KG4 


ti>iji 


r 


^/.. 


^v 


:^^""'^ 


EDiCAl 


'! 


.*     LIBRARY    V7 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/diseasesoflivergOOroll 


PLATE  I. 


DISEASES 

DP 

THE 

VVHR 

GALL-BLADDER 

AND     BILE- DUCTS 

'^                                                                        BY 

H.  D.  ROLLESTON,  M.A.,  M.D.  (Cantab.),  F.R.C.P. 

PHYSICIAN   TO   ST.   GEORGE'S   HOSPITAL,    LONDON;    FORMERLY   EXAMINER   IN 

MEDICINE   IN   THE   UNIVERSITY   OF    DURHAM;    AND   FELLOW  OF 

ST.    JOHN'S   COLLEGE,    CAMBRIDGE,    ENGLAND 

Fully 

Illustrated 

PHILADELPHIA- 

-NEW  YORK-LONDON 

W.   B.  SAUNDERS  AND    COMPANY 

1905 

Copyright,  1904,  by  W.  B.  Saunders  &  Company. 


Eegistered  at  Stationers'  Hall,  London,  England. 


PREFACE. 


During  the  past  twelve  years  I  have  paid  special  attention  to  the 
diseases  of  the  liver,  both  from  the  clinical  and  pathological  points  of 
view.  Some  of  my  observations  have  already  appeared  in  various  med- 
ical journals,  Transactions  of  Medical  Societies,  and  in  articles  on  dis- 
eases of  the  liver  in  Vols.  V  and  VI  of  the  Encyclopsedia  Medica  (in  1900). 

Special  Treatises  often  begin  by  dealing  with  the  normal  anatomy 
and  physiology  of  the  part  concerned,  but  to  be  of  any  real  value  or. 
use  to  the  reader  the  anatomy  and  physiology  of  the  liver  must  be  dealt 
with  in  such  detail  as  would  seriously  add  to  the  bulk  of  the  work,  and 
I  have  therefore  decided  to  omit  any  introductory  chapter  of  this  kind. 
I  have  done  so  with  less  regret  as  I  believe  that  in  most  instances  readers 
refer  to  text-books  or  special  monographs  on  the  anatomy  and  physiology 
of  the  subject  rather  than  to  the  introductory  remarks  at  the  com- 
mencement of  a  clinical  treatise. 

In  the  description  of  each  disease  attention  is  first  directed  to  the 
underlying  morbid  changes  as  without  a  grasp  of  these  it  is  impossible 
to  make  a  rational  diagnosis,  to  treat  the  clinical  manifestations  in  a 
satisfactory  manner,  or  to  give  a  reliable  prognosis.  Selected  cases, 
for  many  of  which  I  am  indebted  to  my  colleagues  at  St.  George's  Hos- 
pital, have  been  embodied  in  the  text,  especially  in  the  parts  dealing 
with  the  symptoms  and  clinical  aspects.  These  cases  and  in  most  in- 
stances statistical  details  have  been  set  in  smaller  print.  The  literature 
of  the  subject  is  enormous  and  though  no  trouble  has  been  spared,  it  is 
inevitable  that  omissions  must  exist.  After  full  consideration  I  have 
decided  to  omit,  in  almost  all  cases,  the  bibliographies  which  had  been 
prepared  and  have  only  retained  the  references  to  authors  actually 
quoted. 

The  illustrations  are  nearly  all  original  and  I  must  cordially  acknowl- 
edge my  gratitude  to  many  past  students  of  St.  George's  Hospital 
for  their  help  in  this  respect,  especially  to  Dr.  E.  A.  Wilson  and 
Mr.  Lawrence  Jones  (coloured  plates,  etc.),  to  Dr.  H.  Spitta  and  Mr. 
S.  G.  Penny  (photo-micrographs),  and  to  Messrs.  P.  L.  and  S.  P. 
Mummery,  Dr.  G.  H.  Goldsmith,  and  Mr.  H.  G.  Drake  Brockman. 
To  Dr.  H.  Morley  Fletcher,  Professor  S.  Del^pine,  and  Dr.  T.  Fisher  I 
am  indebted  for  permission  to  use  or  to  copy  figures  which  have  already 
appeared  elsewhere. 

H.    D.    ROLLESTON, 
November,  1904, 
London,  W. 


CONTENTS. 


DISEASES  OF  THE  LIVER. 


PAGE 


Anatomical  Abnormalities 1 

Some  Postmortem  Appearances  of  the  Liver 5 

Postmortem  Discoloration 5 

Cloudy  Swelling 5 

Foaming  Liver 5 

Acquired  Deformities 8 

Tight-laced  Liver 8 

Tongue-like  Lobes 12 

Displaced  Liver 16 

Hepatoptosis    22 

Functional  Disease  of  the  Liver 36 

Diseases  of  the  Hepatic  Artery 43 

Aneurysm 43 

Embolism   45 

Thrombosis 45 

Arteriosclerosis 46 

Enlargement  of  the  Hepatic  Artery 46 

Diseases  of  the  Hepatic  Veins 47 

Thrombosis 47 

Stricture   48 

Chronic  Periphlebitis  and  Endophlebitis 50 

Suppurative  Phlebitis 51 

Embolism 51 

Thrombosis  of  the  Portal  Vein 52 

Suppurative  Pylephlebitis 67 

Other  Affections  of  the  Portal  Vein 80 

Embolism 80 

Endophlebitis 80 

Calcification   81 

Parasites  in  the  Portal  Vein 82 

Morbid  Conditions  of  Lymphatic  Vessels  and  Glands '83 

Lymphatic  Glands  in  tlie  Portal  Fissure 83 

Chronic  Venous  Engorgement  of  the  Liver 85 

V 


VI  CONTENTS. 

PAGE 

Pericarditic  Pseudo-cirrhosis  of  the  Liver .■ 97 

Infarcts  in  the  Liver 102 

Acute  Congestion  of  the  Liver 109 

Acute  Hepatitis 114 

Hepatic  Abscess 120 

Single  or  Tropical  Abscess 120 

Multiple  Abscess '. 156 

Pygemic  Abscesses 156 

Secondary  Abscesses 159 

Perihepatitis 160 

Acute 160 

Chronic 162 

Universal  Chronic  Perihepatitis 164 

Cirrhosis  of  the  Liver 174 

Classification 174 

Portal  Cirrhosis 178 

Pigmented  Cirrhosis 299 

Cirrhosis  anthracotica 300 

Pigmentary  Cirrhosis  of  Hsemochromatosis 300 

Malarial  Pigmentation  of  a  Cirrhotic  Liver 305 

Biliary  Cirrhosis 306 

Hypertrophic  Biliary  Cirrhosis 306 

Obstructive  Biliary  Cirrhosis 326 

Hepatic  Cirrhosis  in  Children 332 

Tuberculosis  of  the  Liver  and  Bile-Ducts 336 

Syphilitic  Disease  of  the  Liver 347 

Hepatic  Lesions  in  Acquired  Syphilis 347 

Secondary  Manifestations  of  Syphilis  in  the  Liver 347 

Tertiary  Lesions  of  Syphilis  in  the  Liver 350 

Congenital  Syphilis  of  the  Liver 367 

Actinomycosis 381 

Lymphadenoma  Affecting  the  Liver 386 

Hydatid  Cysts 389 

Multilocular  or  Alveolar  Hydatid. 419 

Fatty  Liver 423 

Lardaceous  Disease  of  the  Liver    430 

Pigmentation  of  the  Liver 435 

Intrinsic  Pigments 435 

Extrinsic  Pigments 436 

Calcification  of  the  Liver 437 

Leuksemic  Infiltration  of  the  Liver 439 

Simple  Cysts  of  the  Liver 441 

Cystic  Disease  of  the  Liver 445 


CONTENTS.  Vll 

PAGE 

Adenoma 453 

Single 453 

Multiple 455 

Angioma 461 

Lymphangioma   465 

Myxoma    465 

Fibroma    466 

Lipoma   466 

Embryoma 467 

Teratoma 467 

Malignant  Disease  of  the  Liver 468 

Primary  Malignant  Diseases  of  the  Liver 468 

Varieties  of  Primary  Carcinoma 470 

Varieties  of  Primary  Sarcoma 481 

Starting- Place  of  Sarcoma 484 

Secondary  Malignant  Disease  of  the  Liver 485 

Jaundice   526 

Hsematogenous  Jaundice 528 

Urobilin  Jaundice 529 

Toxaemic,  Intra-hepatic,  or  Hsemohepatogenous  Jaundice 530 

Obstructive  Jaundice 532 

Jaundice  in  the  Newly  Born 557 

Mild  Forms 557 

Severe  Forms 560 

Hereditary  Jaundice 563 

Icterus  Gravis 563 

Acute  Yellow  Atrophy 564 

Jaundice  of  Phosphorus  Poisoning 580 

Infectious  Jaundice 583 

Weil's  Disease 584 


DISEASES  OF  THE  GALL-BLADDER. 

Abnormalities 589 

Acute  Cholecystitis 591 

Forms  of  Acute  Cholecystitis 596 

Acute  Catarrhal  Infective  Cholecystitis 597 

Membranous  Cholecystitis 603 

Suppurative  Cholecystitis 604 

Phlegmonous  Cholecystitis 610 

Gangrenous  Cholecystitis ; 611 

Chronic  Catarrhal  Cholecystitis 613 

Atrophic  Sclerosing  Cholecystitis 615 


Vlll  CONTENTS. 

FAQZi 

Parasitic  Affections  of  the  Gall-Bladder . . .  616 

Innocent  Tumors  of  the  Gall-Bladder 617 

Papilloma 617 

Fibroma    618 

Cystic  Adenoma 618 

Cysts   618 

Fatty  Tumors 619 

Primary  Malignant  Disease  of  the  Gall-Bladder 620 

Secondary  Malignant  Diseases  of  the  Gall-Bladder 637 


DISEASES  OF  THE  BILE-DUCTS. 

Abnormalities 639 

Congenital  Obliteration  of  the  Bile-Ducts 639 

Dilatation  and  Cystic  Tumors  of  the  Bile-Ducts 651 

Simple  Stricture  of  the  Bile-Ducts 653 

Simple  Catarrhal  Jaundice  or  Acute  Catarrhal  Cholangitis 655 

Suppurative  Cholangitis 663 

Chronic  Catarrhal  Cholangitis 670 

Pericholangitis 673 

Intra-hepatic  Pericholangitis  .  .  '. 673 

Parasitic  Affections  of  the  Bile-Ducts 676 

Ascaris  Lumbricoides 676 

Distoma 677 

Psorospermosis 678 

Pentastoma  Constrictum 679 

Paramoecium  Coli 680 

Innocent  Tumors  of  the  Bile-Ducts 681 

Papilloma 681 

Malignant  Disease  of  the  Larger  (Extra-Hepatic)  Bile-Ducts  .  .  683 

Carcinoma  of  the  Ampulla  of  Vater 697 

Cholehthiasis    703 

Classification  of  Gall-Stones 717 

Mode  of  Formation  of  Calculi  in  the  Gall-Bladder 718 

Bihary  Cohc 723 

Mechanical  Effects  of  Gall-Stones 735 

Inflammatory  and  Infective  Changes  Set  Up  by  Gall-Stones  .  .  746 

Intermittent  Hepatic  Fever 750 

BiHaiy  Fistula 756 


Index    773 


DISEASES   OF  THE   LIVER 

GALL-BLADDER  AND 

BILE-DUCTS. 


DISEASES    OF  THE    LIVER. 


ANATOMICAL  ABNORMALITIES. 

ABNORMAL  LOBULATION. 

The  liver  is  sometimes  divided  up  into  a  number  of  lobules  so  as  to 
suggest  a  faint  resemblance  to  the  condition  seen  in  some  animals.  This 
lobulation,  which  is  not  homologous  to  foetal  lobulation  of  the  kidneys, 
is  more  marked  on  the  surface  of  the  larger  right  lobe  than  on  the  left 
lobe.  As  many  as  16  lobules  have  been  found.  (Moser.*)  Wliile  these 
lobules  must  be  distinguished  from  irregularities  and  hobnails  of  portal 
cirrhosis  and  from  cicatrices  manifestly  syphilitic,  it  is  probable  that 
this  lobulation  is  due  to  pathological  conditions  and  is  not  a  morpholog- 
ical phenomenon.  It  may  be  due  to  syphilis,  foetal  peritonitis,  or  pos- 
sibly to  tuberculosis. 

Probably  in  many  of  the  cases  syphilitic  hepatitis  of  congenital  origin 
is  responsible  for  the  change,  but  positive  evidence  to  this  effect  is  very 
often  wanting.  When  lobulation  of  the  liver  is  associated  with  peri- 
toneal adhesions,  it  is  possible  that  peritonitis  during  foetal  life  has 
modified  or  interfered  with  the  growth  of  the  organ  so  as  to  lead  to  As- 
suring and  lobulation  of  its  surface. 

The  view  that  lobulation  of  the  liver  might  be  caused  by  poisons 
manufactured  by  the  Bacillus  tuberculosis  was  put  forward  by  Hanot.f 
who  examined  seven  cases  of  lobulated  livers  in  patients  d3ang  with 
tuberculosis,  and  considered  that  the  lobulation  was  due  to  a  coarse 
fibrosis  induced  by  the  toxines  of  tuberculosis. 


ALTERATION   IN  THE   RELATIVE    SIZE    OF    THE   RIGHT  AND  LEFT 

LOBES. 

Occasionally  the  normal  size  of  the  riglit  or  of  the  left  lobe  is  altered 
with  a  corresponding  change  in  the  relative  and  absolute  size  of  the  other 
lobe. 

In  rare  instances  the  liver,  though  in  its  normal  position,  shows  the 
lobulation  seen  in  transposition  of  the  viscera,  the  right  lobe  being  small 
and  the  left  large;  or  transposition  of  the  lobes  without  situs  transversiis. 

J.  Davy  ±  gives  a  description  of  a  case  in  which  the  left  lobe  was  twice  the  size 
of  the  right. 

*  Moser:  Medical  Record,  May  7,  1898,. p.  671. 
t  Hanot:  Gaz.  des  Hop.,  1893,  p.  902. 
:j:Davy,  J.:  Diseases  of  the  Army,  p.  427. 
1  1 


DISEASES    OF   THE    LIVER. 


In  some  instances  there  is  no  manifest  cause  for  this  reversal  of  the 
normal  lobulation  of  the  liver,  and  it  may  be  supposed  that  it  depends 
on  some  alteration  of  the  circulation  in  foetal  or  early  life.     In  other 


Fig.   1. — LiVEK  with   I.ARfiE  Left  Lobe  axd   Small  Right  Lobe;   ihe  Gall-Bladder  was  on 
THE  Right  Lobe,     (iirawn  by  Dr.  G.  H.  (Joklsmith.) 


-/  Lc+f  Lob  a 


Fig.  2. — Shows  E.vtreme  Dwarfixg  ok  the 
Left  Lobe  of  tmk  Livek.  (Drawn  bv 
Dr.  G.  H.  Goldsmith.) 


Ga.ll  BlaidM 


Fi'..    3. — Shows    Dwauking    of    Li:ft    LoitE. 

GaLL-BI.ADDEK  PK0.IECTS   FROM   THE   LEFT 

Margin  of  the  Liver  and  has  its  Long 
Axis  in  the  Transversf,  Axis  of  tmk 
Bonv.     (Drawn  bv  Dr.  (i.  H.  Goldsniilli. ) 


instances  the  diminution  in  size  of  the  right  lobe  is  manifestly  due  to 
syphilitic  changes  leading  to  cicatricial  contraction. 


ANATO:\IICAL    ABNORMALITIES.  O 

Penrose  *  records  this  in  acquired  syphilis  and  Lazarus-Barlow  f  in  tardi\e 
congenital  syphilis. 

Dwarfing  of  the  left  lobe  is  occasionally  seen;  it  may  be  merely  repre- 
sented by  a  little  flap  of  hepatic  tissue.  In  these  cases  the  left  lateral 
ligament  is  correspondingly  small  and  the  falciform  ligament  arises 
from  the  left  margin  of  the  liver.  The  stomach  is  thus  abnormally  ex- 
jjosed,  and  the  whole  of  the  gall-bladder  is  visible  from  the  front  and 
projects  from  the  left  lateral  margin  of  the  liver.  Owing  to  the  dis- 
turbed relation  of  the  lobes  the  gall-bladder  may  be  so  displaced  as  to 
lie  with  its  long  axis  in  the  transverse  axis  of  the  body.     (Vide  Fig.  3.) 

There  is  seldom  any  very  manifest  reason  why  the  left  lobe  should 
he  so  atrophied,  and  it  may  again  be  suggested  that  it  is  due  to  some 
disturbance  of  the  circulation  in  foetal  or  in  early  life.  The  change  may 
be  associated  with  other  congenital  defects. 

In  a  case  reported  by  Garrod  f  extreme  dwarfing  of  the  left  lobe  was  associated 
with  lobulation  of  the  right  lobe  of  the  Uver  and  the  presence  of  two  instead  of 
three  aortic  A-alves. 

In  other  instances  atrophy  of  the  left  lobe  ma}^  be  due  to  syphilis 
or  to  other  pathological  changes  taking  place  later  in  life. 

I  have  seen  atroph}^  of  the  left  lobe  in  a  case  whei"e  a  large  intra-hepatic  cal- 
culus pressed  upon  the  A-essels  entering  the  left  lobe  of  the  liver. 

MINUTE  ACCESSORY  LOBES. 

Small  projections  of  liver  substance — about  the  size  of  the  terminal 
phalanx  of  the  forefinger — which  in  miniature  imitate  the  caudate  lobe, 
are  quite  common  and  of  no  importance  or  pathological  significance. 
Their  usual  situation  is  the  under  surface  of  the  right  lobe,  near  the  por- 
tal and  longitudinal  fissures.  When  markedly  pedunculated,  they  ma}- 
form  "accessory  livers."  The  Spigelian  lobe  is  sometimes  curiously 
pedunculated. 

There  is  a  cast  in  the  Anatomical  Museum  at  Cambridge  of  a  pedunculated 
lobe  attached  to  the  left  border  of  the  left  lobe;  the  pedicle  is  composed  of  hepatic 
tissue.  Lawrence  and  Nabarro  §  described  an  abnormal  process  from  the  left  lol^e 
of  the  liver  in  association  with  absence  of  the  inferior  vena  cava  in  a  female  child 
aged  fourteen  weeks. 

Accessory  Livers. — Isolated  fragments  of  hej^atic  tissue  or  "rests" 
have  Ijeen  fouiid  in  the  su'spensory  ligament;  but  it  is  noteworthy  that 
they  are  very  rarely  seen.  This  contrasts  with  the  frequency  of  accessory 
suprarenal  bodies  and  of  splenunculi. 

Pepere  ||  has  recently  described  a  remarkable  case  in  which  there  were  innumer- 
able small  nodules  of  hepatic  tissue  or  accessory  Uvers  scattered  over  the  poritonomn 
and  great  omentum.  One  with  a  diameter  of  7  cm.  formed  a  sf)lifarv  adenoma 
in  the  liver.     Thirty-one  years  previously  Wagner**  described  a  munl)orol'  nodules 

*  Penrose:  Trans.  Path.  Soc,  vol.  xl,  p.  133. 
t  Lazarus-Barlow:  Trans.  Path.  Soc,  vol.  1,  p.  l.")S. 
X  Garrod,  A.  E.:  Ibid.,  vol.  xlviii,  p.  42. 

§  LawTence  and  Nabarro:  Journ.  of  Anatomy  and  Physiology,  vol.  xxwi,  p.  (i3. 
!|  Pepere:  Archiv  per  le  Se.  Med.,  li)()'2,  vol.  x\\i,  ji.  LI  7. 
**  Wagner:  Archiv  dor  Heilkunde,  ISGI. 


4  DISEASES    OF   THE    LIVEE. 

composed  of  liver  cells  in  the  falciform  ligaments  of  two  infants  aged  nine  days 
and  two  months  respectively. 

Chaillous  *  has  described  a  large  accessory  lobe  attached  to  the  anterior  border 
of  the  liver,  to  the  right  of  and  close  to  the  falciform  ligament,  on  a  level  mth  the 
quadrate  lobe;  it  was  pear-shaped,  like  the  gall-bladder.  It  was  found  in  the 
body  of  an  infant. 

Davy,t  in  the  examination  of  a  man  aged  twenty-three,  dead  of  dysentery, 
found  a  small  mass  about  the  size  of  a  hazelnut,  the  structure  of  which  appeared 
to  be  the  same  as  that  of  the  li-\-er,  attached  to  the  concave  sui'face  of  that  organ 
by  a  dehcate  pedicle. 

Mahomet  J  described  an  accessory  hver  attached  to  the  tip  of  the  gall-bladder 
in  a  case  of  cirrhosis;  the  accessor}^  hver  was  also  cirrhotic.  I  have  seen  a  somewhat 
similar  condition  in  a  lardaceous  liver. 

Accessory  livers  may  also  be  produced  by  atrophy  of  the  liA'er  cells 
in  the  pedicles  of  the  minute  accessory  lobes  so  commonly  seen  on  the 
under  surface  of  the  liver,  with  the  result  that  a  small  peritoneal  liga- 
ment unites  the  accessoiy  liver  to  the  main  organ. 

It  seems  possible  that  some  detached  lobes  seen  in  adult  life  maj^ 
be  due  to  the  effects  of  pressure  or  to  atrophy  of  some  of  the  liver  tissue 
from  interference  with  the  blood-supply.  Constriction  lobes  attached 
to  the  lower  extremity  of  the  right  or  more  rarely  the  left  lobe  are 
described  under  the  deformities  of  the  liver  clue  to  tight  lacing.  (Vide 
p.  8.)  The  following  may  be  regarded  as  examples  of  atrophy  of  the 
intervening  liver  tissue  inducing  the  appearances  of  an  accessory  lobe. 

In  a  specimen  in  St.  George's  Hospital  Museum  the  part  of  the  hver  representing 
the  left  lobe  is  completely  separated  for  a  distance  of  3  inches  from  the  rest  of  the 
liver;  it  was  also  attached  by  a  kind  of  mesentery  to  the  cardiac  end  of  the  stomach.  § 

In  a  man  aged  twenty-four  there  was  a  vestige  only  of  the  left  lolae,  which 
was  not  continuous  with  the  right  lobe.      (Davy.  || ) 

Atrophy  may  involve  the  base  of  attachment  of  the  Spigehan  or  pos- 
sibly of  the  caudate  lobe  and  so  lead  to  a  pedunculated  lobe.  Davy  ** 
described  a  pedunculated  Spigelian  lobe. 

It  may  be  mentioned  that  between  the  peritoneal  layers  of  the  left 
lateral  Hgament  the  remains  of  a  rudimentary  lobe  can  be  seen  in  the 
presence  of  hepatic  and  portal  vessels,  though  the  liver  cells  have  disap- 
peared. 

*  ChaiUous:  BuU.  de  la  Soc.  Anat.,  Paris,  1898,  p.  572. 
t  Davy,  J. :  Diseases  of  the  Army,  1862,  p.  428. 
t  Mahomet:  Trans.  Path.  Soc,  vol.  xxviii,  p.  147. 

iSeries  ix,  161a.  See  also  Dickinson,  AV.  H.:  Trans.  Path.  Soc,  London, 
vol.  xvi,  p.  160. 

II  Davy,  J.:  loc.  cit.  **  Davy,  J.:  Diseases  of  the  Army,  p.  427- 


SOME  POSTMORTEM  APPEARANCES  OF  THE  LIVER. 

A  few  words  may  be  said  about  certain  common  though  striking  post- 
mortem appearances  of  the  liver,  which  will  not  be  described  elsewhere 
in  this  work. 

POSTMORTEM  DISCOLORATION. 

The  surface  of  the  liver  where  it  has  been  in  contact  with  the  stomach 
or  colon  very  commonly  shows  dark  purjole  stains.  These  stains,  which 
are  produced  after  death  and  are  quite  superficial,  are  due  to  the  action 
of  gases,  among  them  sulphuretted  hydrogen,  which  diffuse  through  from 
the  colon  and  stomach  and  meet  with  iron  in  the  liver;  as  a  result,  some 
compound  like  sulphide  of  iron  is  manufactured. 

Irregular  white  areas  on  the  surface  of  the  liver  are  seen  in  cases 
of  fevers  and  other  infections,  and  show  congestion  and  degenerative 
changes.  This  appearance  was  formerly  thought  to  be  merely  due  to 
mechanical  pressure  exerted  after  death  in  laying  out  the  body. 

CLOUDY  SWELLING. 

This  is  a  very  frequent,  if  not  the  commonest,  change  seen  in  the  liver 
in  routine  postmortem  work.  The  liver  is  enlarged,  heavier  than  normal, 
and  looks  as  if  it  had  been  boiled,  and  has  a  duller,  more  opaque,  and  paler 
aspect  than  normal.  These  changes  are  due  to  cloudy  swelling  or  paren- 
chymatous inflammation  of  the  liver  cells  set  up  by  the  toxines  of  numer- 
ous diseases.  The  changes  which  are  shared  by  other  organs,  such  as 
the  kidneys  and  myocardium,  are  especially  well  seen  in  pneumonia. 
In  this  disease  the  enlargement  of  the  liver  is  very  considerable.  Long 
ago  Bright  *  thought  that  the  pneumonic  lung  materially  depressed  the 
liver,  but  it  is  clear  that  any  increased  hepatic  dullness  below  the  costal 
arch  is  mainly  clue  to  cloudy  swelling  and  congestion. 

FOAMING  LIVER. 

Synonym :  Emphysematous  Liver. 

The  formation  of  gaseous  cysts  in  the  internal  organs  has  long  been 
recognized  and  was  formerly  put  down  to  putrefaction.  This  change 
was  shown  by  Welch  and  Nuttall,t  in  1892,  to  be  due  to  a  micro-organism 
— the  Bacillus  aerogenes  capsulatus.  The  infection  with  this  micro- 
organism is  generally  a  secondary  and  terminal  event;  in  other  words, 
this  bacillus  follows  in  the  wake  of  other  pathogenic  bacteria  and  does 
not  appear  till  the  patient  is  moribund.  To  these  general  rules  there 
are   exceptions.     Pure   cultures   of  the   Bacillus   aerogenes   capsulatus 

*  Bright,  R.:  Abdominal  Tumors,  p.  255.     New  Sydenham  Society. 
t  Welch  and  Nuttall:  Bull.  Johns  Hopkins  Hosp.,  1892,  vol.  iii,  p.  8L 


0  DISEASES    OF    THE    LIVER. 

hsLxe  been  obtained  by  Pratt  and  Fulton,*  and  by  Pakes  and  Bryant  ;t 
while  from  a  case  of  infective  endocarditis  G-\Aynl  rejDeatedly  isolated 
the  micro-organism  from  the  blood  during  life. 

The  micro-organism  may  be  present  and  yet  not  give  rise  to  any 
formation  of  gas;  this  was  shown  in  the  cases  recorded  by  GTsyn  and  by 
Pratt  and  Fulton.  Though  this  infection  ma}'  occur  in  the  bod}^  during 
hfe,  there  is  no  evidence  that  it  ever  produces  gas  until  death  has  occurred. 
The  micro-organism  may  give  rise  to  necrosis  of  the  cells  of  the  liver 
and  to  purulent  inflammation,  as  was  shown  in  Pratt's  and  Fulton's 
case  of  cholangitis  with  multiple  abscesses  in  the  liver. 

The  Bacillus  aerogenes  capsulatus  is  anaerobic,  and  must  be  distin- 
guished from  the  bacillus  of  malignant  oedema.  It  stains  ^\dth  Gram's 
method.  It  is  very  frec^uently  present  in  the  alimentary  canal,  and  has 
been  found  to  be  wideh'  distributed  in  nature. 

Besides  the  Bacillus  aerogenes  capsulatus,  other  gas-producing  bac- 
teria must  be  taken  into  account;  thus,  the  colon  bacillus  (Ivanthack, 
Pakes  and  Bryant)  and  other  members  of  the  aerogenes  group,  such  as 
the  Bacillus  mucosus  capsulatus  (W.  T.  Howard,  Jr.§),  .have  been 
described  as  giving  rise  to  gaseous  C3'sts.  Welch,  however,  is  rather 
sceptical  about  their  claim  to  be  regarded  in  this  light. 

The  liver  is  the  organ  most  frequently  affected.  In  23  cases  tabulated 
by  Pakes  and  Brj^ant,  this  organ  was  affected  in  15. 

Etiology. — As  the  formation  of  gaseous  cysts  is  a  death  agony  or 
postmortem  phenomenon,  the  BaciUus  aerogenes  capsulatus  is  often 
foimd  in  association  with  other  micro-organisms.  Other  micro-organisms 
probably  favour  the  development  of  the  BaciUus  aerogenes  capsulatus 
by  diminishing  the  bactericidal  power  of  the  blood,  and  also  by  reducing 
the  resistance  of  parts  of  the  liver.  ]\Iy  friend.  Dr.  J.  H.  Drysdale,  has 
commimicated  to  me  his  unpublished  results,  which  show  that  hot 
weather  is  a  factor  in  the  production  of  foaming  liver,  but  that  this  con- 
dition may  occur  in  the  absence  of  any  of  the  ordinary  signs  of  decom- 
position. It  is  found  much  more  frecjuently  when  there  has  been  recent 
loss  of  blood,  which  seems  to  favour  the  entrance  of  the  micro-organisms 
into  the  blood  or  their  development  in  it.  Ulceration  and  injurj-  of  the 
intestines  also  favour  the  entrance  of  the  micro-organisms,  which  are 
commonly  present  in  the  alimentary  canal,  into  the  tissues  of  the  body. 
Incubation  of  livers,  taken  at  random  from  the  postmortem  room,  did 
not  give  rise  to  the  formation  of  gaseous  cysts,  but  incubation  of  livers 
from  cases  of  haemorrhage  gave  positive  results  showing  that  the  micro- 
organisms had  got  into  the  organs. 

It  is  generally  recognized  that  the  infection  of  the  liver  may  take 
place  either  by  the  blood-stream  or  b}'  the  bile-ducts.  Infection  most 
commonly  arrives  by  the  portal  vein,  and  is  due  to  some  lesion,  such  as 
ulceration,  in  the  intestinal  tract.     The  inlet  of  infection  may  be  in 

*  Pratt  and  Fulton:  Boston  Med.  and  Surgical  Journ.,  June  7,  1900,  p.  599. 

t  Pakes  and  Brvant:  Guv's  Hosp.  Reports,  vol.  liv. 

1  Gw-vn:  Bull.  Johns  Hopkins  Hosp.,  1S99,  vol.  x,  p.  134. 

§  W.T.  Howard,  Jr.:  Journ.  of  Experiment  Med.,  Oct.  25,  1900,  p.  139. 


SOME    POST.AIORTEM    APPEARANCES    OF   THE    LIVEH.  < 

other  situations,  such  as  the  uterus  or  the  urethra.  iJirect  infection  of 
the  bile-duct  and  gall-bladder  from  the  intestine  may  occur.  In  such 
instances  the  bile-ducts  and  gall-bladder  may  contain  gas  either  in  their 
lumen  or  in  the  substance  of  their  walls,  especially  in  the  submucous  coat. 
AVelch*  has  met  with  five  cases  of  interstitial  emphysema  of  the  bile- 
duct  or  gall-bladder. 

Although  the  gas-producing  micro-organisms  may  give  rise  to  a 
septicaemia  and  be  isolated  from  the  blood,  it  is  doubtful  whether  forma- 
tion of  gas  occurs  in  the  living  tissues.  It  may  occur  very  rapidly  after 
death,  or,  as  shown  in  emphysematous  gangrene,  in  a  part  of  the  body 
that  has  lost  its  vitality.     On  reviewing  the  whole  subject  Welch  is 


I'iG.  4. — Photomicrograph  oka  Foamimj  J^ivku,  siiiiwing  Mixutk  (iAsi:ous  Spaces  Linkp  nv  the 
Bacillus  aeeogexes  capsulatvs.     X  1000.     (By  Dr.  U.  Spitta.) 

inclined  to  the  view  that  gas  is  formed  in  the  viscera  before  death.  Clin- 
ically it  has  been  thought  that  tym]ianites  may  be  due  to  the  formation 
of  gas  before  death. 

The  liver  is  in  a  spongy  condition  from  the  presence  of  a  mmil^er  of 
small  gas-containing  cysts  of  various  sizes,  but  mostly  small.  The  organ 
is  usually  of  a  somewhat  grayish  colour  from  its  inflated  condition, 
which  must  not  be  mistaken  for  multiple  cystic  disease.  The  condition 
may  also  be  met  with  in  other  organs— the  kidneys,  brain,  spleen,  in- 
testines, pancreas.  Some  recorded  cases  of  widespread  cystic  change  in 
tlie  organs  of  the  l)ody  may  haA'e  been  of  this  nature. 

*  For  a  full  re.sume  of  tlie  entire  subject  tlie  reader  i^hould  refer  to  Welch's 
Shattuck  Lecture  for  1900,  Philadelphia  Medical  Journ.,  Aug.  4,  1900,  p.  202. 


ACQUIRED  DEFORMITIES. 

TIGHT-LACED  LIVER. 

Synonym:  Corset  Liver. 

Modifications  in  the  shape  of  the  liver  due  to  tight  lacing,  corsets, 
and  belts  are  of  course  common  in  women,  but  considerable  deformity 
may  be  produced  in  men  by  the  pressure  of  a  tight  belt  or  strap.  The 
effect  of  tight  lacing  on  the  liver  varies  to  a  certain  extent  with  fashion, 
or,  in  other  words,  with  the  position  of  the  waist.  Following  Hertz,* 
who  has  studied  the  changes  produced  by  tight  lacing  in  great  detail, 
the  deformities  of  the  liver  may  be  divided  into  two  main  types,  though 
inixed  or  transitional  forms  may  occur. 

I.  The  liver  is  flattened  and  elongated  from  above  downwards  so  that 
the  upper  or  diaphragmatic  surface  is  diminished  while  the  anterior  is 
increased.  From  its  larger  size  the  right  lobe  naturally  shows  the  change 
more  than  the  left.  The  liver  thus  forms  a  flap  which  covers  the  ab- 
dominal viscera,  though  occasionally  coils  of  intestine  may  pass  in  front 
of  it.  AA^iere  the  elongated  right  lobe  passes  over  the  right  kidney  there 
are  atrophy  of  the  hepatic  substance  and  thickening  of  the  capsule,  which 
is  opaque  and  forms  a  hinge-like  ligament  between  the  main  part  of  the 
right  lobe  above  and  the  constricted  lower  portion.  This  lobe  is  variously 
termed  partial  hepatoptosis,  constriction  lobe,  or  the  sustentacular  for- 
mation of  the  right  lobe  (Hertz).  The  constriction  furrow  is  produced 
by  the  pressure  of  the  corset  in  front  and  the  resistance  of  the  kidney 
behind.  The  constriction  lobe  tapers  to  a  point  so  that  the  shape  of 
the  liver,  as  seen  from  the  front,  is  that  of  a  right-angled  triangle  with 
the  apex  do'\;\Ti wards.  This  lobe  is  often  associated  with  an  unduly 
movable  or  floating  kidney.     (Keith. t) 

Clinically  there  is  a  close  resemblance  between  these  constriction 
lobes  of  the  right  lobe  and  the  tongue-shaped  or  Riedel's  lobe,  originahy 
described  as  occurring  in  special  association  with  gall-stones.  The  left 
lobe  is  prolonged  downwards  in  the  same  manner,  though  to  a  less  marked 
degree,  and  may  even  have  a  constriction  lobe  attached  to  it.  It  has 
been  thought  that  in  the  latter  event  the  symptoms  were  much  more 
marked  than  in  cases  where  the  ordinary  tongue-like  lobes  from  the 
right  lobe  were  present.  A  tongue-like  lobe  arising  from  the  left  lobe 
of  the  liver  would  tend  to  exert  pressure  on  the  pylorus,  duodenum, 
pancreas,  and  nerve  plexuses  which  are  supported  behind  by  the  spine. 
Mobile  on  the  right  side  no  important  viscera  or  structures  would  suffer, 
though  the  lobe  would  probably  be  in  contact  with  the  right  kidney. 

*  Hertz,  P.:  Abnormitaten  in  der  Lage  und  Form  der  Bauchorgane  bei  dem  er- 
wachsenen  Weibe,  Berlin,  1894. 

t  Keith,  A.:  Lancet,  1903,  vol.  i,  p.  711. 

S 


ACQUIRED    DEFORAIITIES. 


9 


From  impaired  nutrition  and  diminished  resistance  the  constriction 
lobe  may  be  more  markedly  affected  b}^  morbid  changes  than  the  rest 
of  the  liver,  or  may  even  be  the  only  part  affected.  Thus,  fibrosis  or 
gummatous  change  may  be  confined  to  a  constriction  lobe,  or  secon- 
dary new  gro'U'th  may  be  wholly  or  chiefly  limited  to  the  pendulous 
lobe. 

In  a  case  of  carcinoma  of  the  mamma  in  a  woman  who  died  of  diabetes  the 
constriction  lobe  contained  large  masses  of  secondary  growth,  while  in  the  re- 
mainder of  the  liver  there  were  only  two  small  nodules.  Frerichs*  figures  a  similar 
case 

On  the  other  hand,  the  interference  with  the  l^lood-suppty  may  to 
some  extent  protect  the  constriction  lobe  against  infection  by  the  blood- 
stream. 


Fifi.  5.— CoxsTRicTiox  Lobe  Attached  to  the  Right  Lobe  of  the  Livke,  Divided,  and  ns 
Halves  Sepakated  so  as  to  Display  Largjc  Secondary  Carcinomatous  Nodules  in  ns 
Substance,     l-'rom  case  descriljed  in  the  text.     (Drawn  by  L.  Jones,   M.B.,  K.  R.C.S.) 


In  1890  I  examined  after  death  the  body  of  a  man  who  died  with  carcinoma 
of  the  pylorus;  the  liver  weighed  nine  pounds  and,  except  the  constriction  lobe, 
attached  to  the  right  lolje,  was  full  of  secondary  new  gro\rths. 

The  whole  of  the  li^'e'r,  con.striction  lo1)e  included,  may  be  uniformly 
affected  b}'  cirrhosis. 

II.  In  the  second  variety  of  tight-laced  liver  the  organ  is  displaced 
upwards  as  a  whole  and  lies  high  up  in  the  abdominal  cavity.  It  is 
thicker  above  than  below,  and  is  curved  and  moulded  over  the  spine  so 
that  the  left  lobe  may  touch  or  even  overlap  the  spleen.  Frerichs  f  figures 
such  a  case  in  which  the  left  lobe  of  the  liver  and  the  spleen  were  firml}" 

*  Frerichs:  Diseases  of  the  Li\-er,  \ol.  ii,  p.  .326.  Translation  in  New  Syden- 
ham Society's  Library. 

t  French;^:  Diseases  of  the  Liver,  vol.  i,  p.  41.     Transl.  New  Sydenham  Soc. 


10 


DISEASES    OF   THE    LIVER. 


united  to  each  other.  The  fossa  for  the  inferior  vena  cava  is  exaggerated 
and  deepened,  while  as  the  result  of  pressure  the  right  kidney  is  displaced 
downwards  and  its  lower  end  tilted  forwards.  The  lower  margin  of  the 
right  lobe  being  compressed  by  the  corset  or  belt,  is  atrophied  in  the 
transverse  direction,  and  shows  opacity  and  thickening  of  the  capsule 
from  local  perihepatitis.  A  triangular  constriction  lobe  may  be  found 
attached  to  the  right  lobe,  but  is  not  such  a  constant  feature  as  in  the 
previous  form,  and  is  never  present  in  connexion  with  the  left  lolDe. 

Besides  being  met  with 
in  women,  this  change 
in  the  liver  may  be  met 
with  in  men  who  wear  a 
tight  belt. 

Diaphragmatic  Sul- 
ci.— When  extreme,  tight 
lacing  or  the  pressure  of 
a  belt  may  exercise  so 
m  u  c  h  circumferential 
pressure  in  an  upward 
direction  as  to  throw  the 
convex  surface  of  the 
liver  into  folds.  The 
curve  of  the  convexity 
is  increased,  and  a  num- 
ber of  furrows  appear  on 
the  upper  surface  of  the 
right  lobe  and  in  rare 
instances  on  the  left  lobe ; 
there  may  be  as  many 
as  six  of  these  furrows. 
They  run  anteroposteri- 
orly  and  are  deeper  posteriorly.  When  due  to  the  pressure  of  a  belt,  a 
transverse  band  of  thickening  of  the  liver  capsule  will  be  found  near  the 
anterior  inferior  margin  of  the  liver.*  These  furrows  have  been  called 
"diaphragmatic  furrows"  by  Zahn,t  who  explains  them  as  the  impress 
left  by  hypertrophied  bundles  of  the  diaphragm  and  not  due  to  pressure. 
The  change  in  the  diaphragm  is  due  to  chronic  diseases  of  the  respiratory 
system,  with  which  these  furrows  are  said  to  be  frequently  associated. 
In  58  cases  from  the  Salpetriere  showing  these  furrows  there  were  only 
5  in  which  the  lungs  were  healthy.     (Seglas.J) 

It  is  improbable  that  they  are  due  to  pressure  exerted  by  the  ribs, 
inasmuch  as  the  sulci  do  not  correspond  to  the  position  of  the  ribs. 

Bagaloglu  §  has  described  a  single  deep  furrow  on  the  upper  surface  of  the 
liver  which  had  no  relation  to  either  the  ribs  or  the  diaphragm  and  was  not  tlie 
result  of  cicatrization.     He  regarded  it  as  directly  due  to  the  pressure  of  the  corset. 

*  Weber,  F.  P.:  Trans.  Path.  Soc,  vol.  xlviii,  p.  113;  vol.  li,  p.  236. 
t  Zahn:  Rev.  Med.  de  la  Suisse  Romande,  1882,  p.  19. 
J  Seglas:  Bull.  Soc.  Anat.,  Paris,  1886,  p.  163. 
§  Bagaloglu:  Ibid.,  Paris,  1899,  p.  67. 


Fig.  6. — TiijHT-laced  Liver  Uniformly  Cirrhotic. 

There  are  two  small  cysts  on  the  right  lobe.  From  a  woman 
forty-four  years  old  who  died  with  grave  anfemia.  The 
liver  weighed  forty-one  ounces.  (Drawn  by  P.  L.  Mummery, 
M.B.,F.K.C.S.) 


ACQUIRED    DICFORAIITIES.  11 

Furrows  of  this  kind  seen  in  fa'tuses,  antl  possiljly  due  to  pressure 
in  utero,  must  be  distinguished  from  those  due  to  herechtary  syphihs. 
My  own  opinion  is  that  these  diaphragmatic  sulci  are  chief!}'-  due  to 
pressure. 


Cirrhosis  ma}^  superven*  in  a  liver  the  subject  of  tight  lacing,  and 
give  rise  to  a  uniform  change.  {Vide  Fig.  6.)  Local  changes  probably 
due  to  chronic  venous  engorgement,  and  resulting  in  fibrosis,  may  occur 
in  the  portion  of  the  liver  below  the  tight-lacing  constriction. 

Clinical  Features. — Tight-laced  livers  are  often  associated  with 
dyspepsia,  which  may  be  partly  due  to  the  abdominal  or  gastric  em- 
barrassment produced  by  a  tight  corset.  In  other  cases  the  symptoms 
are  clue  to  visceroptosis,  which  is  often  associated  with  tight  lacing. 
Keith*  has  insisted  on  the  importance  of  tight  lacing  as  a  cause  of  gall- 
stones, and  symptoms  of  cholelithiasis  are  not  uncommon  in  patients 
who  have  tight-laced  livers.  But  in  a  very  considerable  proportion  of 
patients  with  livers  deformed  by  tight  lacing  no  symptoms  referable  to 
that  organ  are  present.  A  point  of  considerable  interest  about  tight- 
laced  or  corset  livers  is  that  the  constriction  lobe  may,  when  accidentally 
detected,  be  easily  mistaken  for  something  more  important,  such  as  a 
floating  kidney,  a  tumor  of  the  pylorus  or  transverse  colon,  a  dilated 
gall-bladder,  cysts  of  the  pancreas  or  of  the  mesentery,  or  in  extreme 
cases  for  a  fibromyoma  of  the  uterus,  an  ovarian  tumor,  or  appendicitis. 
The  connecting  bridge  between  the  constriction  lobe  and  the  main  part 
of  the  liver,  as  has  already  been  pointed  out,  is  sometimes  very  thin, 
and  may  therefore  give  a  resonant  note  on  percussion,  and  its  actual 
continuity  with  the  remainder  of  the  organ  is  therefore  difficult  to  make 
out. 

Treatment. — As  a  rule,  no  active  treatment  for  the  constriction  lobe 
is  either  required  or  justifiable;  tight  lacing  should  as  far  as  possible  be 
prevented,  but  the  practitioner  requires  considerable  tact  to  effect  this 
reform.  A  straight-fronted  corset  should  be  substituted  for  one  which 
tends  to  constrict  the  waist  and  depress  the  liver.  A  properly  adjusted 
belt  should  be  fitted  in  cases  where  there  is  definite  enteroptosis  with 
symptoms  due  to  this  cause.  Dyspeptic  and  other  associated  symp- 
toms should  be  carefully  attended  to  and  constipation  prevented.  In 
cases  where  the  constriction  lobe  is  the  seat  of  much  pain  it  has  been 
removed,  but  this  can  seldom  be  really  necessa^^^  In  such  cases  Bot- 
ticher  f  considers  that  hepatopexy,  or  fixation  of  the  constriction  lobe, 
is  a  more  satisfactory  method  of  surgical  treatment. 

*  Koith,  A.:   Lancet,  1903,  vol.  i,  p.  639. 

t  Botticher:  Deutsche  Zeitschrift  f.  Chirurg.,  July,  1900,  vol.  Ivi. 


12  DISEASES    OF   THE    LIVER. 


TONGUE-LIKE  LOBES. 

Synonyms:  Linguiform   Lobe,   Riedel's   Lobe,   Partial   Hepatoptosis,    Floating   or 

Appendicular  Lobe. 

Although  the  term  partial  hepatoptosis  has  been  employed,  this  con- 
dition is  quite  distinct  from  complete  hepatoptosis  or  wandering  liver, 
as  there  is  no  dropping  of  the  organ  as  a  whole.  No  doubt  confusion 
between  the  two  conditions  has  occurred;  Glenard  considers  that  the 
reputed  greater  incidence  of  wandering  liver  in  women  depends  on  the 
fact  that  some  observ-ers  have  erroneously  described  tongue-like  lobes 
as  wandering  livers.  These  lobes,  which  are  often  spoken  of  as  Riedel's, 
are  really  much  the  same  as  the  constriction  lobes  just  described  {vide 
p.  8)  in  the  account  of  the  corset  liver.  It  has  been  thought,  espe- 
cially by  Riedel,*  that  the  tongue-shaped  lobes  are  dependent  on 
disease  of  the  gall-bladder,  such  as  inflammation,  gall-stones,  distention, 

traction  exerted  by  pericholecystic  adhe- 
sions. But  this  explanation  does  not  apply 
to  all  the  cases. 

It  is  possible  that  some  of  the  cases  of 
do\\TLward  projection  of  the  right  lobe  are 
connected  with  or  depend  on  a  congenital 
anatomical  variation.  This  suggestion  ap- 
plies forcibly  to  cases  where  this  formation 
is  found  in  babies  or  young  children.  As 
pointed  out  by  Fisher,!  there  is  a  consider- 
able amount  of  variability  in  the  outline 
Fig.  7.— a  well-map.ked  Example     of  the  right  lobe,  and  exaggeration  of  this 

OF  Riedel's  Tongue-like  Lobe.  •    i  j.  •  ^       ^ 

(After  Dr.  T.  Fisher.)  migJit  occur  as  an  occasioual  abnormality 

without  any  determining  irritation  or  trac- 
tion on  the  part  of  the  underlying  gall-bladder.  Possibly  the  formation 
of  Riedel's  lobe  in  some  cases  of  cholelithiasis  and  its  absence  in  other 
cases  depend  on  degrees  of  variability  in  the  outUne  of  the  right  lobe  of 
the  liver. 

Dr.  Fisher  has  kindly  sent  me  a  dra^^ing  of  a  potential  Ptiedel's  lobe  in  a  woman 
aged  twenty-five  whose  gaU-bladder  was  normal;  and  I  find  that  six  years  ago 
I  observed  a  similar  abnormal  lobulation  in  the  body  of  a  man  aged  fiftj^-eight. 
If  gall-bladder  disease  arises  in  such  cases,  a  Riedel's  lobe  would  probably  develop 
much  more  readily  and  rapidly  than  in  a  normal  liver.  McPhedran  %  described 
seven  cases,  and  regarded  the  tongue-hke  lobes  as  developmental  and  not  artificial. 
One  of  his  cases  was  in  a  baby  of  eleven  months. 

Tight  lacing  must  also  be  taken  into  account,  especially  as  by  dis- 
placing the  fundus  of  the  gall-bladder  downwards  it  may  lead  to  kinking 
and  occlusion  of  the  cystic  duct  and  so  to  obstruction  to  the  outflow  of 
the  contents  of  the  gall-bladder — a  state  of  affairs  which  favours  catarrhal 
inflammation  and  the  production  of  gaU-stones.     (Keith.  §) 

*  Riedel:  Berlin.  kUn.  Wochen.,  1888. 
t  Fisher,  T.:  Bristol  Mechco-Chirurg.  Journ.,  Sept.,  1901. 
%  McPhedran:  Canadian  Practitioner,  June,  1896. 

§  Keith,  A.:  The  Anatomy  of  Glenard's  Disease.  The  London  Hospital  Gaz., 
Oct.,  1902,  p.  55. 


ACQUIRED    DEFOR-MITIES. 


13 


Incidence. — Tongue-shaped  lobes  are  much  more  frequent  in  women. 
This  depends  on  their  causation,  both  tight  lacing  antl  cholelithiasis 
being  much  commoner  in  that  sex. 

Anatomy. — The  tongue-shaped  lobes  may  either  taper  off  gradually 
into  an  elongated,  thick  process  from  the  right  lobe,  or  the  connecting 
pedicle  may  be  reduced  to  two  layers  of  somewhat  thickened  peritoneum. 
In  the  latter  case  the  tongue-like  lobe  is  freely  movable,  and  during  life 
may  appear  to  be  quite  distinct  from  the  liver.  The  gall-bladder  may, 
but  need  not,  be  situated  on  the  under  surface  of  the  tongue-like  lobe, 
as  in  two  cases  excised  during  life  (Martin,  Bastianelli);  the  cystic  duct 


Section  through  right  lobe  showing  abscesses 
aud  some  healthy  liver. 


h'"  A 


Right  lobe, 
upper  surface. 


W-'  Left  lobe, 
upper 
suiface. 


-^z^' 


Round  ligament, 
iedel's  lobe. 


Fig.  S. — Snows  the  Livek  with  Riedel's  Tongue-like  Lobe  and  Areas  ov  Supihration  due 

TO  Suppurative  Cholangitis. 

From  a  case  of  cholecysto-colic  fistula  due  to  gall-stones.     (Drawn  by  Dr.  E.  A.  Wilson.) 

will  then  run  across  the  pedicle.  As  a  rule,  the  tongue-like  lobe  is  not 
perfectly  normal  in  structure;  from  repeated  attacks  of  congestion  it 
may  show^  fibrosis,  and  degeneration,  atrophy,  and  pigmentation  of  the 
liver  cells,  and  haemorrhages.  It  has  been  found  to  be  affected  with 
gummata  when  the  remainder  of  the  liver  was  healthy,  and  may  be  the 
seat  of  secondary  new-growth.     (Compare  p.  9.) 

Koux  *  has  described  primary  carcinoma  starting  in  a  tongue-like  lobe.  In  his 
case  t  here  was  calrulous  cholecystitis.  In  similar  cases  care  must  be  taken  to  see 
tliat  the  <ir()\vtli  docs  not  start  in  what  is  a  much  commoner  situation,  viz.,  the 
walls  of  the  siall-bhidder. 


*  Roux:  Rev.  Med.  de  la  Suisse  Romande,  Feb.  20,  1S97. 


14  DISEASES    OF    THE    LIVER. 

Physical  Signs. — There  is  a  movable  abdominal  tumor  on  the' right 
side  of  the  abdomen,  which  descends  with  the  diaphragm  and  the  liver 
on  respiration.  It  is  dull  on  percussion,  but  this  is  seldom  continuous 
with  the  liver  dulness,  as  there  is  usually  a  band  of  resonance  between 
it  and  the  liver.  It  may  be  distinctly  tender  on  pressure.  It  may 
descend  as  low  as  the  right  iliac  region  and  give  rise  to  difficult}^  in  diag- 
nosis from  appendicitis,  etc. 

Symptoms. — The  existence  of  a  tongue-like  lobe  may  be  discovered 
accidentally  and  may  not  be  accompanied  by  any  bad  effects.  Usually 
the  symptoms  associated  with  the  existence  of  a  tongue-like  lobe  are 
due  to  calculous  cholecystitis,  which  may  have  played  an  important 
part  in  the  production  of  the  deformity.  The  patient  maj^  have  been 
conscious  for  some  time  of  enlargement  and  alteration  in  shape  of  the 
abdomen  and  of  a  slowly  growing  tumor,  as  in  Martin's  case,  where  a 
tumor  had  existed  for  twelve  years.  There  are  often  a  feeling  of  oppres- 
sion and  heaviness  in  the  right  hypochondrium  and  pain  in  the  back. 
Abdominal  pain  may  be  paroxysmal,  like  gall-stone  colic,  or  may  be 
constant;  the  pain  is  usually  relieved  by  rest  in  the  recumbent  position. 
Intense  venous  engorgement  of  the  lobe  may  give  rise  to  attacks  of 
palpitation,  vomiting,  and  collapse.  Jaundice  and  ascites  are  rare  and 
are  due  to  some  definite  cause,  such  as  gall-stones  or  chronic  peritonitis. 

Diagnosis. — Riedel's  lobe  may  appear  to  have  no  definite  coimexion 
with  the  liver,  and  thus  appears  as  a  movable  abdominal  tumor  and  may 
easily  be  mistaken  for  a  floating  kidne}' .  An  instructive  case  in  point 
is  recorded  by  C.  Martin.* 

A  woman  aged  thirty-six  had  had  a  lump  in  her  abdomen  for  tweh'e  years 
which  had  recently  grown  rapidty  and  become  tender  and  painful.  An  oval  tumor 
about  the  size  of  a  six  months'  pregnancy  filled  the  right  half  of  the  abdoiuen;  it 
was  tense  and  very  mobile,  dull  on  percussion,  and  separated  from  the  liver  by  a 
band  of  resonance.  It  was  thought  to  be  an  unu.sually  mobile  kidney.  Laparotomy 
revealed  a  pedunculated  accessory  lobe  of  the  liver  bearing  the  gall-bladder;  it  was 
successfully  removed.     Its  weight  was  .3J  pounds. 

Bastianelli  t  describes  a  case  in  which  a  displaced  cancerous  kidney  Avas  diag- 
nosed; laparotomy  revealed  a  floating  lobe  of  liA^er,  "with  the  gall-bladder  on  its 
under  surface.  This  piece,  weighing  500  grammes  (18.75  ounces),  was  successfully 
removed;  on  section  there  were  gummata  in  it,  but  not  in  the  remainder  of  the 
liver. 

A  tongue-like  lobe  may  be  thought  to  be  some  other  form  of  abdominal 
tumor,  such  as  a  solid  growth  in  the  omentum,  a  tumor  of  the  pylorus, 
a  distended  gall-bladder,  or  a  cyst  of  the  pancreas  or  mesentery,  or  in 
extreme  cases  a  fibromyoma  of  the  uterus,  ovarian  cyst,  or  appendicitis. 

In  a  case  under  my  care  in  St.  George's  Hospital  the  gall-l>ladder  was  greatly 
thickened,  probably  from  calculous  cholecystitis,  was  adherent  to  the  colon,  and 
accompanied  by  a  well-marked  tongue-like  lobe  which  before  laparotomy  was 
thought  by  some  to  be  a  floating  kidney  or  a  gro^'th  in  the  transverse  colon. 

Treatment. — In  cases  where  a  tongue-like  lobe  is  diagnosed,  treat- 
ment is  only  necessary  when  pain  or  discomfort  is  present.     If  there 

*  C.  Martin:  Birmingham  Med.  Rev.,  Feb.,  1898,  p.  92. 

t  Bastianelli :  II  PolicUnico,  April,  1895.  Epitome,  Brit.  Med.  Journ.,  Mav  i, 
1895. 


ACQUIRED    DEFOR:\irnES.  15 

is  any  underlying  cholec3'stitis  or  cholelithiasis,  treatment  should  be 
directed  to  those  conditions.  In  seven  cases  where  the  morbid  condi- 
tion of  the  gall-bladder  was  treated  the  tongue-like  lobe  disappeared 
(Terrier  and  Auvray*).  An  ill-fitting  corset  or  one  which  presses  on  the 
liver  should  be  replaced  by  a  straight-fronted  corset,  and  tight  lacing 
or  constriction  of  the  waist  by  a  belt  should  be  prevented.  It  is  not 
often  that  radical  treatment,  such  as  stitching  the  lobe  to  the  abdominal 
parietes  or  its  complete  removal,  is  necessary. 

In  three  cases  the  tongue-like  lobe  has  been  stitched  to  the  aljdominal  parietes 
with  success  (Billroth, f  Tscherning,J  Langenbuch^.  Removal  of  the  lobe  has  been 
carried  out  b)^  Bastianelli,  Martin,  and  Lockwood.  || 

Effect  of  Tight  Lacing  on  the  Gall-bladder. — The  gall-bladder  is 
frequently  dilated.  Hertz  **  found  it  so  in  24  out  of  41  cases.  The 
downward  displacement  of  the  duodenum  brings  tension  to  bear  on  the 
cystic  duct,  which  even  under  normal  conditions  requires  a  spiral  valve 
to  keep  it  open  (Keith  ft);  and  thus  leads  to  obstruction.  The  resulting 
retention  of  bile  and  mucus  in  the  gall-bladder  may  tend  to  elongation  of 
the  right  lobe,  and  so  give  rise  to,  or  accentuate,  the  tongue-like  lobe 
seen  in  many  corset  livers.  Retention  of  bile  in  the  gall-bladder  disposes 
to  cholecystitis  and  cholelithiasis,  and  the  predominance  of  female  suf- 
ferers from  gall-stones  is  no  doubt  in  part  due  to  the  bad  effects  of  the 
corset. 

When  calculi  are  present  in  the  gall-bladder,  the  pressure  exerted  by 
the  corset  may,  as  suggested  by  Fiitterer,:|::j:  increase  the  friction  between 
the  gall-stones  and  the  mucous  membrane  of  the  gall-bladder,  and  thus 
help  to  explain  the  greater  frequenc}'  of  primar}-  carcinoma  of  the  gall- 
bladder in  women.  In  this  connexion  it  is  noteworthy  that  the  larger 
bile-ducts,  which  are  not  affected  in  the  same  way  by  corsets  or  belts, 
are  more  often  the  site  of  primary  carcinoma  in  man. 

*  Terrier  et  Auvray:  Rev.  de  Chirurg.,  1897. 

t  Bilhoth:  AViener  med.  Wochen.,  1886,  No.  14. 

t  Tscherning:  Centralblatt  f.  Chirurg.,  1888,  p.  426. 

§  Langenbuch:  Deutsche  med.  Wochen.,  1888. 

II  Lockwood,  C.  B.:  Lancet,  1903,  vol.  ii,  p.  223. 

**  Hertz:  Abnormitaten  in  der  Lage  und  Form  der  Bauchorgane,  1894. 

tt  Keith,  A. :  Lancet,  1903,  vol.  i,  p.  639. 

ti  Fiitterer,  G. :  Chicago  Medical  Society,  April  1,  1897 


DISPLACED  LIVER. 

SYNOPSIS  OF  THE  FORMS  OF  MALPOSITION. 

Congenital. 
Transposition. 
Ectopia. 
In  diaphragmatic  hernia. 

Acquired. 

In  diaphragmatic  hernia. 

In  spinal  curvature  and  in  riclcets. 

In  tight  lacing. 

Thoracic  conditions  displacing  the  liver. 

Pleural  effusion  and  pneumothorax. 
Malignant  disease  of  lung,  etc. 
Pericardial  effusion. 

Abdominal  conditions  displacing  the  liver. 

Downwards. 
Forwards. 
Backwards. 
Laterally. 

Apart  from  enlargement  due  to  tumors  or  other  causes,  the  liver  may 
occupy  an  abnormal  position  under  numerous  and  very  various  condi- 
tions. A  displaced  liver  which  is  at  the  same  time  freely  movable  is  a 
wandering  liver,  and  is  dealt  with  under  that  heading  {tide  p.  22).  Here 
we  are  only  concerned  with  displaced  livers  which  are  not  more  movable 
than  normal.  Malposition  may  conveniently  be  divided  in  the  first 
instance  into  (a)  those  of  congenital  origin  and  (6)  those  acquired  in  later 
life ;  the  latter  class  is  by  far  the  larger. 

CONGENITAL  MALPOSITIONS. 

Transposition. — In  complete  transposition  of  the  viscera  the  liver 
will  be  on  the  left  side,  but  occasionally  the  heart  may  be  congenitally 
transposed  without  the  liver  sharing  in  the  change.  Transposition  of 
the  liver  without  the  other  viscera  being  affected  is  very  rare  indeed. 

Complete  transposition  of  the  viscera  may  lead  to  an  erroneous  diag- 
nosis if  the  condition  is  not  recognized.  In  a  case,  recorded  by  Billings,* 
of  cholelithiasis  in  a  patient  with  situs  transversus  a  physician  had  diag- 
nosed acute  yellow  atrophy  from  absence  of  the  hepatic  dulness  on  the 
right  side. 

Congenital  Ectopia  of  the  Liver. — (Synonyms:  Hepatomphalos, 
Hepatocele.) — From  congenital  defect  of  the  muscles  of  the  abdominal 

*  BiUings:  Philadelphia  Med.  Journ.,  1900,  p.  670. 
16 


DISPLACED    LIVER.  17 

wall  the  liver  may  project  under  the  skin  either  at  the  umbilicus  or  in 
the  middle  line  between  the  umbilicus  and  the  ensiform  cartilage.  Con- 
genital hernia  or  ectopia  of  the  organ  at  the  umbilicus  has  been  called 
hepatomphalos.  The  tumor  is  firm,  dull  on  percussion  unless  coils  of 
intestine  are  also  present  in  the  sac,  and  is  continuous  with  the  liver 
dulness.  It  ma}^  be  easily  reduced,  but  reappears  on  removal  of  the 
pressure.  On  the  other  hand,  the  liver  may  become  adherent  to  the 
walls  of  the  umbilical  sac  and  thus  be  irreducible.  This  was  the  case  in 
a  baby  aged  three  weeks.*  Bullarcl  f  met  with  a  case  where  the  liver 
was  described  as  being  herniated  into  the  umbilical  cord. 

Displacement  of  the  Liver  as  the  Result  of  Congenital  Diaphrag- 
matic Hernia. — Congenital  defects  of  the  diaphragm  may  give  rise 
either  to  a  free  communication  between  the  peritoneal  and  pleural  cav- 
ities or,  from  deficiency  of  the  muscular  tissue  of  the  diaphragm  only, 
to  a  membranous  pouch  which  projects  up  into  the  thorax.  Congenital 
deficiency  of  the  diaphragm  is  commoner  on  the  left  side  (Jaffe  {)  and 
may  allow  the  left  lobe  of  the  liver  to  enter  freely  into  the  thorax. 

In  a  case  of  Porak  and  Durante's  §  the  peritoneum  communicated  freely  with 
the  left  pleura,  and  the  left  lobe  of  the  liver  was  found  behind  the  sternum. 

ACQUIRED  DISPLACEMENTS. 

In  Diaphragmatic  Hernia. — This  may  occur  as  part  of  a  severe 
injury,  the  diaphragm  being  torn  across  and  the  stomach,  colon,  spleen, 
or  part  of  the  liver  may  pass  into  the  thoracic  cavity.  Diaphragmatic 
hernia  when  found  in  adult  life  without  any  history  of  injury  may  of 
course  be  congenital  in  origin,  and  in  cases  where  the  herniated  viscera 
have  been  found  enclosed  in  a  sac  composed  of  the  attenuated  remains 
of  the  diaphragm  or  merely  of  the.  opposed  pleura  and  peritoneum,  this 
would  appear  probable.  Pouching  due  to  weakness  near  the  oesophagus 
or  xiphoid  cartilage  may,  however,  be  an  acquired  condition.  In  some 
cases  a  rent  in  the  diaphragm  may  have  been  due  to  an  injury  received 
years  before  and  almost  or  c^uite  forgotten.  The  nature  of  the  defect 
may  then  be  regarded  as  congenital,  whereas  it  is  really  acquired.  In  a 
considerable  number  of  cases  of  diaphragmatic  hernia  the  condition  is 
found  to  have  been  preceded  by  traumatism  years  before. 

Traumatic  diaphragmatic  hernia  is  nearly  always  on  the  left  side, 
since  the  support  provided  by  the  liver  tends  to  protect  the  right  leaflet 
from  rupture.  The  liver  is  much  less  often  displaced  into  the  cavity  of 
the  thorax  than  the  stomach,  colon,  intestines,  or  spleen. 

Blum  and  Ombredanne  ||  refer  to  three  cases  of  traumatic  diaphragmatic 
hernia  in  which  the  liver  projected  into  the  pleural  cavity.  In  one  of  these,  in 
which  there  was  a  history  of  a  fall  fourteen  years  before,  part  of  a  cancerous  liver 
projected  into  the  left  pleura.     (Dietz's  case.) 

*  J.  Hutchinson:   Medical  Times,  1870,  vol.  i,  p.  397. 
t  BuUard:  American  Medicine,  Nov.  8,  1902. 
t  Jaffe:  Trans.  Path.  Soc,  vol.  xlv,  p.  224. 
§  Porak  et  Durante:  Bull.  Soc.  Anat.  Paris,  1901,  p.  354. 
II  Blum  et  Ombredanne:  .\rchiv.  General  de  M6d.,  1896,  vol.  i,  p.  1,  178. 
2 


18  DISEASES    OF   THE    LIVER. 

Part  of  the  liver  may  pass  through  the  rent  and  become  tightly  con- 
stricted at  the  margin  of  the  rent  like  a  strangulated  hernia. 

The  folloT\-ing  case,  the  postmortem  examination  of  which  I  saw,  was  recorded 
by  Dr.  Ogle  in  the  transactions  of  the  Pathological  Society,  vol.  xlviii,  p.  114.  -A 
boy,  aged  sixteen  years'  who  had  had  an  accident  six  years  before,  was  admitted 
mth  frequent  vomiting  and  signs  of  a  left  pleural  effusion;  aspiration  did  not 
remove  any  fluid.  At  the  autopsy  the  cardiac  end  of  the  stomach  and  the  left 
lobe  of  the  hver  were  found  in  the  left  pleural  cavity,  ha^dng  passed  through  a 
rent  in  the  central  tendon  of  the  diaphragm,  which  had  a  diameter  of  IJ  inches. 
The  intrathoracic  part  of  the  left  lobe  was  connected  by  a  thin  atrophied  pedicle 
with  the  rest  of  the  li-\^er  and  formed  a  lump  5  by  4  inches  which  looked  very  like 
a  hard,  deeply  congested  spleen.  On  section  it  was  deep  red  in  parts  with  white 
areas,  and  was  mottled.  Microscopically  there  were  much  hgemorrhage,  a  quantity 
of  blood-pigment,  and  degeneration  of  the  liver  cells. 

In  Spinal  Curvature  and  in  Rickets.— The  liver  though  structurally 
normal  may  be  very  considerably  displaced  by  spinal  deformity.  Its 
lower  edge  may  be  below  the  umbilicus  and  the  organ  may  be  unduly 
movable.  In  rickets  the  deformity  of  the  chest  to  some  extent  depresses 
the  liver,  which  is  usually  somewhat  enlarged  from  the  action  of  intes- 
tinal poisons.  The  view  that  the  liver  is  enlarged  in  rickets  is  true,  but 
the  increase  in  the  downward  extent  of  the  hepatic  dulness  is  often  partly 
due  to  displacement  by  thoracic  deformity. 

Tight  Lacing,  etc. — The  deformities  of  the  liver  resulting  from 
tight  lacing  and  artificial  constriction  of  the  lower  part  of  the  thorax  are 
described  elsewhere  (p.  8).  In  these  conditions  the  liver  may  be 
displaced  upwards  as  a  whole,  or  even  downwards,  according  to  the 
position  of  the  "waist,"  but  most  commonly  the  right  lobe  is  elongated 
downwards  and  has  a  constricted  area,  corresponding  to  the  Hne  of 
pressure,  uniting  the  floating  lobe  to  the  main  part  of  the  right  lobe. 

Thoracic  Conditions  Giving  Rise  to  Displacement  of  the  Liver. 
— Effusion  into  the  Right  Pleural  Cavity. — ^A  large  serous  effusion  or 
empyema  wiU  effect  this,  but  inasmuch  as  these  conditions  are  usually 
reheved  by  paracentesis,  the  best  examples  of  displacement  of  the  hver 
due  to  disease  of  the  pleura  are  seen  in  cases  of  right  pneumothorax. 
A  neglected  or  latent  pleural  effusion  may,  however,  reach  a  large  size 
and  then  produce  marked  displacement  of  the  liver. 

A  man  aged  forty-three  years  arrived  at  the  hospital  in  a  state  of  collapse 
and  died  in  a  few  minutes.  At  the  autopsy,  which  I  performed,  the  right  pleura 
contained  10  pints  of  pus,  the  liver  was  greatlj^  depressed,  its  lower  edge  being  on 
a  level  with  the  anterior  superior  spines  of  the  iha. 

Besides  being  displaced  downwards  the  liver  is  rotated  on  its  antero- 
posterior axis.  The  right  leaflet  of  the  diaphragm  being  depres.sed  or 
even  'presenting  its  convexity  downwards,  the  right  lobe  is  much  more 
depressed  than  the  left,  and  the  left  lobe  swings  upwards,  the  wliole  organ 
being  pushed  towards  the  left. 

A  pneumothorax  on  the  right  side  may  in  rare  cases  lead  to  acute 
dislocation  of  the  liver  when  the  intrathoracic  pressure  is  raised,  as  a 
result  of  a  \'alvular  communication  between  the  lung  and  the  pleural 
ca^dt3^ 


DISPLACED   LIVER.  19 

Stiller  *  records  a  case  where  a  pneumothorax  developed  as  the  result  of  sneezing 
in  a  healthy  man  and  the  liver  was  depressed  so  as  to  form  a  large  abdominal  tumor. 

A  pleural  effusion  or  pneumothorax  on  the  left  side  may  give  rise, 
if  excessive,  to  downward  displacement  of  the  left  lobe  of  the  liver. 

Malignant  Disease  of  Lung. — Ver}'-  extensive  malignant  disease 
affecting  the  lung  and  greatly  increasing  its  volume  may  displace  the 
liver  downwards. 

This  displacement  was  very  marked  in  a  boy  with  an  enormous  calcifying 
sarcoma  in  the  thorax,  secondary  to  sarcoma  of  the  thigh,  who  died  in  St.  George's 
Hospital  under  the  care  of  Dr.  Penrose  in  April,  1898.  Tlie  growth  pressed  the 
right  leaflet  of  the  diaphragm  do^^^l  so  that  its  under  surface  was  convex,  the  liver 
was  depressed,  and  its  lower  border  was  on  a  level  with  the  umbilicus.  It  was  not 
more  freely  movable  than  normal. 

In  mediastinal  growths  the  liver  is  not  displaced  unless,  as  not  in- 
frequently occurs,  there  is  a  large  pleural  effusion  at  the  same  time. 

In  emiphyseina  the  downward  displacement  of  the  liver  is  often  easily 
detected,  but  the  increased  do^^nward  extent  of  the  liver  is  not  extreme 
unless  there  is,  in  addition,  chronic  venous  engorgement  due  to  failure 
of  the  right  side  of  the  heart. 

Pneumonia. — Bright  t  thought  that  pneumonia  was  the  direct  phy- 
sical cause  of  the  liver  being  below  the  costal  arch.  But  the  cloudy 
swelling  of  the  liver  is  in  part  responsible  for  the  projection  of  the  liver 
downwards.  When  the  whole  lung  is  solid,  the  diaphragm  may  be  in 
the  position  of  maximum  inspiration,  and  as  a  result  the  liver  is  some- 
what depressed.  I  have  seen  downward  displacement  of  the  right  half 
of  the  diaphragm  and  of  the  liver  at  the  autopsy  of  a  child  with  extensi^■e 
tuberculous  pneumonia  of  the  right  lung. 

Pericardial  Effusion. — A  large  pericardial  effusion  will  depress  the 
diaphragm  and  with  it  the  liver. 

In  a  case  figured  by  Sibson,t  where  the  pericardium  contained  3^-  pounds  of 
fluid,  the  right  lobe  of  the  liver  was  displaced  and  tilted  just  in  the  same  manner 
as  in  a  right-sided  pleural  effusion. 

Abdominal  Conditions  Leading  to  Displacement  of  the  Liver. — 

Generally  speaking,  abdominal  conditions  which  displace  the  liver  do  so 
in  an  upward  direction,  but  occasionally  the  liver  may  be  depressed, 
while  in  other  cases  it  may  be  pushed,  drawn,  or  rotated  laterally. 
Growths  arising  from  the  retroperitoneal  space  may  push  the  liver  for- 
wards and,  conversely,  gak  free  in  the  peritoneal  cavity  or  under  certain 
conditions  tympanitic  distension  of  the  intestines  may  separate  the  liver 
from  the  anterior  aljdominal  wall. 

Abdominal  Conditions  Displacing  the  Liver  Downwards. — A  subdia- 
phragmatic or  subphrenic  abscess  on  the  right  side  may  pass  between 
the  diaphragm  and  the  convexity  of  the  right  lobe  and  displace  the  liver 
downwards.  A  right-sided  subphrenic  abscess  may  l^e  the  result  of  a 
gastric  ulcer  situated  near  the  pylorus,  of  a  perforating  duodenal  ulcer, 

*  Stiller:  Wien.  med.  Wochen.,  May  4,  1901. 

t  Bright,  R. :  Abdominal  Tumours,  p.  255,  New  Sydenham  Society. 

X  Sibson:  Russell  Rejniolds'  System  of  ^led.,  vol.  iv. 


20  DISEASES    OF   THE    LIVER. 

though  the  resultmg  peritonitis  unfoi-tiinately  is  rarely  localized,  and  may 
then  contain  gas  as  ^Yell  as  pus,  or  tract  up  from  perforation  of  an  in- 
flamed appendix,  situated  in  what  is  not  an  infrequent  abnormal  posi- 
tion, viz.,  running  up  over  the  right  kidney.  Besides  these  extrinsic 
origins  for  a  right-sided  subphrenic  abscess,  an  abscess  in  the  liver  itself, 
a  suppurating  hydatid  cyst  or  the  multiple  abscesses  of  pylephlebitis 
may  perforate  into  the  potential  space  between  the  liver  and  diaphragm 
and  give  rise  to  a  collection  of  pus  there  and  so  to  downward  displace- 
ment of  the  liver.  In  these  cases  the  liver  is  itself  enlarged  and  the 
condition  is  almost  the  same  as  hepatic  abscess. 

A  hydatid  cyst  projecting  from  the  convexitj^  of  the  liver  rather  encroaches 
on  the  thorax  than  pushes  the  hver  do'wnwards.  Shattuck  *  described  a  single 
cystic  adenoma  of  the  bile-ducts  containing  a  gallon  of  clear  fluid  which  pushed 
the  liver  doT\Tiwards. 

As  the  result  of  peritoneal  adhesions  due  to  local  peritonitis,  e.  g.,  from 
appendicitis  or  inflamed  tuberculous  glands,  as  in  a  case  of  Sir  F.  Treves,t 
the  liver  may  be  pulled  downwards  towards  the  pelvis.  A  liver  which 
in  the  first  instance  was  freely  movable  may  subsequently  become  fixed 
in  an  abnormal  position  by  local  peritonitis  or  perihepatitis.  Thus 
Richelot  J  found  the  liver  fixed  in  the  right  iliac  fossa  close  to  the  caecum. 

Upward  Displacement  of  the  Liver. — Ascites,  fiatulent  distension  of 
the  intestines,  excessive  dilatation  of  the  colon,  or  the  presence  of  large 
abdominal  tumors,  such  as  o^-arian  cysts,  uterine  fibromyomata,  etc., 
push  the  liver  and  diaphragm  up  and  thereby  encroach  A^ery  seriously 
on  the  capacity  of  the  thorax.  The  convexity  of  the  diaphragm  may 
then  be  on  a  level  with  the  third  rib  or  even  higher. 

As  an  example  of  extreme  displacement  of  the  liver  from  the  pressure  exerted 
by  ovarian  cysts  reference  may  be  made  to  a  remarkable  case  recorded  by  F.  A. 
Bald^van  §  in  which  there  were  four  o\'arian  cysts,  two  large  and  two  small,  in 
the  abdomen  of  a  woman  aged  fifty-nine  years.  The  cysts  contained  18  gallons 
of  fluid  and  were  estimated  to  weigh  185^  poimds.  The  highest  point  of  the  liver 
was  on  a  level  with  the  upper  border  of  the  third  rib  in  the  nipple  line. 

When  this  upward  displacement  is  very  considerable,  the  liver  may 
largely  or  even  entirely  cease  to  be  in  contact  with  the  anterior  abdominal 
wall  and  undergoes  a  very  striking  alteration  in  its  relation  to  other 
organs.  The  anterior  surface  travels  backwards  and  becomes  posterior, 
while  the  inferior  surface  looks  forwards  and  upwards  instead  of  down- 
wards and  backwards.  This  is  due  to  the  liver  moving  upwards  on  a 
transverse  axis  running  through  its  connexion  with  the  inferior  vena 
cava,  which  is  relatively  a  fixed  point. 

Displacement  Forwards. — A  retroperitoneal  growth  or  a  pancreatic 
cyst  may  in  rare  cases  push  the  liver  fonvards,  a  gro^^i;h  of  the  right 
suprarenal  capsule  may  displace  the  right  lobe  forwards,  while  a  pan- 
creatic cyst  will  tend  to  force  the  left  lobe  into  undue  prominence.     An 

*  Shattuck:  Boston  Med.  and  Surg.  Journ.,  April  2(),  1900. 

t  Treves,  F. :  Brit.  Med.  Journ.,  1896,  vol.  i,  p.  1. 

X  Richelot:  Gaz.  des  Hop.  Paris,  p.  783. 

§  Baldwin:  Brit.  Med.  Journ.,  1900,  vol.  ii,  p.  80. 


DISPLACED    LIVER.  21 

aortic  aneurysm  near  the  pillars  of  the  diaphragm  ma}'  so  displace  the 
liver  forwards  as  to  suggest  a  new-growth  in  that  organ.  In  Beatty's  * 
case  of  aortic  aneurysm  in  this  situation  the  liver  appeared  steadily  to 
increase   in   size. 

Displacement  Backwards.— Occa,sionsi\\y  coils  of  intestine  or  the 
colon  may  intervene  between  the  liver  and  the  anterior  abdom- 
inal wall,  thus  displacing  the  liver  backwards.  This  occurs  in  acute 
yellow  atrophy  where  the  great  diminution  or  even  complete  disap- 
pearance of  the  liver  dulness  is  largeh'  due  to  the  flabby  liver  allowing 
resonant  bowel  to  come  between-  it  and  the  abdominal  parietes.  In 
cases  of  perforation  free  gas  in  the  peritoneum  may  pass  between  the 
liver  and  the  anterior  abdominal  wall  and  displace  the  organ  backwards. 
In  rare  cases  a  distended  piece  of  small  intestine  or  colon  may  get  between 
the  anterior  surface  of  the  liver  and  the  abdominal  wall.  This  accounts 
in  all  probability  for  the  occasional  absence  of  liver  dulness  seen  in  cases 
during  life  for  which  no  definite  cause,  such  as  acute  yellow  atrophy,  a 
subphrenic  pyopneumothorax,  or  perforation,  is  forthcoming.  In  these 
cases,  in  which  there  may  be  no  abdominal  symptoms,  a  thickening  of 
the  capsule  of  the  liver  corresponding  to  the  abnormally  situated  piece 
of  intestine  may  sometimes  be  found  after  death. 

Dilatation  of  the  stomach  or  extreme  degrees  of  dilatation  of  the 
descending  colon  will  tend  to  rotate  the  liver  towards  the  right. 

T.  Fisher  t  figures  cases  of  this  kind  and  I  have  seen  several  examples  of  this 
condition  in  the  postmortem  room.  In  one  case  the  colon  lay  just  anterior  to  the 
atrophied  bridge  of  Hver  substance  connecting  the  constriction  lobe  witli  the  re- 
mainder of  a  tight-laced  liver. 

A  displaced  liver  is,  as  a  rule,  not  more  movable  than  one  in  its  normal 
position.  It  differs  from  a  wandering  liver  in  this  respect,  and  also  in 
the  fact  that  it  cannot  be  replaced  in  its  normal  position,  while,  in  addi- 
tion, a  definite  cause  for  its  displacement  is  often  forthcoming.  Symp- 
tonxs  which  might  be  referred  to  a  displaced  liver,  such  as  weight,  pain, 
and  heaviness,  are  generally  thrown  into  the  shade  by  those  of  the  con- 
dition responsible  for  the  displacement.  The  various  forms  of  enlarge- 
ment of  the  liver,  fatty,  lardaceous,  leuka;mia,  new-growth,  abscess,  cir- 
rhosis, etc.,  must  be  differentiated  from  a  displaced  liver  by  a  careful 
physical  examination  of  each  individual  case. 

The  treatment  of  a  displaced  liver  is  that  of  the  condition  giving  rise 

to  it. 

*  Beatty:  Dublin  Hosp.  Reports,  vol.  v. 

t  Fislier,  T. :  Bristol  Medico-chirurg.  .Journ.,  Sept.,  1901. 


HEPATOPTOSIS. 

Synonyms:    Wandering    Liver,    Movable    Liver,   Prolapse    or   Dislocation   of  the 

Liver. 

By  the  term  wandering  or  movable  liver  is  meant  one  which,  being 
unduly  displaceable,  leaves  its  normal  position  and  forms  an  abdominal 
tumor. 

Historical. — Cantani  *  in  1866  described  a  clinical  case  of  movable 
liver,  but  there  was  no  autopsy.  Though  Cantani's  name  is  connected 
with  the  recognition  of  its  clinical  features,  the  anatomical  condition  had 
been  described  long  before. 

Heister,  as  far  back  as  1754,  published  the  account  of  an  autopsj^,  with  a  plate 
showing  tlie  position  of  the  liver.  Gunzius  (1744),  Buchoby  (1768),  and  Sauvage 
(1768)  also  referred  to  cases.  Wickham  Legg  t  first  drew  attention  to  the  subject 
in  this  country.  Li  recent  times  Glenard  t  has  done  much  to  direct  attention  to 
the  subject. 

Hepatoptosis  is  analogous  to  a  wandering  spleen.  Both  these  organs 
are  normally  "floating"  in  the  abdominal  cavity,  for  while  tethered  in 
their  normal  positions  by  peritoneal  ligaments,  they  are  supported  by 
the  mutual  pressure  of  the  other  abdominal  viscera,  especially  the  elastic 
pad  formed  by  the  intestines,  and  are  not  fixed  and  packed  round  by  fat 
in  the  way  that  the  kidneys  are.  The  term  "floating,"  which  is  accu- 
rately applied  to  an  unduly  movable  kidney,  is  an  equally  appropriate 
epithet  for  a  normal  liver  or  spleen,  and  therefore  does  not  describe  an 
abnormally  mobile  condition  of  these  viscera.  The  liver  normally  moves 
during  respiration,  descending  with  the  diaphragm  on  inspiration  half  an 
inch  below  the  costal  arch  in  the  right  nipple  line.  A  dilated  stomach 
or  distension  of  the  colon  on  the  left  side  will  rotate  the  hver  to  the  right. 
When  this  displacement  is  greatly  exaggerated,  the  state  of  affairs  in 
wandering  hver  is  imitated. 

There  is  a  great  difference  between  an  unduly  movable  hver  on  the 
one  hand,  and  one  which  is  merely  pushed  out  of  place  by  a  tumor  or 
pleural  effusion  on  the  other  hand.  A  displaced  liver  is  not  necessarily, 
or  indeed  usuaUy,  more  movable  than  one  in  the  normal  position.  Again, 
the  tongue-like  and  constriction  lobes  attached  to  the  right  lobe  of  the 
liver  in  tight  lacing  and  other  conditions  must  be  distinguished  from  a 
wandering  liver.  The  wandering  liver  may  be  spoken  of  as  total  hepat- 
optosis, w^hile  the  constriction  and  tongue-like  lobes  have  been  called 
partial  hepatoptosis. 

Existence  of  Total  Hepatoptosis. — From  the  collected  cases  of 
Faure,  Einhorn,  Graham,  Botticher,  Glenard,  and  Telaky,  it  has  been 

*  Cantani:  Annali  Universali  de  Medecina,  vol.  clxxxxviii,  p.  373,  1866. 
t  W.  Legg:  St.  Bartholomew's  Hosp.  Reports,  vol.  xiii,  p.  141,  1877. 
X  Glenard:  Les  ptoses  Visc^rales,  Paris,  1899. 

22 


HEPATOPTOSIS.  23 

estimated  b}^  Button  Steele  *  that,  in  all,  about  100  cases  of  undoubted 
total  hepatoptosis  are  on  record,  of  which  44  have  been  confirmed  by 
operation  or  autopsy.  Its  existence,  therefore,  admits  of  no  reasonable 
doubt,  but  from  its  intimate  attachment  to  the  diaphragm,  the  liver  is 
not  so  often  affected  by  visceroptosis  as  the  other  abdoininal  organs. 

The  existence  of  movable  livers  has  been  doubted  from  time  to  time,  and  the 
clinical  signs  of  the  condition  have  been  explained  as  due  to  causes  such  as  floating 
kidneys,  renal  or  other  tumors.  This  was  the  view  taken  by  Wicldiam  Legg,t 
the  first  -m-iter  (1877)  on  this  subject  in  this  country.  In  some  cases  where  a 
floating  hver  was  diagnosed  during  hfe  the  liver  has  been  found  in  its  natural  position 
after  death  (P.  MiiUer,J  Cra-n-furd). 

According  to  Hertz  §  and  Glenard,  ||  some  at  anj^  rate  of  the  cases  described 
as  wandering  hvers  were  in  reaUty  constriction  lobes  attached  to  a  thinned  and 
elongated  right  lobe.  The  part  below  the  corset  furrow  may  thus  be  mistaken  for 
the  whole  liver,  especially  when  it  is  very  mobile  and  the  abdomen  is  lax  and  pendu- 
lous. Glenard,  indeed,  considers  that  the  predominance  of  the  female  sex  in  the 
recorded  cases  of  movable  liver  is  thus  explained. 

Frequency. — Well-marked  examples  of  hepatoptosis  with  definite 
symptoms  are  rare.  ]\Iinor  degrees,  however,  are  fairly  often  found 
when  looked  for;  thus  Glenard,**  from  researches  on  a  large  number 
(3500)  of  invalids  suffering  from  various  disturbances  of  nutrition,  esti- 
mated that  20  per  cent,  of  these  patients  present  some  degree  of  it.  He 
put  the  numbers  at  25  per  cent,  for  males  and  15  per  cent,  for  females, 
thus  reversing  the  usual  incidence  of  really  movable  livers  in  the  two 
sexes.  For  there  can  be  no  doubt  that  cases  with  characteristic  symp- 
toms are  usually  met  with  in  women  with  pendiilous  abdominal  walls 
who  have  borne  many  children.  It  is  noteworthy  that  Glenard  has  found 
some  degree  of  hepatoptosis  with  greater  frequencj"  in  his  later  papers; 
thus,  in  1886,  he  estimated  that  it  occurred  in  2  per  cent,  and  in  1892 
in  20  per  cent,  of  patients  with  diseases  of  nutrition.  It  is  fairly  safe  to 
assume  that  many  of  the  latter  cases,  which  would  escape  observation 
in  less  practised  hands,  do  not  suffer  from  the  effects  of  the  condition. 

Sex. — The  female  sex  provides  the  vast  majority  of  cases  of  wandering 
livers.  In  80  cases  described  as  hepatoptosis  and  collected  from  Htera- 
ture  by  Glenard,tt  69  at  least  were  in  women.  In  Graham's  J}  70  cases 
56  were  in  women.  Max  Einhorn§§  in  private  practice  noted  21  women 
and  9  men.  As  alread}^  mentioned,  Glenarcl's  own  obserA-ations,  which 
include  minor  degrees  of  hepatoptosis,  were  to  the  effect  that  hepatoptosis 
is  really  more  frequent  in  men,  its  apparently  greater  incidence  in  females 
being  explained  by  cases  of  partial  hepatoptosis  (Riedel's  lobes,  constric- 
tion lobes)  erroneous^  regarded  as  complete  hepatoptosis. 

Age. — -The  majority  of  patients  suffering  from  hepatoptosis  are  over 

*  Dutton  Steele:  University  of  Penna.  Med.  Bull.,  Jan.,  1903,  p.  424. 

t  Legg:  St.  Bartholomew's  Hosp.  Reports,  vol.  xiii,  p.  141, 1877. 

t  P.  MuUer:  Deutsch.  Archiv  f.  klin.  Med.,  1874,  Bd.  xiv,  S.  146. 

§  Hertz:  Abnormitaten  in  der  Lage  und  Form  der  Bauchorgane,  1894. 

II  Glenard:  Les  ptoses  Viscerales,  Paris,  1899. 
**  Glenard:  Les  ptoses  Viscerales,  Paris,  1899,  p.  503. 
ft  Glenard:  Les  ptoses  Viscerales,  Paris,  1899,  p.  625. 
XX  J-  E.  Graham:  Canadian  Practitioner,  June,  1895. 
§§  Einhorn,  Max:  Medical  Record,  Sept.  16,  1899. 


24  DISEASES    OF   THE    LIVER. 

forty  years  of  age.  Treves  *  puts  the  age  at  between  thirty-five  and 
sixty.     In  exceptional  instances  it  is  met  with  in  children. 

Freeman,t  in  496  autopsies  on  children,  met  with  four  examples  of  hepatoptosis 
due  to  relaxation  and  elongation  of  the  suspensory  ligament;  the  right  lobe  came 
down  into  the  pelvis,  the  left  lobe  being  the  only  part  of  the  liver  touching  the 
diaphragm,  while  the  upper  surface  was  turned  to  the  riglit. 

Factors  Responsible  for  the  Normal  Position  of  the  Liver. — As 

bearing  on  the  causation  of  hepatoptosis  it  will  be  w^ell  to  refer  to  the 
factors  which  maintain  the  liver  in  its  normaL position.  These  are:  (1) 
The  attachment  of  the  liver  by  the  inferior  vena  cava  to  the  diaphragm. 
This,  according  to  Faure,J  is  the  most  important  agent  in  retaining  the 
liver  in  its  place,  and  by  itself  is  capable  of  sustaining  a  weight  of  27 
kilogrammes,  as  against  20  kilogrammes  which  the  other  suspensory 
ligaments  can  support.  (2)  The  peritoneal  ligaments,  the  falciform, 
coronary,  and  lateral,  and  the  connective  tissue  uniting  the  right  lobe 
of  the  liver  to  the  diaphragm  (the  mesohepaticon).  Graham's  §  ob- 
servations on  the  dead  body  showed  that  they  can  support  the  liver 
independently  of  the  abdominal  walls,  and  both  he  and  Button  Steele  || 
found  that  cutting  these  ligaments  led  to  a  condition  which  was  much 
the  same  as  that  in  hepatoptosis.  These  observations  show  that  in 
spite  of  Symington's**  statement  that  under  ordinary  conditions  the 
suspensory  ligaments  are  not  tense,  they  can,  when  intact  and  healthy, 
prevent  any  abnormal  or  excessive  descent  of  the  liver.  (3)  The  healthy 
tone  of  the  abdominal  muscles  which  keeps  up  the  intra-abdominal 
pressure  and  makes  the  intestines  act  as  an  elastic  pad  or  support  for 
the  liver.  In  the  rare  cases  of  congenital  absence  of  the  muscles  of  the 
abdominal  wall  the  liver  has  been  found  to  be  extremely  movable. 
(Guthrie.tt) 

Intra-hepatic  blood  tension  may  possibly  play  a  part  in  keeping  the  liver  in  its 
normal  position.  Injection  of  water  into  the  vessels  of  the  liver  was  found  by 
Glenard  and  Siraudtf  not  only  to  increase  its  size,  but  to  straighten  out  its  under 
or  concave  surface,  which  became  more  convex.  It  is  further  stated  that  in 
chronic  congestion  of  the  liver  the  organ  keeps  well  in  its  place  even  though  the 
abdominal  walls  are  flaccid.  Alteration  in  the  intra-hepatic  blood-pressure  may 
therefore  possibly  have  something  to  do  with  dropping  of  the  liver. 

Causation  of  Hepatoptosis. — An  unduly  movable  liver  might 
depend  on  some  congenital  defect  or  abnormality  of  the  suspensory 
apparatus,  such  as  an  imperfect  development  of  the  falciform  or  coronary 
ligaments,  or  upon  elongation,  which  when  extreme  might  justify  the 
term  "mesohepar."  There  is,  however,  very  little  anatomical  evidence 
to  support  this  theory.     It  is  quite  reasonable  to  suppose  that  elongation 

*  Treves,  F. :  Lancet,  1900,  vol.  i,  p.  1339. 

t  Freeman:  Arcliives  of  Pediatrics,  1900,  p.  81.        t  Faure:  These,  Paris,  1892. 

§  Graham,  J.  E. :  In  Loomis  and  Thompson's  System  of  Practical  Med.,  vol.  iii, 
p.  414. 

II  Dutton  Steele:  University  of  Pennsylvania  Med.  Bull,  vol.  xv,  p.  424,  Jan  , 
1903. 

**  Symington:  Trans.  Medico-cliirurg.  Soc,  Edinburgh,  vol.  vii,  p.  53. 

tt  Guthrie,  L.  G. :  Trans.  Path.  Soc,  vol.  xlvii,  p.  139. 

It  G16nard  and  Siraud:  Lyon  Medical,  .June,  July,  1895. 


HEPATOPTOSIS.  2o 

of  the  suspensory  ligaments  ma}'  be  congenital  in  the  sense  that  there 
is  an  hereditary  weakness  which,  like  that  underh'ing  hernia  and  general 
dropping  of  the  viscera  (Glenard's  disease),  allows  elongation  of  the 
ligaments  to  occur  later  in  life  under  conditions  which  in  ordinary  persons 
would  not  have  this  effect.  Another  equallv  tenable  view  is  that  the 
tendency  to  elongation  is  acquired  and  depends  on  degeneration  or 
atrophy  of  the  suspensory  ligaments  induced  by  malnutrition  and  gen- 
eral debility.  The  associated  enteroptosis,  pendulous  abdominal  walls, 
and  linese  albicantes  may  be  regarded  as  manifestations  of  the  same 
process,  and,  as  will  be  seen  later,  they  favour  the  production  of  hepato- 
ptosis.  Elongation  of  the  suspensory  ligaments  must  occur  in  order  to 
allow  the  liver  to  become  movable. 

In  cases  where  the  suspensory  ligaments  are  unduly  extensible,  drag- 
ging on  the  liver  by  peritoneal  adhesions,  tumors,  cysts,  or  large  accu- 
mulations in  the  gall-bladder  may  lead  to  elongation  of  the  ligaments, 
and  so  to  an  excessively  movable  and  displaced  liver.  This  condition 
resembles  a  simple  displaced  liver  (vide  p.  16),  but  differs  from  it  in 
excessive  mobility.  Total  hepatoptosis  due  to  traction  is  a  rare  event, 
and  must  be  distinguished  from  the  elongation  of  the  right  lobe  (Riedel's 
lobe,  partial  hepatoptosis)  seen  in  many  cases  of  cholelithiasis  (ndep.  12). 

Thus  in  a  case  of  Sir  F.  Treves,*  a  young  woman  aged  twenty-two  years, 
the  liver  descended  2  inches  on  assuming  the  erect  posture ;  there  was  general  enter- 
optosis due  to  traction  exerted  by  the  great  omentum,  which  was  firmly  adherent 
to  calcified  tuberculous  glands  in  the  right  iliac  fossa. 

Tight  lacing  and  corsets  are  probably  extremely  important  in  the 
production  of  a  freely  movable  liver.  The  pressure  of  the  corset  and  the 
traction  exerted  by  a  heavy  skirt  at  the  waist  tend  to  displace  the  ab- 
dominal viscera  downwards.  The  suspensory  ligaments  of  the  liver,  if 
degenerate,  would  thus  be  easily  elongated.  Further,  tight  lacing  leads 
to  weakness  of  the  abdominal  muscles,  and  so  increases  the  conditions 
favourable  to  hepatoptosis. 

Landau  f  and  Hertz, |  however,  who  have  paid  considerable  attention  to  the 
effects  of  tight  lacing,  oppose  this  view. 

Failure  of  the  healthy  tone  of  the  abdominal  muscles,  leading  to  a 
]3endulous  condition  of  the  abdomen  with  a  diminution  of  intra-abdom- 
inal pressure,  is  an  important  factor  in  hepatoptosis.  A  flaccid  abdominal 
wall  removes  the  support  provided  to  the  liver  by  the  intestines,  and 
thus  throws  the  weight  of  the  liver  onto  the  suspensory  ligaments,  which 
if  not  sufficiently  strong  will  stretch  and  elongate.  Weakness  of  the 
abdominal  walls  alone  is  not  sufficient  to  cause  hepatoptosis,  and,  con- 
versely, hepatoptosis  may  occur  when  the  abdominal  walls  are  healthy. 

In  55  cases  of  hepatoptosis  collected  l^y  Graham  §  only  19  were  definitely 
stated  to  have  pendulous  abdomens. 

*  Treves:  Brit.  Med.  Journ.,  1896,  vol.  i,  p.  1. 

t  Landau:  Deutsrh.  Archiv  f.  klin.  Med.,  Bd.  xiv,  1S75.  J  Hertz:  Loc.  cit. 

§  Graham,  .J.  E. :  Loomis  and  (i.  Thompson's  Sj'stcm  of  Practical  Medicine, 
vol.  iii,  p.  414. 


26  DISEASES    OF   THE    LIVER. 

The  causes  which  lead  to  weakening  of  the  abdominal  parietes  are 
chiefl}^  those  that  produce  abdominal  distension,  such  as  repeated  preg- 
nancy, ascites,  intra-abdominal  tumors,  persistent  flatulence,  and  accu- 
mulations of  fat.  In  addition,  the  wearing  of  stays  and  want  of  exercise 
diminish  the  healthy  tone  of  the  abdominal  muscles,  while  anaemia, 
debilitating  diseases,  and  neurasthenia  have  the  same  effect.  This 
weakening  of  the  abdominal  walls  is  a  most  important  factor  in  dimin- 
ishing the  intra-abdominal  tension.  These  conditions  being  more  fre- 
quently present  in  women,  abdominal  tension  is  much  lower  among 
them  than  among  athletic  men.  In  men  who  lead  a  sedentary  Hfe, 
such  as  tailors  and  cobblers,  however,  the  intra-abdominal  pressure 
may  be  low.     In  women  it  may  even  be  negative.     (Bruce  Clarke.*) 

Glenard  f  lays  stress  on  "hepatism"  as  a  factor  in  the  production  of  movable 
liver.  By  "  hepatism  "  he  means  a  chronic  nutritional  change  which  may  be  heredi- 
tary or  acquired,  and  may  be  of  two  kinds,  (a)  chol^mic,  (b)  uricsemic,  corresponding 
to  "arthritism"  of  some  French  authors,  and  to  Murchison's  "hthsemia."  (Vide 
p.  39.) 

To  sum  up:  The  important  disposing  factors  in  the  production  of 
hepatoptosis  are  (1)  a  weak,  extensible  condition  of  the  suspensory  liga- 
ments and  (2)  a  low  intra-abdominal  tension  due  to  an  atonic  condition 
of  the  abdominal  walls.  These  conditions  of  impaired  nutrition  are  very 
prone  to  go  together  and  to  be  accompanied  by  general  visceroptosis. 

Associated  Conditions. — Visceroptosis. — Hepatoptosis  may  be  part 
of  general  enteroptosis  and  the  most  prominent  manifestation  of  that 
condition,  or  it  may  occur  in  cases  where  there  is  no  other  manifestation 
of  visceroptosis  or  only  a  floating  kidney.  The  association  of  a  floating 
right  kidney  with  hepatoptosis  is  comparatively  frequent. 

In  44  cases  of  hepatoptosis,  verified  eitlier  by  laparotomy  or  autopsy,  Button 
Steele  J  found  9  cases  of  floating  right  kidney,  or  20.4  per  cent.  In  330  cases  of 
nephroptosis  recognized  clinically  by  Glenard  §  in  women,  there  were  70  cases  of 
hepatoptosis. 

Neurasthenia,  etc. — As  already  mentioned,  neurasthenic  conditions 
and  general  debility  with  loss  of  muscular  tone  may  accompany  total 
hepatoptosis  and  are  probably  closely  related  to  the  low  intra-abdominal 
pressure.  Schwerdt,  ||  indeed,  regards  visceroptosis  as  primarily  depen- 
dent on  muscular  atony  of  nervous  origin. 

Exciting  Causes. — A  wandering  liver  in  the  majority  of  cases  de- 
velops gradually,  so  that  there  is  no  definite  onset.  But  in  a  certain 
proportion  of  the  cases — according  to  Graham,  in  5  per  cent. — there  is 
an  acute  onset  of  symptoms  suggesting  sudden  dislocation  of  the  organ. 
This  acute  onset  may  in  rare  instances  be  due  to  severe  injuries  leading 
to  rupture  or  laceration  of  the  peritoneal  suspensory  ligaments,  such  as 
the  passage  of  a  wheel  over  the  body,  falls,  or  blows.  In  less  extreme 
cases    sudden    exertion   in   lifting    heavy   weights,    violent   expiratory 

*  Bruce  Clarke,  W. :  Brit.  Med.  Journ.,  1896,  vol.  ii,  p.  1493. 

t  Glenard:  Les  ptoses  Viscerales,  Paris,  1899,  p.  736  et  passim. 

t  Steele,  Dutton :  Loc.  cit. 

§  Glenard:  Les  ptoses  Viscerales,  Paris,  1899,  p.  503. 

II  Schwerdt:  Deutsch.  med.  Wochen.,  Jan.  23,  1896. 


HEPATOPTOSIS. 


27 


efforts,  such  as  sneezing,  coughing,  vomiting,  laughing,  or  straining,  may 
have  the  same  effect. 

Max  Einhorn  *  refers  to  a  singer  on  whom  the  laborious  work  of  the  diaphragm 
incident  to  his  profession  probably  led  to  laceration  of  the  hepatic  ligaments. 

Forms  of  Total  Hepatoptosis. — In  hepatoptosis  the  liver  tends  to 
be  rotated  in  two  different  directions,  (1)  on  its  transverse  axis,  so  that 
its  upper  (diaphragmatic)  surface  comes  in  contact  with  the  abdominal 
wall,  while  the  anterior  surface  points  do^\mwards;  this  is  anteversion. 
(2)  On  its  vertical  axis;  usually  the  convexity  of  the  liver  is  turned 
to  the  right  and  the  under  surface  to  the  left. 

While  the  liver  is  more  coixmionly  displaced  downwards  and  to  the 
right,    it    may    be     displaced 
downwards     and     rotated    to 
the  left.     Thus,  the  liver  may 

(2) 

to 

(3) 

to 


be  (1)  simply  anteverted; 
anteverted  with  rotation 
the  right,  the  usual  form; 
anteverted  with  rotation 
the  left. 

Hepatoptosis  with  Antever- 
sion.— ^The  liver  being  more 
fixed  posteriorly,  where  the  in- 
ferior vena  cava  runs  through 
it,  than  elsewhere,  movement 
is  least  in  this  situation.  The 
liver  moves  downwards,  the 
sharp  anterior  margin  sinking 
down  towards  the  pelvis  while 
the  superior  or  diaphragmatic 
surface  slides  forwards  and 
downwards  so  as  to  come 
under  the  anterior  abdominal 
wall.  The  inferior  surface  of 
the  liver  at  the  same  time 
becomes  more  posterior.  The 
liver  becomes  much  flattened  out  and  elongated.  (Vide  Fig.  9.)  As 
the  result  of  tight  lacing,  the  front  of  the  liver  may  show  a  transverse 
line  of  fibrous  atrophy.  This  grooved  condition  of  the  liver  {le  foie  corde; 
Schnurleber)  when  exaggerated  has  been  spoken  of  as  the  "pilgrim's 
bottle  liver"  ("le  foie  en  gourde  de  pelerin"). 

The  following  case,  in  which  the  condition  was  recognized  only  on 
the  postmortem  table,  is  a  good  example  of  hepatoptosis  with  ante- 
version. 

On  opening  the  body  of  a  widow  aged  fifty  who  died  of  bronchitis  after  being 
only  one  day  in  St.  George's  Hospital,  I  found  the  liver  extremely  mobile,  and 
occupying  the  front  of  the  abdomen  like  a  flattened  cake  and  reaching  1^  inches 
below  the  umbilicus;  both  lobes  were  much  elongated,  as  shown  in  the  figure. 

*  Max  Einhorn :  Medical  Record,  Sept.  16,  1899. 


Fig.  9. — Partially  Antevkkted  Liver  with  Elos- 
GATiox  OF  Both  Lubes.  (Drawn  by  Dr.  H.  B. 
Roderick.) 


28  DISEASES    OF   THE    LIVER. 

The  coronary  ligaments  were  verj^  much  elongated,  measuring  2^  inches.  There 
was  also  evidence  of  constriction  from  tight  lacing;  the  lower  part  of  the  liver 
below  the  constriction  could  be  easily  turned  up  so  as  to  form  a  double  fold  of 
liver  substance.  The  commencement  of  the  cystic  duct  contained  a  calculus, 
and  the  neck  of  the  gall-bladder  was  much  elongated.  The  kidnej^s  appeared  more 
movable  than  natural,  and  the  pn-sence  of  linea;  albicantes  on  the  abdomen  as 
well  as  the  character  of  the  os  uteri  made  it  probable  that  she  had  had  children. 
This  case  was  e^ddently  one  of  partially  anteverted  wandering  liver.  Somewhat 
similar  cases  are  described  by  Crawfurd,*  Peters,!  and  Griffiths.! 

The  following  is  a  good  example  of  a  moA'-able  liver  with  rotation  on 
its  vertical  axis  to  the  right: 

Morestin  §  found  the  gall-bladder  and  right  lobe  of  a  man's  liver  in  the  right 
iliac  fossa.  The  liver  was  elongated  and  rotated  so  that  the  convexity  pointed 
to  the  right  and  the  under  surface  to  the  left.  The  left  lobe  was  reduced  in  size 
to  a  mere  tongue  of  hepatic  tissue.  There  was  no  morbid  change  in  the  liver  sub- 
stance. 

In  cases  of  such  rotation  the  right  lobe  may  simulate  disease  around 
the  appendix. 

Complications. — Generally  speaking,  a  movable  liver  can  be  replaced 
in  its  normal  position,  but  this  is  not  always  possible;  in  80  cases  collected 
by  Glenard  this  could  not  be  effected  in  14,  while  in  3  more  it  could  only 
partially  be  accomplished.  A  movable  Hver  may  contract  adhesions 
when  displaced  downwards,  and  so  become  fixed  to  the  lower  part  of  the 
abdomen.  L'nder  these  circumstances  it  readily  gives  rise  to  great  diffi- 
culty in  diagnosis  and  may  resemble  some  abclominal  tumor  or  inflam- 
matory formation. 

Richelot,  ||  in  an  exploratory  laparotomy  for  an  abdominal  tumor  of  doubtful 
origin,  found  the  liver  rotated  and  fixed  in  the  right  ihac  region. 

A  movable  and  displaced  liver  has  been  found  to  be  cirrhosed,  to  be 
associated  with  calculous  cholecystitis,**  gall-stones,  or  in  exceptional 
instances  to  be  occupied  by  malignant  disease  or  a  hydatid  cyst.  (Ned- 
wiU.ft)  A  certain  amount  of  atrophy  and  subsequent  fibrous  substitu- 
tion may  be  due  to  torsion  and  twisting  of  the  portal  vessels  and  bile- 
duct  in  the  lesser  omentum. 

Tn  80  cases  collected  by  Glenard  J  J.  the  liver  was  healthy  in  50;  in  26  it  was 
the  subject  of  disease,   u.suaUy  cirrhosis  or  gall-stones.      In  one  each  cancer  or 

hydatid  cyst  was  present. 

Physical  Signs. — There  is  an  abdominal  tumor  which  is  readily 
displaceable,  and  can  be  put  back  into  the  normal  position  of  the  liver, 
to  which,  indeed,  it  tends  to  return  when  the  patient  lies  down,  only 
to  fall  when  a  sitting  or  erect  posture  is  assumed,  the  organ  dropping 
two  or  more  inches.     The  liver  still  descends  on  respiration;    l)ut  the 

*  Crawfurd,  R.  P.:  Lancet,  1897,  vol.  ii,  p.  1182. 

t  Peters:  New  York  Med.  Gaz.,  1882,  p.  412. 

X  Griffiths,  T.  D. :  Trans.  Path.  Soc,  vol.  xxviii. 

§  H.  Morestin:  Bull,  de  la  Soc  Anat.,  Paris,  1896,  p.  201. 

II  Puchelot:  Gaz.  des  Hop.,  1893,  p.  783. 
**  Lennander:  Gaz.  des  Hop.,  Mav  10,  1900. 
tt  Xedwill :  Lancet,  1901,  vol.  h,  p.  914. 
Jl  Glenard:  Les  ptoses  Viscerales,  Paris,  1899. 


HEPATOPTOSIS.  29 

nu^re  marked  the  displacement,  the  less  is  this  apparent.  When  the 
organ  is  very  freely  movable,  and  when  presumably  the  lateral  ligaments 
are  greatly  stretched  or  but  ill  developed,  it  can  be  readily  rotated  on  its 
vertical  axis,  which  passes  through  the  inferior  vena  cava.  This  rota- 
tion is  an  exaggeration  of  that  which  a  dilated  stomach  or  colon  may 
induce  in  the  liver  under  normal  conditions.  The  freedom  of  movement 
may,  indeed,  be  so  marked  that  the  liver  seems  to  turn  over  in  its  descent. 
When  the  patient  turns  on  the  left  side,  it  travels  in  the  same  direction. 

The  displaced  liver  is  visible  under  the  relaxed  abdominal  walls  as  a 
rounded  tumor  on  the  right  side  about  the  level  of  the  umbilicus.  It 
is  dull  on  percussion,  firm,  and  smooth.  The  outline  of  the  liver  and 
perhaps  the  depression  for  the  fundus  of  the  gall-bladder  and  the  notch 
between  the  left  and  right  lobes  for  the  round  ligament  can  also  be  made 
out.  When  the  organ  has  fallen  away  from  the  right  hypochondrium, 
the  normal  liver  dulness  is  replaced  by  resonance.  In  such  cases  the 
hand  may  be  passed  some  way  over  the  upper  surface  of  the  liver,  between 
it  and  the  diaphragm.  There  is  a  sinking  or  hollow  in  the  right  hypo- 
chondrium and  a  compensatory  swelling  or  tumor,  formed  by  the  dis- 
placed liver,  in  the  right  flank  or  in  the  abdomen  below  the  umbilicus. 
The  empty  state  of  the  upper  part  of  the  abdomen  below  the  right  costal 
arch  may  be  very  striking. 

The  abdominal  walls  may  be  so  lax  and  thin  as  to  allow  peristaltic 
action  to  be  plainly  visible,  and  divarication  of  the  recti  and  a  pendu- 
lous condition  of  the  abdomen  may  be  brought  out  when  the  patient  rises 
from  the  horizontal  position.  According  to  Glenard,  the  lower  part  of 
the  umbilicus  becomes  hidden  by  a  fold  of  skin,  upon  which  tension  is 
brought  to  bear  by  the  displaced  liver  through  the  attachment  of  the 
round  and  falciform  ligaments.  Other  manifestations  of  visceroptosis, 
such  as  a  floating  kidney,  a  displaced  uterus  or  stomach,  may  be  present. 

Onset. — Generally  this  is  insidious  and  attracts  no  attention,  but  in 
some  instances  (Graham*  says  5  per  cent.)  it  may  be  sudden,  and  then 
resembles  a  traumatic  dislocation.  There  is  then  a  feeling  of  something 
giving  way,  accompanied  by  sudden,  twisting  pain,  which  may  be  so 
severe  as  to  make  the  patient  faint,  and  may  then  be  regarded  as  biliary 
colic. 

A  good  case  of  sudden  dislocation  of  the  liver  is  recorded  by  Garnett  f  in  a 
woman  aged  fifty,  who,  when  hurriedly  stooping  to  pick  something  up  from  the 
floor,  felt  a  sudden  wrench 'in  the  right  side  of  the  abdomen.  The  liver  was  found 
reaching  to  the  right  iliac  crest.  Rest  in  bed  and  the  application  of  an  appropriate 
bandage  were  followed  by  recovery.  Graham  f  has  seen  a  movable  displaced  liver 
due  to  the  wheel  of  a  wagon  passing  over  the  abdomen  in  a  boy  aged  seventeen. 

Symptoms. — The  symptoms  of  floating  liver  may  be  summed  up 
under  different  heads,  as  cases  may  present  the  features  of  one  or  jnore 
of  the  following  symptom-groups: 

(1)  Pain,  dragging,  and  heaviness  in  the  hepatic  region. 

*  Graham,  J.  E. :  Loomis  and  Thompson's  System  of  Practical  Med.,  vol.  iii, 
]\  41.5. 

t  Garnett,  A. :  American  .Journ.  Med.  Sciences,  1881,  p.  110. 
j  Graham,  .J.  E. :  Canadian  Practitioner,  1895. 


30  DISEASES    OF   THE    LIVER. 

(2)  Symptoms  referable  to  the  intestinal  tract,  viz.,  dyspepsia, 
vomiting,  and  mucous  colic. 

(3)  Imitating  biliary  colic,  viz.,  pain  and  jaundice. 

(4)  Imitating  hepatic  cirrhosis,  viz.,  ascites,  hsematemesis,  melsena. 
These  symptoms  are  very  rare. 

(5)  Symptoms  belonging  to  the  respirator}^  system,  viz.,  cough, 
dyspnoea. 

(6)  H}T30chondriasis,  hysteria. 

There  may,  however,  be  no  sj^mptoms  at  all. 

Hepatic  Pain. — ^Wlien  symptoms  are  present,  the  commonest  is  a 
feeling  of  discomfort,  weight,  or  actual  pain  in  the  right  h}^ochondrium. 
The  dragging  feeling  is  commonly  felt  in  the  right  hypochondrium  or 
epigastrium,  but  it  may  be  more  extensive  and  radiate  behind  the  sternum 
or  even  to  the  base  of  the  neck,  the  traction  exerted  on  the  diaphragm 
by  the  liver  being  perhaps  transmitted  through  the  pericardium  to  the 
cervical  fascia.  The  pain  and  discomfort  are  usually  reheved  in  the 
horizontal  position,  but  are  aggravated  by  movement,  and  may  quite 
prevent  the  patient  from  walking  or  getting  about,  or  even  from  lying 
on  the  right  side.  The  pain,  however,  may  be  constant  and  verj^  dis- 
tressing, and  is  then  quite  probably  due  to  chronic  cholecystitis,  chole- 
lithiasis, or  stretching  of  adhesions.  There  are  frequently  attacks  of 
very  severe  pain,  exactly  like  biliary  colic,  but  not  necessarily  accom- 
panied by  jaundice. 

In  44  cases  of  hepatoptosis  these  colicky  attacks  occurred  in  37,  or  84  per 
cent.,  and  were  only  accompanied  by  jaundice  in  14.     (Button  Steele.*) 

This  subject  is  referred  to  again  later  on. 

Symptoms  Referable  to  the  Intestinal  Tract. — In  other  cases  the  symp- 
toms are  mainly  of  a  dyspeptic  nature.  Nausea  and  vomiting  maj' 
occur  and  may  be  set  up  by  lying  on  the  right  side.  Intestinal  disturb- 
ance, such  as  flatulent  distension  and  constipation,  may  be  present. 
Glenard  f  considers  that  the  vascular  disturbance  resulting  from  a  wan- 
dering liver  is  the  cause  of  mucous  or  "membranous"  colitis  (or  colic), 
which  he  thinks  is  often  associated  vdth  enteroptosis.  Probably  many 
of  the  symptoms  observed  in  hepatoptosis,  such  as  hysterical  mental 
disturbance  and  irritability,  leucorrhoea,  menorrhagia,  albuminuria,  are 
rather  the  results  of  enteroptosis  in  general  than  of  hepatoptosis  in 
particular. 

Symptoms  Imitating  Biliary  Colic. — As  already  mentioned,  attacks 
of  pain  resembhng  bihary  colic  are  very  frequently  met  with,  in  cases  of 
wandering  liver. 

In  44  cases  in  which  the  liver  was  seen  to  be  displaceable  either  at  a  laparotomy 
or  autopsy,  attacks  of  colic  occurred  in  37,  or  84  per  cent. ;  in  14  of  these  37  there 
was  jaimdice  and  in  10  calcuU.  In  15  cases  attacks  of  colic  and  transient  jaundice 
occurred  without  gall-stones.     (Button  Steele.) 

*  Button  Steele:  University  of  Pennsylvania  Med.  Bull.,  vol.  xv,  p.  424,  Jan., 
1903. 

t  Glenard :  Academic  de  M^decine,  April  20,  1897. 


HEPATOPTOSIS.  31 

The  colic  may  be  due  to  at  least  three  causes,  viz.,  calculi,  the  presence 
of  a  floating  kidney  on  the  same  side,*  or  torsion  of  one  of  the  bile-ducts. 
In  the  absence  of  gall-stones  and  a  floating  kidney  on  the  right  side  the 
attacks  of  colic  are  probably  due  to  torsion  of  the  cystic  duct  at  its  junc- 
tion with  the  common  bile-duct,  which  would  not  necessarily  give  rise 
to  jaundice  or  to  kinking  of  the  common  bile-duct  at  its  commencement. 

In  Crawfurd's  f  case  of  hepatoptosis  with  jaundice  a  twist  seemed  to  have 
occurred  at  the  commencement  of  the  common  bile-duct.  In  this  case  I  had  an 
opportunity  of  examining  sections  of  the  hver  which  showed  dilatation  of  the 
lymphatics  and  oedema  in  the  portal  spaces,  as  if  the  lymphatics  had  also  been 
twisted  and  obstructed ;  but  as  bile  had  evidently  passed  into  the  general  circulation, 
the  obstruction  must  have  been  intermittent. 

Button  Steele  discusses  the  question  why  jaundice  is  not  always  met 
with,  and  points  out  that  the  obstruction  need  not  always  be  in  the 
common  bile-duct  and  that  the  kinking  may  be  very  transitory^,  the  liver 
returning  towards  its  normal  position.  His  experiments  showed  that 
the  further  the  liver  was  displaced  towards  the  pelvis,  the  greater  was 
the  pressure  required  to  drive  an  injection  from  the  biliary  papilla  into 
the  gall-bladder. 

In  some  instances  jaundice  may  occur  without  pain;  Steele  refers 
to  two  cases.     It  may  be  catarrhal,  as  in  Snowman's  J  case. 

It  may  be  pointed  out  that  a  displaced  liver  may  by  traction  on  the 
ducts  lead  to  stagnation  of  bile  in  the  ducts,  and  so  favour  hydrops  of 
the  gall-bladder,  cholecystitis,  and  the  production  of  gall-stones. 

In  Newman's  §  case  the  gall-bladder  contained  thirty  ounces  of  straw-coloured 
fluid  and  numerous  gaE-stones. 

Symptoms  Imitating  Hepatic  Cirrhosis. — As  very  exceptional  results, 
reference  may  be  made  to  the  occurrence  of  ascites,  probably  caused  by 
twisting  of  the  portal  vein,  and  oedema  of  the  legs,  probably  due  to  a  kink 
of  the  inferior  vena  cava.  Twisting  of  the  portal  vein,  by  obstructing 
the  circulation,  might  be  expected  to  give  rise  to  venous  oo?:ing  into  the 
stomach  and  intestines  and  so  to  hsematemesis  and  mela?na.  Hismat- 
emesis  is,  however,  extremely  rare. 

McNaughton  Jones  ||  describes  a  case  of  a  woman  aged  thirty-eight,  the  mother 
of  seven  children,  who  had  hsematemesis  on  several  occasions,  the  first  at  the  age 
of  nineteen.  The  last  attack  was  very  severe,  and  at  this  time  a  tumor,  thought 
to  be  renal,  was  discovered.  At  the  laparotomy  the  tumor  was  found  to  be  liver, 
which  extended  into  the  rigl)t  iliac  fossa. 

Symptoms  Referable  to  the  Respiratory  System. — In  some  cases  classed 
by  Max  Einhorn  **  as  asthmatic  there  is  dyspnoea  in  addition  to  a  feeling 
of  fulness  and  constriction  in  the  upper  part  of  the  abdomen. 

A  dry  cough  of  eighteen  years'  duration,  which,  however,  disappeared  when 
the  patient  was  in  the  recumbent  posture,  was  found  by  L.  Veneft  to  be  associated 

*  Compare  J.  Hutchinson,  Jr. :  Practitioner,  Feb.,  1902. 

t  Crawfurd:  Lancet,  1897,  vol.  ii,  p.  1182.         %  Snowman:  Lancet,  1896,  vol.  i. 

§  D.  Newman:  Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  249. 

II  McNaughton  Jones:  Lancet,  1898,  vol.  i,  p.  1327. 
**  Max  Einhorn :  Medical  Record,  Sept.  16,  1899. 
tt  Louis  Vene:  Journal  de  M^decine  Interne,  Oct.  15,  1898. 


32  DISEASES    OF   THE    LIVER. 

with  hepatoptosis,  and  was  cured  by  the  apphcation  of  a  flannel  bandage.  It  was 
thought  that  the  cough  was  due  to  excitation  of  the  diaphragm  by  traction  of  the 
liver  on  the  inferior  vena  cava. 

Some  instances  of  cough  usually  put  clown  to  hysteria  may  in  reality 
be  due  to  hepatoptosis. 

Hysteria  or  hypochondriasis  is  frequently  observed  to  be  associated 
with  hepatoptosis;  the  mental  depression  may  result  in  the  patient 
acquiring  the  morphia  habit. 

Absence  of  Symptoms. — A  freely  movable  liver  may  be  found  acci- 
dentally in  patients  who  do  not  suffer  any  inconvenience  from  it.  Bed- 
dard  *  refers  to  a  case  in  a  placid  unmarried  lady  who  lived  at  her  ease 
and  in  whom  "the  tumor ^'  formed  by  the  prolapsed  liver  merely  aroused 
an  "amused  curiosity."  It  is  probable  that  the  presence  or  absence  of 
symptoms  largely  depends  on  the  life  the  individual  leads  and  on  her 
temperament.  Women  of  a  high-strung  and  nervous  nature  often  feel 
pain  and  suffer  inconvenience  from  conditions^  such  as  peritoneal  adhe- 
sions and  floating  kidneys,  of  which  their  more  robust  sisters  are  uncon- 
scious. 

Diagnosis. — In  some  cases  where  movable  livers  have  been  felt 
clinically  the  organ  has  at  the  postmortem  examination  been  found  in 
its  normal  position,  so  that  a  doubt  has  naturally  been  thrown  on  the 
correctness  of  the  diagnosis.  But  if  in  such  a  case  the  suspensory  liga- 
ments are  found  to  be  much  elongated,  it  is  quite  possible  that  the  organ 
has  returned  to  its  natural  condition  as  the  result  of  collapse  of  the 
lungs  and  ascent  of  the  diaphragm,  on  the  one  hand,  and  gaseous  dis- 
tension of  the  intestines,  on  the  other  hand,  pushing  the  liver  up. 

The  chief  points  in  the  diagnosis  are  the  presence  of  a  movable  abdom- 
inal tumor,  resembling  the  liver,  which  can  be  replaced  in  the  position 
of  that  organ,  and  the  fact  that  the  hepatic  region  is  sunken  and  resonant 
on  percussion  when  the  tumor  is  in  the  middle  of  the  abdomen.  In 
addition,  other  conditions,  such  as  a  floating  kidney,  etc.  {ride  Differ- 
ential Diagnosis),  must  be  excluded. 

Differential  Diagnosis. — A  freely  movable  or  wandering  liver  must 
be  distinguished  from  an  enlarged  liver,  from  a  tongue-like  lobe  with  or 
without  a  distended  gall-bladder,  and  from  mere  downward  displacement 
of  the  liver  such  as  may  result  from  pleural  effusion,  pneumothorax,  or 
other  causes. 

In  Packard's  f  case  of  movable  liver  the  diagnosis  during  life  was  subphrenic 
abscess  following  typhoid  fever. 

From  Floating  Kidney. — The  most  frequent  mistake  seems  to  consist 
in  regarding  a  wandering  liver  as  a  floating  kidney  or  as  some  other  form 
of  enlargement  of  the  right  kidney.  Floating  kidneys  are  much  com- 
moner than  hepatoptosis,  and  the  general  symptoms  are  so  much  alike 
that  the  condition  of  the  liver  may  be  overlooked,  especially  when,  as 
is  by  no  means  infrequent,  there  is  a  floating  kidney  as  well  as  a  wander- 

*  Beddard,  A.  P. :  Guy's  Hospital  Reports,  vol.  Ivii,  p.  179,  1902. 
t  Packard :  Trans.  Coll.  Physicians,  Philadelphia,  1896,  p.  230. 


HEPATOPTOSIS.  33 

ing  liver.  Alteration  in  the  position  of  a  floating  liver  may  imitate  an  in- 
termittent hydronephrosis,  while  concomitant  distension  of  the  gall- 
bladder may  have  the  same  effect. 

Newman  *  operated  on  a  floating  liver  and  let  out  30  ounces  of  bile  from  the 
gall-bladder.     The  symptoms  had  suggested  a  hydronephrosis. 

A  careful  bimanual  examination,  if  necessary  under  an  anaesthetic, 
should  be  made;  the  liver  dulness  should  be  percussed,  and  an  attempt 
to  displace  the  abdominal  tumor  into  the  right  loin  should  be  made. 

From  Tumors  and  Hydatid  Cysts  in  the  Liver. — A  wandering  liver  may 
suggest  malignant  disease  of  the  organ,  especially  when,  as  in  rare  cases 
like  Crawfurd's,t  jaundice  and  ascites  are  present  from  torsion  of  the 
common  bile-duct  and  portal  vein  in  the  lesser  omentum.  The  ease 
with  which  the  liver  is  displaced  ought  to  prevent  any  mistake  of  this 
kind,  while,  on  the  other  hand,  irregularities  of  the  surface  of  the  liver 
and  signs  of  chronic  obstruction  of  the  colon  make  malignant  disease 
probable. 

Hydatid  cysts  projecting  from  the  upper  surface  of  the  liver,  or,  in 
rare  instances,  between  the  liver  and  diaphragm,  give  rise  to  downward 
displacement  of  the  organ,  but  there  is  no  absence  of  the  hepatic  dulness 
below  the  sixth  rib  in  the  right  nipple  line,  as  there  would  be  if  the  liver 
had  dropped  away  from  its  normal  position.  The  converse  mistake 
has  occurred,  and  laparotomies  undertaken  for  supposed  hydatid  cysts 
have  led  to  the  discovery  of  a  wandering  liver.     (Marchant  J,  Areilza.§) 

Gall-stones. — ^The  pain  and  jaundice,  presumably  due  to  twisting  of 
the  bile-duct,  may  give  rise,  as  in  a  case  of  Mathieu's,  ||  to  a  diagnosis  of 
biliary  colic.  Max  Einhorn**  has  seen  five  cases  of  wandering  liver  that 
had  previously  been  erroneously  diagnosed  as  cholelithiasis.  The  tAvo 
conditions  may  both  be  present. 

Tumors  and  Inflammatory  Thickenings  of  the  Omenta,  Mesentery,  etc. — 
Tumors  and  cysts  of  the  omentum  and  of  the  mesentery,  though  movable, 
cannot  be  displaced  to  the  same  extent  from  above  downwards  as  a 
wandering  liver;  moreover,  they  are  separated  by  a  zone  of  resonance 
from  the  liver  dulness.  Inflammatory  thickenings  in  the  omentum  are 
comparatively  fixed  and  are  hardly  likely  to  give  rise  to  any  difficulty 
in  diagnosis. 

In  some  exceptional  cases  it  is  just  conceivable  that  a  question  might 
arise  whether  a  movable  tumor  is  the  Uver  or  a  mass  of  growth  in  the 
stomach,  colon,  or  inflammation  around  the  appendix;  but  under  ordinary'- 
conditions  there  is  little  or  no  resemblance  between  hepatoptosis  and 
these  conditions. 

Treatment. — Tight  lacing  and  corsets  which  constrict  the  lower  part 
of  the  thorax  and  tend  to  displace  the  liver  downwards  must  be  discon- 

*  Newman:  Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  249. 
t  Crawfurd,  R. :  Lancet,  1897,  vol.  ii,  p.  1182. 
t  G.  Marchant:  Acad,  de  M(5d.,  Paris,  Aug.  11,  1891. 
§  Areilza:  Rev.  Med.  y  Cirug.  pract.,  1896. 
II  Mathieu:  Gaz.  des  hop.,  1893,  p.  1152. 
**  Max  Einhorn:  Medical  Record,  Sept.  16,  1899. 


34  DISEASES    OF   THE   LIVER. 

tinued.  The  "straight-fronted"  corset  should  be  worn,  as  it  supports 
the  abdomen  from  below  and  does  not  compress  the  waist  unduly.  A 
suitable  abdominal  belt,  binder,  or  elastic  bandages  should  be  applied 
so  as  to  support  the  lower  abdomen  in  an  upward  direction,  and  thus, 
by  increasing  the  intra-abdominal  pressure,  to  support  the  liver  in  its 
proper  position.  The  belt  or  binder  must  reach  below  the  hips  and 
should  be  fixed  in  position  while  the  patient  is  still  in  bed  in  the  morning 
and  before  the  liver  has  become  prolapsed.  This  method  of  replacing 
the  healthy  tone  of  the  abdominal  muscles  is  much  more  effective  than 
applying  a  supporting  pad  to  the  liver  alone.  The  treatment  of  mova- 
ble liver  is  on  the  same  lines  as  that  of  enteroptosis  or  Glenard's  disease. 

Diet  is  a  matter  of  importance  and,  as  a  rule,  the  patient  requires 
liberal  feeding  so  as  to  improve  the  general  state  of  nutrition.  The  subjects 
of  hepatoptosis  are  usually  weakly,  but  when  there  is  decided  corpulence, 
the  amount  and  quality  of  food  taken  should  be  supervised  by  the  medical 
attendant,  and  any  excessive  eating  interdicted.  There  will  be  no  diffi- 
culty in  distinguishing  the  weakly,  flabby  patient  whose  muscles  and 
tissues  are  in  want  of  better  food  from  the  heavy  eater  whose  liver  and 
tissues  are  congested  from  the  presence  of  the  products  of  excessive  pro- 
teid  metabohsm.  It  is  important  to  keep  the  bowels  freely  open,  for  in 
this  wa}^  portal  congestion  and  flatulent  distension  are  relieved  and  a 
distended  gall-bladder  may  be  emptied,  conditions  which  may  conceivably 
dispose  to  or  exaggerate  hepatoptosis. 

In  order  to  improve  the  tone  of  the  abdominal  muscles  carefully 
planned  gymnastic  exercises  may  be  employed.  The  exercises  should  be 
simple  and  readily  carried  out.  Lea*  speaks  of  the  following  as  very 
efficient : 

(1)  The  patient  hes  on  the  back  without  any  pillows,  the  arms  being 
folded  in  front,  and  gradually  raises  herself  into  the  sitting  posture 
without  any  help  from  the  arms. 

(2)  The  patient,  being  in  the  same  position  as  before,  raises  first  one 
lower  limb,  then  both,  with  the  knees  extended,  to  a  right  angle  with 
the  trunk. 

(3)  Deep  breathing,  especially  inspiratory  movements  with  the 
glottis  closed  and  after  a  forced  expiration.  This  exercise  is  useful  in 
drawing  up  the  viscera. 

Lea  directs  that  each  of  these  exercises  should  be  performed  six  to 
twelve  times  night  and  morning. 

Massage  may  be  used  in  order  to  improve  the  muscular  tone. 

Electrical  stimulation  has  been  applied  to  the  abdominal  muscles 
and  has  been  found  to  be  beneficial.  Griffith  f  obtained  a  good  result 
by  daily  stimulating  the  muscles  with  an  interrupted  current  for  three 
months,  but  the  long  duration  of  the  treatment  would  render  it  unsuitable 
in  many  cases. 

If  the  application  of  a  belt  and  the  other  palliative  measures  referred 
to  fail  to  relieve  the  symptoms,  and  the  pain  is  so  se^'ere  as  to  in- 

*  A.  W.  W.  Lea:  Medical  Chronicle,  July.  1902. 
t  Griffith:  Brit.  Med.  Journ.,  1878,  vol.  i,  p.  89. 


HEPATOPTOSIS.  35 

capacitate  the  patient  from  ordinary  life  and  work,  the  advisabiUty  of 
surgical  interference  must  be  considered.  The  operation  of  fixing  the 
liver  by  sutures  or  other  means  in  its  proper  position  is  known  as 
hepatopexy  or  hepatorrhaphy.  Various  methods  have  been  adopted, 
such  as  passing  sutures  through  the  liver  substance  and  the  abdominal 
wall,  tying  the  round  ligament  up  to  the  cartilage  of  the  seventh  rib  and 
at  the  same  time  promoting  adhesions  between  the  diaphragm  and 
convexity  of  the  liver  by  rubbing  the  peritoneum  with  aseptic  gauze. 
When  the  gall-bladder  contains  calculi,  the  operation  for  cholecystotomy 
usually  leads  to  fixation  of  the  liver. 

In  1891  Gerard  Marchant  *  fixed  the  anterior  margin  of  the  Uver  to  the  costal 
margin  by  four  silk  sutures,  and  was  followed  by  Langenbuch  t  and  Richelot,J 
who  performed  somewhat  similar  operations.  Treves  §  utilized  the  round  ligament 
to  support  the  sutures.  Lannelongue  and  Faquet  ||  in  1895  sutured  the  liver  to  tlie 
anterior  abdominal  waU  and  roughened  the  opposed  surfaces  of  the  liver  and  dia- 
phragm so  as  to  get  adhesions.  Union  of  the  liver  to  the  opposed  peritoneal  surface 
of  the  diaphragm  has  also  been  obtained  b)^  swabbing  the  surface  of  the  liver  with 
strong  carbolic  acid. 

Pean  **  supported  the  liver  b}^  uniting  the  peritoneum  of  the  anterior  abdominal 
wall  with  that  of  the  postero-lateral  part  of  the  abdomen  below  the  replaced  liver. 

In  fifteen  cases  of  hepatopexy  collected  byTerrier  and  Auvray  ft  there 
were  eleven  cures. 

The  drawbacks  to  operative  measures  are, — (1)  that  the  underlying 
condition  disposing  to  enteroptosis  in  general  and  hepatoptosis  in  par- 
ticular is  not  removed;  (2)  that  the  incision  through  the  abdominal 
walls  is  ver}'  prone  to  become  the  seat  of  hernial  protrusion,  inasmuch 
as  their  tone  and  nutrition  are  especially  defective. 

On  the  other  hand,  hepatopexy  may  succeed  after  all  other  mechan- 
ical and  palliative  measures  have  failed,  and  it  does  so  by  compensating 
for,  though  not  removing,  the  disposing  factors  of  hepatoptosis.  The 
danger  of  hernial  protrusion  in  the  scar  is  probably  greater  in  old  women 
with  permanently  pendulous  abdomens  than  in  j^ounger  women  who  are 
temporarily  in  a  Iom'  state  of  nutrition  from  several  rapidly  succeeding 
pregnancies.  In  any  case  an  abdominal  belt  should  be  worn  after  the 
operation. 

With  regard  to  prophylaxis,  the  practice  of  tight  lacing  should  be 
prevented  and  care  should  be  taken  that  a  pendulous  condition  of  the 
abdominal  wall  is  not  induced  or  aggravated  by  getting  up  too  soon 
after  parturition  and  by  neglecting  the  use  of  a  proper  binder. 

*  Gerard  Marchant:  Acad,  de  Med.,  Aug.  11,  1891. 
t  Langenbuch:  Deutsch.  med.  Wochen.,  1891,  S.  1241. 
X  Richelot:  Gaz.  Hebd.  de  M6d.  et  de  Chirurg.,  1892,  p.  242. 
§  Treves:  Brit.  Med.  Journ.,  Jan.  4,  1896. 

|l  Lannelongue  et  Faquet:  Congres  de  Bordeaux,  189.5.     Quoted  by  Treves: 
Lancet,  1900,  vol.  i,  1344. 

**Pean:  Congres  de  Chirurg.,  Paris,  1896.  Quoted  by  Treves:  Lancet,  1900, 
vol.  i,  1.344. 

tt  Terrier  et  Auvray:  Rev.  de  Chirurg.,  1897,  p.  746. 


FUNCTIONAL  DISEASE  OF  THE  LIVER. 

Before  entering  on  the  rather  difficult  subject  of  functional  disease 
of  the  hver  it  will  be  convenient  to  enumerate  the  important  functions 
of  the  liver. 

(1)  The  secretion  of  bile. 

(2)  The  metabohc  processes  in  connection  with  the  formation,  stor- 
age, and  supply  of  gtycogen. 

(3)  In  connection  with  proteid  metabohsm.  The  liver  is  very  largely 
concerned  in  the  conversion  of  ammonia  into  urea,  but  there  is  no  reason 
to  believe  that  it  plays  any  part  of  importance  in  the  production  of  uric 
acid.  In  some  diseases,  in  which  the  liver  cells  are  degenerated,  the 
amount  of  urea  is  diminished  while  the  quantity  of  nitrogen  excreted  in 
the  urine  as  ammonia  is  increased.  It  has,  therefore,  naturally  been 
assumed  that  the  fall  in  the  output  of  urea  was  due  to  failure  in  the  func- 
tional activity  of  the  liver  cells.  This,  however,  is  not  the  true  explana- 
tion. The  real  reason  is  that  in  these  diseases  organic  acids,  of  the  fatty 
acid  series,  are  formed  and  unite  with  any  available  bases,  among  which 
is  ammonia,  present  in  the  blood.  The  ammonia,  which  under  ordinaiy 
conditions  would  be  changed  by  the  liver  into  urea,  is  now  in  a  form 
which  cannot  undergo  this  transformation,  and  therefore  appears  in 
the  urine  linked  "udth  an  organic  acid.  This  occurs  in  acute  yellow 
atrophy,  phosphorus  poisoning,  and  some  cases  of  cirrhosis  and  fatty 
liver.  In  such  cases  ammonia  given  by  the  mouth  increases  the  amount 
of  urea  in  the  urine,  thus  showing  that  the  liver  cells  have  not  lost  their 
power  of  transforming  ammonia  into  urea.  It  is  only  in  the  very  latest 
stages  of  such  diseases,  shortly  before  death,  that  the  hver  cells  appear 
to  lose  this  power.* 

(4)  Its  antitoxic  or  protective  function.  Poisons,  whether  intro- 
duced into  the  alimentary  canal  or  manufactured  there  as  the  result  of 
bacterial  activity,  are  normally  arrested,  or  converted  into  harmless 
bodies  by  the  liver  ceUs.  The  detoxicating  action  of  the  hver  is  shown 
by  the  difference  in  the  action  of  poisons,  such  as  strychnine,  conia,  snake 
poison,  albumoses,  when  introduced  into  the  portal  circulation,  on  the 
one  hand,  and  into  the  general  circulation,  on  the  other  hand.  It  appears 
from  Roger's  j  observations  that  the  antitoxic  function  of  the  liver  varies 
with  its  richness  in  glycogen  and  its  power  of  stopping  sugar  and  formhig 
glycogen,  and  that  if  the  liver  loses  its  power  of  stopping  sugar  it  is  also 
unable  to  arrest  poisonous  bodies  brought  to  it  from  the  portal  area. 
In  complete  biliary  obstruction  the  antitoxic  power  of  the  liver  fails, 
and  the  grave  manifestations  seen  imder  these  conditions  are  chiefly  due 

*  For  a  lucid  account  of  this  question  the  reader  should  refer  to  Hertcr's  Lectures 
on  Chemical  Pathology,  p.  338. 

t  Roger:  La  Presse  -Mddicale,  June  26.   1897. 

36 


FUNCTIONAL    DISEASE    OF  THE   LIVER.  37 

to  the  poisons  which  flood  the  body,  and  only  depend  in  a  minor  degree 
on  the  presence  of  the  bile  pigments  in  the  blood. 

From  the  number  and  importance  of  the  functions  of  the  liver  it  is 
clear  that  failure. in  discharge  of  these  duties  must  be  followed  by  very 
definite  symptoms.  Functional  disturbance  is  undoubtedly  common  in 
the  liver,  but  the  folloTving  questions  require  some  consideration: 

(!)  Are  the  disorders  of  hepatic  function  primar}^  in  the  Uver  ?  and 
(2)  Are  the}'  entirely  independent  of  structural  change  in  the  organ? 

Numerous  conditions,  many  of  them  in  no  way  connected  with  the 
liver,  Avere  formerly  described  as  due  to  functional  disease  of  that  organ. 
The  idea  was  attractive  to  the  lay  mind  and  is  recklessly  appealed  to  in 
everyday  life.  Flatulence,  dyspepsia,  constipation,  and  the  bad  effects 
of  overeating  and  drinking  are  often  eupheixiistically  described  as  "liver." 
As  a  reaction  against  this  inaccurate  though  comforting  doctrine  the 
tendency  at  the  present  time  among  most  English  medical  -^Titers  is 
to  ignore  the  subject  or  to  deny  the  existence  of  primar}'  functional 
disease  of  the  Hver.  This  s\\dng  of  the  pendulum  to  the  opposite  extreme 
— for  it  must  be  admitted  that  the  idea  originated  with  the  profession — 
is  due  to  the  knowledge  that  the  symptoms  ascribed  to  functional  disease 
of  the  hver  can  in  great  part  be  explained  as  due  to  other  factors,  such 
as  indigestion,  auto-intoxication,  constipation,  or  to  subacute  congestion 
or  even  inflammation  of  the  organ,  often  secondary  to  intestinal  disturb- 
ance or  to  absor]3tion  of  toxic  products  from  the  intestine.  In  other 
words,  the  hepatic  disturbances  formerly  regarded  as  due  to  primary 
functional  insufficiency  are  in  the  vast  majority  of  cases  dependent  on 
morbid  processes  elsewhere,  and  therefore  secondary,  or  are  associated 
with  definite  organic  change  in  the  Hver. 

Thus,  to  consider  the  symptoms  commonly  referred  to  functional 
disorder  of  the  liver,  the  distaste  for  food,  dyspepsia,  flatulence,  con- 
stipation or  diarrhoea,  are  the  expression  of  gastro-intestinal  catarrli  set 
up  b}'  poisonous  or  unsuitable  food.  The  icteric  tint  of  the  conjunctivae, 
the  muddy  skin,  and  some  of  the  mental  depression  are  either  due  to  the 
spread  of  the  gastro-duodenal  catarrh  to  the  l^ihar}-  papilla  and  the  slight 
obstruction  to  the  flow  of  bile  thus  induced;  or  possibly  to  catarrh  of 
the  minute  intra-hepatic  ducts  set  up  by  poisons  absorbed  from  the 
alimentar}'  canal  and  subsequently  excreted  into  the  ducts;  and  in  either 
case  to  the  passage  of  bile,  which  often  contains  toxic  constituents,  into 
the  general  circulation.  The  pale  colour  of  the  fajces  may  be  due  to 
catarrh  of  the  bile-duct  and  a  deficient  amount  of  bile,  but  in  cases  where 
there  is  no  evidence  of  jaundice  elsewhere  it  is  often  the  result  of  the 
faeces  being  permeated  with  bubbles  of  gas  from  excessive  carbohydrate 
fermentation.  This  colour  of  the  faeces  is  often  mentioned  by  the  patients 
as  proof  that  "the  liver  is  not  acting"  and  that  there  is  an  imperfect  for- 
mation of  bile. 

The  headache,  giddiness,  muscse  volitantes,  malaise,  muscular  debility, 
mental  depression,  and  irritability  are  due  to  the  local  action  on  the 
nervous  system  of  poisons  absorbed  from  the  alimentary  canal.  These 
toxic  bodies  are  either  produced  in  s^ich  quantities  that  the  liver  fails 


38  DISEASES    OF   THE    LIVER. 

to  Stop  them,  or  more  probably  they  act  on  the  Hver  cells  and  impair 
their  vitality  and  function;  in  either  case  the  general  circulation  becomes 
flooded  with  toxic  bodies.  The  piles,  the  feehng  of  weight  in  the  right 
hypochondrium,  and  shoulder  pain  depend  on  hepatic  congestion  or 
even  slight  hepatitis  brought  on  by  constipation  and  the  advent  to  the 
liver  of  digestive  products  in  excessive  amounts  and  probably  of  altered 
(i.  e.,  toxic)  quality.  This  state  of  hepatic  congestion  is  especially  apt 
to  be  set  up  in  patients  who  have  suffered  from  malaria  in  the  tropics. 
{Vide  Tropical  Liver.)  Nevertheless  there  can  be  no  doubt  that  in  some 
instances  morbid  results  are  referred  to  the  functional  disturbance  of 
the  liver  without  its  being  always  possible  to  determine  satisfactorily  that 
this  disturbance  is  secondary.  Thus,  in  some  forms  of  glycosuria  it  is 
possible  that  there  is  an  excessive  activity  of  the  glycogenic  function, 
while  again  in  ahmentary  glycosuria  the  liver  fails  to  discharge  efficiently 
its  function  of  stopping  the  sugar  brought  to  it  by  the  portal  vein.  As 
a  rule,  in  alimentary  glycosuria  there  is  some  definite  underlying  cause, 
such  as  pancreatic  disease,  but  it  cannot  be  recognized  in  ah  cases. 
These  conditions,  however,  are  not  ordinarily  spoken  of  as  functional 
disease  of  the  liver. 

It  has  recently  been  urged  that  pueiperal  eclampsia  is  in  many  cases 
due  to  hepatic  insufficiency,  and  that  the  renal  symptoms  are  secondary 
to  a  primary  hepatic  toxaemia.  During  pregnancy  toxaemia  is  favoured 
by  several  factors,  such  as  the  retention  of  bodies  which  are  normally 
removed  in  the  menstrual  flow,  the  passage  of  toxic  bodies,  derived  from 
metaboHc  processes  in  the  foetus,  into  the  maternal  circulation,  and  ■ 
auto-intoxication  from  constipation,  which  is  so  common  during  preg- 
nancy. In  a  woman  who  inherits  a  diminished  hepatic  activity  and 
resistance  the  liver  fails  to  rise  to  the  occasion  and  to  stop  and  destroy 
the  poisons  which  reach  it.  The  blood  then  becomes  flooded  with  poisons, 
and  symptoms  of  toxsemia  result.  These  are  dyspepsia,  severe  vomiting, 
ptyalism,  oedema  without  albuminuria,  pruritus,  and  pigmentation.  In 
more  marked  instances  there  are  intractable  vomiting,  jaundice,  acute 
yellow,  atrophy,  mania,  eclampsia,  etc.  In  fatal  cases,  however,  changes 
are  constant  in  the  liver,  and  consist  in  focal  or  more  extensive  necroses, 
degeneration  of  the  liver  cells,  and  haemorrhages. 

As  has  already  been  admitted,  functional  disorder  of  the  liver  is  no 
doubt  responsible  for  many  symptoms.  The  difficulty  in  regard  to  the 
subject  is  to  prove  that  the  functional  disturbance  is  primary  in  the  liver 
and  not  secondary  to  disease  or  morbid  factors  elsewhere.  The  discus- 
sion is  not  a  mere  academic  exercise,  but  has  a  practical  bearing  on  the 
treatment.  Thus,  if  it  were  thought  that  there  was  a  primary  failure 
of  hepatic  activity,  as  is  implied  by  the  common  phrase  ''torpid  liver," 
the  rational  course  would  be  to  stimulate  the  organ.  Whereas,  if  there 
was  an  underlying  and  primary  factor  elsewhere,  this  should  be  attacked. 

The  difficulties  about  the  recognition  of  primary  functional  disorders 
of  the  liver  may  be  best  explained  by  referring  to  some  of  the  conditions 
which  it  has  been  supposed  to  cause. 


FUNCTIONAL    DISEASE    OF   THE    LIVER.  39 

Liihcemia  was  described  by  Murchison  *  as  a  condition  of  innate  de- 
fect of  power,  often  hereditar}^,  in  the  liver,  in  virtue  of  which  its  healthy 
functions  are  liable  to  be  deranged  by  the  most  ordinary  articles  of  diet. 
As  a  result  of  this  hepatic  insufficiency  uric  acid,  instead  of  urea,  was 
said  to  be  produced  in  the  liver  and  turned  out  into  the  blood.  Among 
the  results  of  lithsemia  Murchison  enumerates  such  different  conditions 
as  dyspepsia,  constipation,  gout,  urinary  calculi,  biliary  calculi,  and 
acute  and  chronic  renal  disease. 

This  conception  has  been  revived  in  France  under  a  different  name — "  hepatism  " 
— by  Glenard  f  It  is  regarded  as  a  chronic  nutritional  change  which  may  be 
hereditarj'  or  acquired.  It  may  take  (a)  the  cholaBmic  form ;  this  condition  is  much 
the  same  as  the  simple  family  cholsemia  more  recently  described  by  Gilbert  and 
Lereboullet,J  in  which  the  blood-serum  contains  bile-pigment  though  the  urine 
usuall}^  does  not.  Its  primary  signs  are  pigmentation  of  the  skin,  which  may  be 
of  the  nature  of  slight  jaundice,  or  dark  and  resembling  Addison's  disease,  moles, 
freckles,  or  brown  areas  (the  biliary  mask)  resembling  the  melasma  of  pregnancy, 
and  xanthelasma  of  the  ej^elids.  As  secondary  results  such  various  conditions  as 
the  following  may  arise :  dyspepsia,  abdominal  pain,  hajmatemesis,  epistaxis, 
mucous  colitis,  megrim,  albuminuria,  and  rheumatic  pains,  while  it  is  closely  related 
to  transient  and  chronic  jaundice,  biliary  cirrhosis,  and  similar  conditions.  (6)  The 
uricsemic  form,  which  corresponds  to  the  diathesis  termed  "arthritism"  by  some 
French  writers,  or  to  Murchison's  lithsemia.  A  mixture  of  these  two  forms  corre- 
sponds to  the  diathesis  of  "  herpetism  "  described  by  some  French  writers.  Hepatism, 
according  to  Glenard,  is  a  functional  disturbance  of  the  liver  and  is  the  cause  of 
a  large  number  of  diseases,  including  those  incriminated  by  Murchison,  and,  in 
addition,  neurasthenia,  diabetes,  chlorosis,  and  visceroptosis.  It  may  be  pointed 
out  that  the  choltemic  form  is  probably  dependent  on  slight  catarrh  of  some  part 
of  the  bile-ducts,  either  in  the  liver  or  close  to  the  termination  of  the  common 
bile-duct  in  the  duodenum. 

?iIurchison's  theory  of  lithfemia  is  very  far-reaching,  and  among  other 
things  offers  an  explanation  of  gout;  in  fact,  many  of  the  manifestations 
of  lithsemia  are  those  of  irregular  gout.  Among  recent  writers  Yeo  § 
has  supported  the  view  that  hepatic  inadequacy  is  an  underlying  factor 
in  the  production  of  gout.  The  protean  manifestations  of  neurasthenia 
include  many  of  those  formerly  ascribed  to  functional  failure  on  the 
part  of  the  liver. 

This  theory  of  lithaemia  depends  on  the  assumption  that  as  the  result 
of  imperfect  metabolism  uric  acid,  instead  of  urea,  is  manufactured  by 
the  liver.  There  are  two  mistakes  here.  In  the  first  place,  it  is  now 
universally  agreed  that  uric  acid  and  urea  are  the  products  of  entirely 
distinct  metabolic  processes,  and  that  there  is  nothing  to  support  the 
view  that  if  the  formation  of  urea  is  left  incomplete  uric  acid  results. 
As  Woods  Hutchinson  ||  graphically  expresses  it,  they  are  practically  as 
distinct  from  each  other  as  the  urine  from  fasces.  In  the  second  place, 
it  has  been  shown  since  Murchison's  time  that  the  liver  does  not  play 
any  predominant  part  in  the  manufacture  of  uric  acid.  Uric  acid  is 
produced  in  the  body  generally,  and  more  especiallj'  from  lymphoid 

*  Murchison,  C. :  Croonian  Lectures;  Royal  College  of  Physicians,  1S74.  Dis- 
eases of  the  Liver,  p.  594,  ed.  ii,  1877. 

t  Gl^niard:   Les  ptoses  Viscdrales,  Paris,  1899. 

j  Gilbert  and  Lereboullct:  Gaz.  Hcbdom.  de  Med.  et  de  Chirurg.,  Sept.  21, 
1902,  p.  889. 

§  Yeo:  Brit.  Med.  Journ.,  1901,  vol.  i,  p.  1457. 

II  Woods  Hutchinson:  Lancet,  1903,  vol.  i,  p.  288. 


40  DISEASES    OF   THE    LIVEK. 

tissue;  it  is  closely  associated  with  leucocytosis,  uric  acid  being  derived 
from  the  nuclein  of  the  cells.  This  is  well  seen  in  the  excessive  excretion 
of  uric  acid  in  leukaemia.  According  to  P.  W.  Latham,  KoHsch,  and 
Luff,*  uric  acid  is  manufactured  in  the  kidneys.  It  is,  therefore,  too 
narrow  a  view  of  the  faulty  metabolism  of  proteid  material  which  results 
in  an  excessive  production  of  uric  acid  to  say  that  it  depends  on  functional 
disorder  of  the  liver  to  the  exclusion  of  the  rest  of  the  body. 

Habitual  high  arterial  tension  and  its  accompaniments,  such  as 
migraine,  might  be  thought  to  depend  on  a  failure  of  the  liver  to  stop  and 
destroy  the  poisonous  bodies  that  are  continually  being  carried  to  it 
from  the  intestines.  The  liver  undoubtedly  exerts  this  important  func- 
tion of  protecting  the  body  from  auto-intoxication,  but  it  is  difficult  to 
prove  that  failure  in  the  discharge  of  this  duty  leads  to  high  arterial 
tension;  since  in  cases  of  extensive  disorganization  of  the  liver — for  ex- 
ample, in  cirrhosis — hepatic  insufficiency  must  exist,  but  the  arterial 
tension  is  low  and  not  raised.  It  is  much  more  likely  that  high  arterial 
tension  is,  like  gout,  due  to  some  general  disorder  of  metabolism  of  the 
body. 

In  cases  popularly  described  as  "biUousness"  or  "toipid  hver"  the 
symptoms  are  indigestion,  some  hepatic  pain,  headache,  slight  icteric  tinge- 
ing  of  the  conjunctivge  with  an  apparent  or  real  deficiency  of  colouring- 
matter  in  the  faeces.  The  most  probable  explanation  of  these  symptoms 
is  gastro-duodenal  catarrh  with  slight  catarrhal  jaundice  and  not  a 
primary  diminution  in  the  secretion  of  bile.  In  these  cases  it  is  possible 
either  that  there  is  catarrhal  swelling  of  the  biliary  papilla  in  the  duo- 
denum or  that,  as  the  result  of  indigestion,  poisonous  products  are  carried 
to  the  liver  and  then,  when  excreted  into  the  bile-ducts,  set  up  a  certain 
amount  of  catarrh  in  the  small  intra-hepatic  ducts.  This  leads  to  re- 
absorption  of  the  bile  with  the  poisons  contained  in  it,  which  pass  into  the 
general  circulation  and  act  on  the  body  as  a  whole.  Sir  Lauder  Brun- 
ton  t  has  shown  that  it  is  probable  that  the  proverbial  bitter  taste  of 
the  bile  is  pathological  and  due  to  the  presence  of  poisons  absorbed  from 
the  bowel  and  then  excreted  into  the  ducts,  and  that  in  health  the  bile 
is  tasteless. 

It  must  be  borne  in  mind  that  the  liver,  like  other  organs,  must  vary 
greatly  in  different  individuals  as  to  its  functional  activity  and  reserve 
power,  and  that  an  amount  of  food-products  which  can  be  satisfactorily 
dealt  with  b}'  the  liver  in  one  individual  would  in  another  be  entirely 
beyond  its  capabilities.  This  difference  in  the  inherent  powers  of  the 
liver  in  different  persons  is  analogous  to  variations  in  their  muscular  and 
mental  powers,  and  the  less  powerful  should  not  be  described  as  suffer- 
ing from  functional  disease  of  their  muscles  or  brain  because  they  fail  to 
accomplish  the  work  which  their  better  developed  companions  have  no 
difficulty  with.  If,  therefore,  an  individual  consumes  an  amount  of 
food  that  is  excessive  for  his  powers  of  digestion,  fermentation  and 
auto-intoxication  will  result.     These  poisons  Avill  impair  the  functional 

*  Luff,  A.  P. :  Practitioner,  March,  1898. 

t  Sir  T.  L.  Brunton:  Clinical  Journ.,  Jan.  10,  1900. 


FUNCTIOXAL    DISEASE    OF  THE   LIVER.  41 

activity  of  the  liver,  and  as  a  result  the  poisonous  products  of  digestion 
will  be  allowed  to  pass  into  the  general  circulation  and  give  rise  to  the 
various  toxic  manifestations  already  referred  to.  From  what  has  gone 
before,  it  is  evident  that  the  well-known  symptoms  ascribed  to  a  "tor- 
pid" or  "inactive  liver"  are  chiefly  due  to  factors  which  secondarily 
interfere  with  the  functional  activity  of  the  liver  and  not  to  a  primar}^ 
functional  failure  on  the  part  of  that  organ.  But  because  the  ingenious 
conception  of  lithsemia  and  other  views  as  to  primar}^  functional  disease 
of  the  liver  do  not  commend  themselves  in  the  light  of  later  knowledge, 
it  does  not  follow  that  hepatic  insufficiency  or  inadequacy  is  a  negUgible 
factor.  It  is  quite  possible  that  primary  functional  disorder  of  the  liver 
does  occur,  but  in  the  present  state  of  our  knowledge  its  existence  is  almost 
impossible  to  recognize  with  accurac)'. 

The  symptoms  of  secondary  functional  disturbance  of  the  liver  have 
already  been  referred  to  (p.  41);  a  few  lines  as  to  their  treatment  will 
now  be  given. 

Treatment. — The  treatment  of  the  symptoms  of  secondary  hepatic 
inadequacy  must  therefore  be  directed  to  the  causes  and  not  to  the  liver 
itself.  In  the  first  place,  the  alimentary  canal  should  be  cleared  out; 
this  is  most  satisfactorily  effected  by  the  use  of  calomel,  grs.  iij,  or  of 
the  old-fashioned  blue  pill,  grs.  v,  followed  by  haustus  sennse,  or  saline 
purgatives,  such  as  sulphate  of  magnesium  or  soda,  phosphate  of  soda, 
or  some  natural  mineral  water  with  purgative  properties.  The  mercury 
drives  the  bile  out  of  the  gall-bladder,  unloads  the  bile-ducts,  and  by 
sluicing  the  common  duct  tends  to  remove  the  causes  of  catarrh  of  its 
lower  end.  At  the  same  time  it  acts  as  an  intestinal  antiseptic  and 
inhibits  excessive  fermentation,  and  thus  puts  a  stop  to  further  auto- 
intoxication. The  saline  removes  the  mercury  from  the  intestinal  sur- 
face and  prevents  prolonged  irritation,  while  at  the  same  time  it  dimin- 
ishes portal  engorgement.  The  purgative  action  of  these  two  remedies 
removes  poisons  from  the  alimentary  canal.  Intestinal  fermentation  and 
putrefaction  can  be  most  satisfactorily  prevented  by  careful  dieting  and 
by  the  administration  of  minute  doses  of  calomel  {j-q  to  ^tt  grain)  three 
times  a  day,  which  is  preferable  to  salol,  /5-naphthol,  and  other  popular 
drugs  employed  for  this  purpose.  It  is,  of  course,  important  that  the 
bowels  should  be  kept  properly  open.  The  ordinary  purgatives  already 
mentioned  may  be  used  for  this  purpose,  or  a  pill  containing  euonymin 
and  iridin.  These  two  drugs  are  often  employed  and  spoken  of  as  if 
they  had  some  special  action  other  than  that  of  purgatives,  but  witliout 
any  satisfactory  reason. 

Plenty  of  water  should  be  taken  so  as  to  wash  out  the  poisonous 
products  from  the  circulation  and  stimulate  the  functional  activity  of 
the  kidneys.  It  is  better  not  to  take  water  in  considerable  quantities 
either  with  or  directly  after  food,  but  to  take  it  one-half  an  hour  or  so 
before  a  meal.  Hot  water  may  be  sipped  first  thing  in  the  morning  and 
last  thing  at  night.  During  the  existence  of  symptoms  a  liquid  diet, 
of  Avhich  milk  is  the  staple,  should  be  adopted,  while  alcohol  in  an}'  form 
should  be  rigidly  avoided.     In  the  second  place,  the  patient  should  be 


42  DISEASES    OF   THE    LIVER. 

warned  to  avoid  the  forms  of  food  likely  to  set  up  intestinal  catarrh  and 
fermentation.  The  articles  of  food  that  must  be  avoided  as  indigestible 
will,  of  course,  vary  in  individual  cases,  but,  generally  speaking,  the 
following  should  be  forbidden:  Concentrated  and  highly  spiced  soups; 
rich  fish,  such  as  salmon,  mullet,  eels,  kippered  fish;  duck,  hare,  made 
dishes,  entrees,  pickles,  rich  sauces,  melted  butter,  tea  cakes,  crumpets, 
sweets,  cream,  cheese,  and  much  proteid  food.  Alcohol  should  be  avoided 
or  taken  in  great  moderation,  well  diluted,  and  with  meals.  Claret, 
hock,  or  whisky  are  the  forms  that  may  be  taken  if  it  is  thought  desirable, 
but  beer,  stout,  cider,  champagne,  sherry,  Madeira,  Port,  Burgundy,  and 
liqueurs  should  be  strictly  prohibited. 

Exercise  is  important.  The  form  of  exercise  most  suitable  to  indi- 
vidual requirements  varies  somewhat,  and  a  stereotyped  direction 
cannot  be  given  to  all  cases.  In  some  instances  where  the  symptoms 
have  existed  for  a  considerable  time  and  where  muscular  debility  is 
present,  active  exercise  is  unsuitable,  at  any  rate  at  first,  and  may  lead 
to  exhaustion  and  exaggeration  of  the  symptoms.  Under  such  circum- 
stances massage  may  give  very  good  results  and  may  be  followed  by 
carefully  regulated  exercise,  such  as  Ling's  Swedish  gymnastics.  In 
ordinary  cases,  however,  massage  and  g5.''mnastics  are  hardly  necessary. 
In  some  persons  walking  briskly  is  sufficient,  but  in  many,  probably  in 
the  majority,  a  more  active  form  of  exertion  is  more  effective,  such  as 
horse-riding,  bicycling,  golf,  or  lawn  tennis.  There  is  the  additional 
advantage  that  these  forms  of  exercise  distract  the  attention  from  the 
individual's  private  business  or  worries.  Open-air  exercise  is  better 
than  indoor,  but  when  the  weather  is  bad,  fencing,  racquets,  boxing,  or 
gymnastics  may  be  of  great  use  in  improving  the  conditions  of  health. 

It  is  important  to  get  the  skin  to  act,  and  for  this  purpose  Turkish 
baths  or  hot  baths  with  vigorous  friction  of  the  skin  by  rough  towels 
are  useful.  When  the  skin  has  been  acting  vigorously  after  exercise 
the  underclothing  should  be  changed  as  soon  as  the  individual  comes  in, 
so  as  to  avoid  chilling  the  surface  of  .the  body.  The  body  should  be  well 
but  not  too  warmly  clad,  and  care  must  be  taken  to  avoid  chills  to  the 
legs,  abdomen,  and  neck. 

A  visit  to  a  spa,  either  in  this  country,  such  as  Harrogate,  Llandrin- 
dod  Wells,  or  Strathpeffer,  or  abroad,  Homburg,  Ems,  Neuenahr,  Vichy, 
Carlsbad,  Marienbad,  etc.,  may  be  followed  by  improvement  or  cure. 
The  patient  not  only  undergoes  a  carefully  regulated  course  of  treat- 
ment (''the  cure"),  but  gets  change,  holiday,  and  rest  from  the  cares 
of  business  or  other  worries. 

As  to  the  prognosis,  the  digestive  disturbances  which  give  rise  to  these 
symptoms  are  much  the  same  as  those  leading  to  cirrhosis,  and  indeed 
the  symptoms  of  functional  disease  of  the  liver  may  in  some  instances 
be  the  early  manifestations  of  cirrhosis.  As  a  rule,  however,  the  prog- 
nosis is  good  provided  the  patient  conforms  to  medical  advice. 


DISEASES  OF  THE  HEPATIC  ARTERY. 

Aneurysm;  Embolism;  Thrombosis;  Arteriosclerosis;  Etc. 

ANEURYSM. 

Aneurysms  of  the  hepatic  artery  have  been  recorded  in  rather  more 
than  twenty  instances;  but  examination  of  metropolitan  and  other 
museums  would  increase  the  number  of  cases;  thus  there  is  a  large 
hepatic  aneurysm,  the  size  of  a  cocoanut,  in  the  Museum  of  Surgeon's 
Hall,  Edinburgh,  and  another  the  size  of  a  turkey's  head  in  the  Museum 
of  St.  George's  Hospital. 

Age  and  Sex. — In  24  cases  where  the  ages  were  given,  the  average 
age  was  34.5  years,  the  extremes  being  56  and  17  years.  In  24  cases, 
8  were  females  and  16  males.  The  average  age  in  the  women  was  a  little 
higher  (36  years)  than  in  the  men  (33.5). 

Causation. — Some  of  these  aneurysms  may  be  due  to  embolism, 
and  from  the  comparatively  unsupported  condition  of  the  visceral  arteries 
in  the  abdoixdnal  cavity,  simple  non-infective  embolism  is  more  likely 
to  be  foUowed  b}^  aneurysm  there  than  in  other  situations,  except,  per- 
haps, in  the  circle  of  Willis,  where  the  arteries  he  on  a  yielding  water-bed, 
the  subarachnoid  space.  Traumatism  has  been  noted  as  a  cause  of 
hepatic  aneurysm;  thus,  Mester's  *  patient  was  kicked  in  the  abdomen 
by  a  horse.  In  most  cases  of  hepatic  aneurysm  there  is  no  evidence  of 
embolism  or  traumatism  and  yet  these  factors  seem  more  probable  than 
mere  chronic  endarteritis.  Perhaps  in  some  instances  the  cause  of  the 
embolus,  such  as  a  calcareous  plate  from  the  aorta,  has  naturally  been 
overlooked,  or  has  passed  away  before  the  patient's  death.  Often, 
howe^'er,  no  antecedent  condition,  except  endarteritis,  is  recorded. 

A  very  interesting  specimen  of  an  aneurysm  the  size  of  a  walnut  was  found 
by  the  late  Dr.  Pearson  Irvine  t  inside  an  abscess  in  the  left  lobe  of  the  liver ;  here 
the  aneurj^sm  was  produced  by  inflammation  and  ulceration  of  the  outer  coats  of 
the  arten.^  in  the  same  wa}^  that  aneurysms  are  formed  in  vomicse  during  the  course 
of  pulmonary  tuberculosis. 

Aneurj^sms  of  the  hepatic  artery  or  its  branches  may  be  due  to  ulcera- 
tion starting  in  the  walls  of  the  gall-bladder  or  the  bile-ducts  and  eroding 
the  wall  of  the  artery.  At  first  an  aneurysm  would  result,  and  later, 
by  extension  of  the  ulceration,  the  aneurysm  would  be  opened  into  the 
bile-duct. 

This  ulceration  may  be  due  to  gall-stones.  Naunyn  X  regards  Lebert's  case  of 
rupture  of  an  hepatic  aneurysm  into  the  gall-bladder  of  a  woman  aged  thirty,  with 
fatal  gastro-intestinal  hajmorrhage,  as  due  to  gall-stones,  and  quotes  M.  B.  Schmidt's 
case  of  ulceration  of  the  bile-duct,  in  connection  with  an  impacted  gall-stone,  opening 

*  Mester:  Zeitsrhrift  f.  klin.  Med.,  Bd.  xxviii,  S.  93,  1895. 
t  Pearson  Irvine:  Trans.  Path.  Soe.,  vol.  xx'ix,  p.  128. 
t  Naun^•n  :  On  Cholelithiasis,  p.  141.     Translation,  New  Sydenliam  Soc. 

43 


44  DISEASES    OF   THE    LIVER. 

into  an  aneurysm  of  the  hepatic  artery.  Schmidt  has  recently  reported  another 
case  in  which  cholelithiasis  probably  set  up  ulceration  of  the  gall-bladder  and  an 
aneurysm  of  a  branch  of  the  hepatic  artery. 

In  connexion  with  the  production  of  hepatic  aneurysm  by  ulceration 
starting  in  the  gall-bladder  or  bile-ducts  and  possibly  due  to  cholelithiasis, 
it  is  significant  that  in  24  cases  of  hepatic  aneurysm  where  the  sex  is 
noted  8  were  in  women  and  1 6  in  men.  Aneurysms  are  so  rare  in  women, 
while  gall-stones  are  so  common,  that  it  is  probable  this  large  proportion 
of  female  cases  in  aneurysm  of  the  hepatic  artery  may  to  some  extent 
be  due  to  the  mechanism  of  ulceration  of  the  artery  from  without.  Usu- 
ally there  is  a  single  aneurysm  on  the  trunk  or  extra-hepatic  branches  of 
the  hepatic  artery,  but  in  some  instances  more  than  one  or  even  multiple 
aneurysms  have  been  recorded. 

In  a  boy  aged  seventeen  there  were  two  intra-hepatic  aneurysms  (Borcher*), 
and  in  a  boy  aged  eighteen  Hale  White  t  found  an  aneurysm  on  each  of  the  main 
branches  of  the  hepatic  artery,  one  of  which  was  embedded  in  the  substance  of  the 
liver.  Multiple  aneurj'-sms  of  small  size  may  occur  in  great  profusion  in  the  liver 
in  the  rare  disease  periarteritis  nodosa.  Intra-hepatic  aneurysms  have,  however, 
attracted  very  little  attention,  and  are  very  rarely  seen. 

Symptoms  of  Hepatic  Aneurysm.^ — Pain  is  nearly  always  present, 
and  maybe  mistaken  for  that  of  bihary  colic ;  in  fact  "pseudo-bihary  "  colic 
may  be  due  to  the  pressure  of  the  aneurysm  on  the  bile-ducts.  Jaundice, 
from  pressure  on  the  bile-ducts,  very  frequently  occurs,  though  the 
jaundice  may  be  slight  and  not  appear  until  late  in  the  course  of  the 
disease.  Aneurysm  and  new-growth  in  the  portal  fissure  behave,  in  a 
miniature  fashion,  just  as  the  corresponding  lesions  in  the  anterior 
mediastinum  do  with  regard  to  the  adjacent  venous  trunks.  Aortic 
aneurysm  rarely  obstructs  the  superior  vena  cava,  while  mediastinal 
growth  frequently  does.  In  the  same  way  aneurysm  of  the  hepatic  ar- 
tery, though  it  may  push  the  portal  vein  aside,  does  not  obliterate  it 
or  give  rise  to  ascites. 

Hepatic  aneurysm  may  perforate  into  the  peritoneum  and  give  rise 
to  fatal  collapse.  Usually  it  ruptures  into  some  part  of  the  bile-ducts, 
and  the  blood  thus  poured  out  passes  into  the  alimentar}'-  canal  and  may 
be  vomited,  or  more  often  passed  by  the  bowel  alone;  repeated  leakage 
and  haemorrhages  may  occur  before  a  fatal  one.  Rupture  of  the  aneu- 
rysm may  take  place  into  the  hepatic  or  common  bile-ducts,  the  gall- 
bladder, colon,  and  possibly  stomach. 

A  pulsating  tumor  may  be  felt  in  the  epigastrium,  and  a  bruit  may 
be  heard  over  it. 

Aneurysm  of  the  hepatic  artery,  as  in  a  case  recorded  by  Ledieu, 
may  obstruct  the  circulation  in  its  branches.  By  experimental  hgation 
of  the  hepatic  artery  in  dogs  Dujarier  and  Castaigne  J  have  found  that 
the  flow  of  bile  is  retarded  and  that  infection  of  the  bile-ducts  is  thus 
rendered  more  easy.  This  may  explain  cases  where  multiple  abscesses 
in  the  liver  are  found  associated  with  an  aneurysm  of  the  hepatic  artery. 

*  Borcher:  Aneurysma  d.  Art.  hepat.,  Kiel,  187S. 

t  Hale  White:  Brit.  Med.  Journ.,  1892,  vol.  i,  p.  223. 

I  Dujarier  and  Castaigne:  Bull.  Soc.  Anat.,  Paris,  1899,  p.  329. 


DISEASES   OF  THE    HEPATIC   AKTERY.  45 

Ross  and  Osier  *  have  recorded  a  remarkable  case  where  the  sac  of  an  hepatic 
aneurysm  became  septic  and  multiple  emboli  passed  into  the  liver,  leading  to  numer- 
ous abscesses. 

Diagnosis. — The  diagnosis  of  hepatic  aneurysm  is  very  difficult. 
Most  of  the  recorded  cases  have  been  regarded  as  duodenal  ulcer  or 
cholelithiasis.  It  would  be  very  difficult  to  distinguish  with  certainty 
between  an  hepatic  aneurysm  and  one  of  the  abdominal  aorta  in  the 
immediate  neighbourhood;  especially  as  the  latter  may  press  on  the 
bile-duct  and  give  rise  to  jaundice. 

Treatment  is  usually  merely  palliative.  Of  four  cases  treated  sur- 
gically, three  died;  in  the  fourth,  which  recovered,  Kehrf  successfully 
ligated  the  hepatic  artery  and  removed  the  aneurysm. 

EMBOLISM. 

Embolism  of  the  main  trunk  of  the  hepatic  artery  is  very  rarely  ob- 
served; possibly  it  is  sometimes  missed,  from  the  fact  that  the  artery  is 
not  systematically  examined.  Chiari  J  in  a  case  of  embolism  involving 
the  main  trunk  of  the  hepatic  artery  found  complete  necrosis  of  the  liver. 
Lancereaux  §  and  Ogle  !|  have  recorded  cases  of  embolism  at  the  bifur- 
cation. In  Lancereaux's  case  hepatic  pain  set  in  ten  hours  before  death 
and  was  referred  to  the  embolism.  In  Ogle's  case  there  Avere  anaemic 
infarcts  in  the  liver,  but  no  general  necrosis  of  the  liver.  Necrosis  of 
the  liver  has  been  recorded  by  Lancereaux  and  by  Chiari  in  man,  and 
experimentaUy  embolism  of  the  hepatic  artery  in  the  hands  of  Cohnheim 
and  Litten,**  and  of  Doyon  and  Dufourt,f  f  has  led  to  the  same  result. 
Short  of  this  extreme  result  the  flow  of  bile  is  retarded  and  infection  of 
the  bile-ducts  rendered  easier.  In  Lancereaux's  cases  of  obstruction 
of  the  hepatic  artery  the  liver  became  very  greatly  engorged  from  the 
absence  of  the  driving  power  or  vis  a  tergo  normally  supplied  by  the 
hepatic  artery.  In  rare  cases  infarction  of  the  liver  may  follow  embolism. 
{Vide  p.  104.) 

Septic  embolism  of  the  small  branches  of  the  hepatic  artery  occurs 
in  hsemic  infections  and  gives  rise  to  pyaemic  abscesses.  Embolism  also 
occurs  in  generalized  tuberculosis  and  sarcomatosis,  especially  in  melan- 
otic sarcoma. 

THROMBOSIS. 

This  is  also  a  pathological  curiosity.  Lancereaux  J  J  describes  a  case 
of  a  clot  in  the  trunk  of  an  atheromatous  hepatic  artery  in  a  man  aged 
sixty-five  who  died  with  arteriosclerosis  and  gangrene  of  the  feet  which 
may  have  been  either  embolic  or  thrombotic, 

*  Ross  and  Osier:  Canadian  Med.  Journ.,  vol.  vi. 

tKehr,  H:  Miinchen.  med.  Wochen.,  1903,  S.  1861. 

t  Chiari:  Zeitschrift  f.  Heilkunde,  Bd.  xix,  S.  507. 

§  Lancereaux:  Traitd  des  Maladies  du  foie  et  du  pancreas,  p.  541. 

II  Ogle,  C:  Trans.  Path.  Soc,  vol.  xlvi,  p.  72. 
**  Cohnheim  and  Litten:  Virchow's  Archiv,  Bd.  Ixvii,  S.  153. 
tt  Doyon  and  Dufourt:  Archiv  de  Physiol.,  5th  Series,  vol.  x,  p.  522,  1S9S. 
Xt  Lancereaux:  Traits  des  Maladies  du  foie  et  du  pancreas,  1899,  p.  543. 


46  DISEASES   OF  THE   LIVER. 


ARTERIOSCLEROSIS. 

The  trunk  of  the  hepatic  artery  is  sometimes,  in  common  with  the 
rest  of  the  arterial  system,  found  to  be  atheromatous.  When  affected, 
the  hepatic  artery  usually  shows  endarteritis  deformans  rather  than 
endarteritis  obliterans,  or  is  dilated  and  varicose  from  loss  of  elasticity 
rather  than  narrowed.  It  thus  disposes  to  the  rare  events,  aneurysm 
and  thrombosis  of  the  hepatic  arter}^  It  is  noticeable  that  arterio- 
sclerosis does  not  lead  to  a  fibrotic  atrophy  of  the  hver  in  any  way  re- 
sembHng  a  granular  arteriosclerotic  kidney,  though  senile  atrophy  of 
the  liver  with  some  fibrous  replacement  might  be  thought  to  depend  on 
a  similar  process.  Inside  the  liver  the  branches  of  the  hepatic  artery 
show  endarteritis  in  the  neighbourhood  of  syphilitic  gummata.  In 
hsemochromatosis  the  hepatic  artery  shows  endarteritis;  occasionally 
in  ordinary  cirrhosis  there  is  endarteritis  obliterans.  Bonome  describes 
hsemorrhagic  and  necrotic  infarcts  due  to  endarteritis  obliterans  in  cir- 
rhosis. In  general  paralysis  of  the  insane,  which  has  been  regarded 
by  Bruce  and  by  Ford  Robertson  as  a  chronic  toxaemia  of  intestinal 
origin,  Angiolella  has  observed  endarteritis  of  the  hepatic  artery. 

BIBLIOGRAPHY. 

Adami:  Montreal  Med.  Journ.,  Dec,  1896. 

AngioleUa:  II  Manicomio  Moderno,  1894,  1895.     Quoted  by  Robertson. 

Bonome:  Sperimentale,  anno  53,  fasc.  4.     Quoted  in  Rev.  Generale  de  Pathologic 

interne,  1900,  p.  70. 
Brace:  Brit.  Med.  Journ.,  1901,  vol.  i.,  p.  1600. 
Hasonfeld:  Deutsch.  Archiv  f.  klin.  Med.,  1897. 
Robertson,  Ford:  Brit.  Med.  Journ.,  1901,  vol.  i,  p.  1602. 

ENLARGEMENT  OF  THE  HEPATIC  ARTERY. 

Enlargement  of  the  hepatic  artery  is  seen  in  cases  of  new-growth, — 
though  not  in  all  instances, — in  cases  of  portal  thrombosis  of  some 
standing,  and  in  ordinary  cirrhosis. 

In  a  case  where  the  liver  weighed  14  pounds  from  carcinomatous  infiltration, 
secondary  to  a  primary  gro'ni:!'!  in  the  oesophagus,  the  hepatic  artery  was  dissected 
out  and  was  small  in  size. 


DISEASES  OF  THE  HEPATIC  VEINS. 

Thrombosis;    Stricture;   Chronic  Periphlebitis  and  Endophlebitis ;   Sup- 
purative Phlebitis;  Embolism. 

THROMBOSIS. 

Thrombosis  of  the  hepatic  veins  is  somewhat  rare;  it  is  usually  a 
secondary  effect  of  some  other  hepatic  lesion,  but  may  spread  from  the 
inferior  vena  cava.  It  may  give  rise  to  a  nutmeggy  condition  of  the 
liver  and  produce  such  stagnation  and  other  changes  that  portal  throm- 
bosis results.     It  may  be  set  up  in  the  following  ways: 

(1)  New-growth  in  the  liver  may  extend  into  the  hepatic  veins  and 
give  rise  to  thrombosis. 

(2)  ''Adenomata"  in  nodular  hepatitis  may  rupture  into  the  hepatic 
veins  and  thus  lead  to  thrombosis.*  The  occurrence  of  such  clots  in 
the  portal  or  hepatic  veins,  containing  liver  cells,  has  probably  led  some 
writers  to  consider  that  such  cases  of  multiple  adenomata  in  cirrhosis  are 
carcinomatous,  on  the  grounds  that  the  growth  has  extended  into  the 
veins. 

(3)  In  portal  cirrhosis.  Thrombosis  of  the  hepatic  veins  is  found  in 
rare  instances  in  cirrhotic  livers.  It  may,  as  has  just  been  pointed  out, 
occur  in  cases  of  cirrhosis  with  multiple  adenomata  or  nodular  cirrhosis. 
Further,  thrombosis  of  the  hepatic  veins  may  be  due  to  intercurrent 
acute  or  subacute  infections  falling  on  a  cirrhotic  liver  and  setting  up 
inflammation  which  involves  the  thin  walls  of  the  hepatic  veins.  It 
may  be  mentioned  that  in  some  cases,  where  thrombosis  of  the  hepatic 
veins  is  associated  with  a  slight  degree  of  cirrhosis,  the  latter  may  be  the 
result  of  thrombosis,  being  merely  a  secondary  fibrous  replacement. 

(4)  Thrombosis  may  be  due  to  stricture  and  narrowing  of  the  hepatic 
veins.  Examples  of  this  rare  condition  will  be  found  on  page  49,  under 
the  heading  "Stricture."  It  is  possible,  as  suggested  by  Fisher,t  that 
the  contraction  of  the  veins  is  secondary  to  thrombosis  and  not  the 
cause  of  it. 

(5)  Thromb'osis  may  extend  from  the  inferior  vena  cava. 

I  have  seen  a  parietal  thrombus  in  the  inferior  vena  cava,  where  it  grooves 
the  hver,  associated  with  thrombosis  in  the  hepatic  veins;  there  was  more  recent 
clot  in  the  portal  vein.  In  a  case  of  obhteration  of  the  inferior  vena  cava  recorded 
by  Reynaud  the  right  hepatic  vein  was  thrombosed.  In  a  case  of  obhteration  of 
the  inferior  vena  caA-a  recorded  by  Dixon  Mann  and  Hall  X  there  were  thrombi  in 
the  hepatic  veins.  In  this  case  peritonitis  was  thought  to  have  set  up  periphlebi- 
tis and  endophlebitis  and  the  subsequent  changes  in  the  inferior  vena  cava  and 
hepatic  veins. 

*  Compare  Del6pine:  Trans.  Path.  Soc,  vol.  xli,  p.  362. 
t  Fisher,  T. :  Bristol  Medico-cliirurg.  Journ.,  vol.  xx,  p.  209. 
+  Dixon  Mann  and  W.  Hall:  Edinburgh  Med.  Journ.,  July,  1904,  p.  57. 

47 


48  DISEASES    OF   THE    LIVER. 

■  Osier  *  has  described  considerable  stenosis  of  the  orifices  of  the  hepatic 
veins  in  a  case  of  obliteration  of  the  inferior  vena  cava,  a  condition  which 
would  readily  dispose  to  thrombosis. 

(6)  Thrombosis  of  the  hepatic  veins  may  also  occur  in  association 
with  widespread  venous  thrombosis. 

Pittf  records  thrombosis  in  the  aorta^  in  the  splenic,  left  renal,  and  right 
middle  cerebral  arteries,  and  in  the  right  hepatic  vein.  Softening  and  therefore 
older  thrombi  were  found  in  the  portal  vein. 

It  appears  probable  that  thrombosis  of  the  hepatic  veins  may  be 
due  to  the  same  causes  that  set  up  portal  thrombosis,  or  to  an  extension 
of  that  process. 

(7)  It  may  not  be  possible  to  assign  a  definite  cause  for  thrombosis 
of  the  hepatic  veins  in  all  cases.  Possibly  toxines  or  micro-organisms 
stopped  by  the  liver  may  be  responsible  for  some  cases.  Fisher  J  reports 
a  case  of  hepatic  vein  thrombosis  in  a  child  with  bronchopneumonia. 
Thrombosis  of  the  hepatic  veins  occurs  as  an  early  stage  in  suppurative 
inflammation  due  to  hepatic  abscess,  pylephlebitis,  etc. 

Clinically  thrombosis  of  the  hepatic  veins  presents  itself  in  much  the 
same  light  as  thrombosis  of  the  portal  vein;  in  fact,  portal  thrombosis 
may  follow  on  hepatic  vein  thrombosis,  as  in  the  case  mentioned  on 
page  57.  Ascites  is  generally  present  and  may  last  for  as  long  as  four 
months;  the  liver  may  be  palpably  enlarged  and  gastro-intestinal  haemor- 
rhages may  occur.  In  cases  of  some  standing  the  subcutaneous  veins 
of  the  abdominal  wall  may  be  very  greatly  dilated.  The  diagnosis  from 
portal  thrombosis  is  very  difficult;  in  both  ascites  may  occur  suddenly 
in  a  patient  previously  in  good  health.  Ascites  appears  to  be  more 
rapidly  fatal  in  thrombosis  of  the  portal  vein  than  in  hepatic  vein  throm- 
bosis. Treatmerd  should  be  directed  to  any  causal  factor  or  associated 
condition  likely  to  give  rise  to  it,  but  as  the  diagnosis  is  seldom  made, 
treatment  is  chiefly  symptomatic. 

STRICTURE  OF  THE  HEPATIC  VEINS. 

Stricture  of  the  hepatic  veins  chiefly  occurs  at  or  close  to  their  junc- 
tion with  the  inferior  vena  cava.  Pressure  from  tumors,  hydatid  cysts, 
or  cicatricial  adhesions  may  obstruct  branches  of  the  hepatic  veins  in 
the  liver  and  lead  to  local  venous  engorgement.  {Vide  Cardiac  Liver.) 
Stenosis  of  the  main  trunks  is  rare.  It  may  be  due  to  the  following- 
causes  : 

(I)  Cicatricial  contraction  starting  outside  the  veins,  either  in  the 
liver  or  in  its  neighbourhood.  Under  the  name  of  phlebitis  hepatica 
adhsesiva,  Frerichs  §  described  great  narrowing  of  the  hepatic  veins  due 
to  inflammation  spreading  in  from  dense  adhesions  in  the  neighbourhood. 
His  case  was  in  an  alcoholic  married  man  aged  forty-five ;  no  mention  of 
syphilis  is  made.     He  had  ascites  and  jaundice;  there  were  perihepatitis 

*  Osier:  Journ.  Anat.  and  Phys.,  vol.  xiii,  p.  291. 

t  Pitt,  G.  N. :  Trans.  Path.  Soc,  vol.  xlvi,  p.  75.  $  Fisher,  T. :  Loc.  cit. 

§  Frerichs:  Diseases  of  Liver,  vol.  ii,  pp.  432-437,  New  Sydenham  Soc. 


DISEASES   OF  THE    HEPATIC   VEINS.  49 

and  23robably  some  cirrhosis  as  well  as  a  nutnieggy  condition  of  the  liver. 
Kelynack  *  met  with  a  similar  state  of  affairs  in  a  woman  aged  thirty- 
two  who  had  probably  had  sjq^hilis.  There  were  adhesions  around  the 
hepatic  veins,  with  marked  stenosis  and  thrombosis;  the  adhesions  were 
thought  to  have  produced  the  stenosis.  When  stenosis  and  thrombosis 
are  associated,  the  stenosis  is  generally  assumed  to  be  primary;  T. 
Fisher  f  suggests  that  in  some  cases  the  contraction  of  the  veins  msij 
be  the  result  of  primary  thrombosis. 

(II)  To  the  effect  of  gummatous  disease  or  S3qohilitic  fibrosis  in  the 
immediate  neighbourhood  of  the  main  hepatic  veins.  A  gumma  may 
be  so  situated  as  to  lead  to  obliteration  and  thrombosis  in  one  or  both  of 
the  hepatic  veins.  Fagge  {  refers  to  a  case  where  one  of  the  hepatic 
veins  was  so  much  narrowed  by  the  pressure  of  a  gumma  that  it  only 
admitted  a  probe.  In  rare  instances  a  gumma  has  been  found  involving 
the  inferior  vena  cava  and  obliterating  the  openings  of  the  hepatic  veins. 
(Wilks,§  West.ll) 

(III)  To  extensive  hepatic  fibrosis  and  cirrhosis.  In  some  cases  the 
cicatricial  formation  is  very  extensive  and  is  associated  with  general 
hepatic  fibrosis.  There  is  not  in  all  cases  a  certain  syphilitic  histor}-, 
but  there  is  sufficient  evidence  to  suggest  that  congenital  syphilis  is  a 
probable  factor  in  the  general  and  extensive  fibrosis. 

In  a  man  aged  twenty-six  years  under  Dr.  Churton's  **  care  ascites  suddenly 
set  in,  and  death  occurred  nine  days  later  from  exhaustion.  Very  marked  cirrhosis 
of  the  Uver  thought  to  be  due  to  congenital  syphilis  with  thrombosis  and  thickening 
of  the  walls  of  the  hepatic  veins  was  found  at  the  autopsy;  there  was  no  portal 
thrombosis.  A  good  example  of  cicatricial  contraction  involving  and  causing 
tlirombosis  of  the  hepatic  veins  was  found  in  the  body  of  a  boy  aged  thirteen  who 
died  in  St.  George's  Hospital  with  very  marked  cirrhosis  of  the  liver.  The  patient 
had  never  taken  alcohol,  but  there  was  reason  to  believe  he  was  the  subject  of  con- 
genital syphilis,  as  his  mother  had  three  miscarriages  after  his  birth  and  as  there 
was  marked  fibrosis  in  the  spleen,  which  weighed  16  ounces.  The  liver  weighed 
42  oimces  and  was  considerably  enlarged;  it  was  most  extensively  fibrosed,  and 
the  large  mass  of  cicatricial  tissue  involving  the  hepatic  veins  suggested  early  gum- 
matous change;  no  caseation,  however,  could  be  seen  microscopically.tf 

The  following  case  is  probably  a  combination  of  syphilitic  cirrhosis  with  endo- 
phlebitis  obliterans:  Dr.  Gee  J  J  describes  complete  obliteration  of  the  orifices  of 
the  hepatic  veins  in  a  child  aged  seventeen  months.  Ascites  rapidly  developed  at 
the  age  of  fourteen  months,  and  paracentesis  was  twice  performed.  The  liver  weighed 
16f  ounces  and  was  cirrhotic.  There  was  considerable  perihepatitis  around  the 
orifices  of  the  hepatic  veins.  The  hepatic  veins  ended  abruptly,  just  short  of 
entering  the  inferior  vena  cava,  being  cut  off  from  it  by  a  thin  membrane  only. 
The  lining  membrane  of  the  vena  cava  where  the  mouths  of  the  hepatic  veins  should 
have  been  showed  dimples  which  had  not  at  all  the  look  of  scars.  Dr. 
Gee  did  not  think  this  was  congenital  and  due  to  a  failure  of  union  of  tlie  vena3 
revehentes  hepaticse  with  the  inferior  vena  cava,  for  then  the  ductus  venosus  should 
have  remained  open.  He  regarded  the  primary  change  as  cirrhosis  which  led  to 
stenosis  and  obliteration  of  the  hepatic  veins.  Some  of  the  hepatic  veins  contained 
firm  clot.     The  liver  was  nutmeg.     There  was  a  free  collateral  circulation  especially 

*  Kelynack :  Med.  Press  and  Circular,  June  23,  1897. 
t  Fisher,  T. :  Bristol  Medico-chirurg.  Journ.,  vol.  xx,  p.  209,  Sept.,  1902. 
i  Fagge:  Principles  and  Practice  of  Medicine,  vol.  ii,  p.  295,  Ed.  1886. 
§  Willcs,  S. :  Trans.  Path.  Soc,  vol.  xiii,  p.  123. 

II  West,  S. :  Ibid.,  vol.  xlii,  p.  155.     **  Churton :  Trans.  Path.  Soc,  vol.  1,  p.  145. 
tt  Lazarus-Barlow,  W.   S. :  Path.  Trans.,   vol.  1,  p.   147.     St.  George's    Hosp. 
Museum,  Ser.  ix,  174  l. 

Xt  Gee:  St.  Bartholomew's  Hospital  Reports,  vol.  vii,  p.  144,  1S71. 
4 


50  DISEASES    OF   THE    LITER. 

around  the  left  branch  of  the  portal  vein.     Similar  cases  have  been  described    by 
Rosenblatt,*  and  Penkert.f 

(R^)  To  primary  obliterative  endophlebitis  of  the  hepatic  veins.  In 
a  few  cases  there  is  marked  or  ahiiost  complete  stenosis  of  the  openings 
of  the  hepatic  veins  into  the  inferior  vena  cava  without  any  evidence 
that  the  inflammatory'  process  has  spread  to  the  veins  from  adjacent 
parts.  Craven  Moore  j  has  collected  12  cases  of  this  primar}-  obUterative 
inflammation  of  the  hepatic  veins.  The  openings  into  the  inferior  vena 
cava  may  be  mere  dimples. 

In  some  instances,  as  in  Chiari's  §  three  cases,  syphihs  was  regarded  as 
responsible,  but  there  is  no  reason  to  think  that  this  holds  good  in  aU 
cases.  The  entrance  of  the  ductus  venosus  into  the  inferior  vena  cava 
in  the  immediate  neighbourhood  of  the  hepatic  veins  suggests  that  the 
process  of  obhteration  of  that  foetal  vessel  may  spread  to  the  orifices  of 
the  hepatic  veins  and,  by  excess  of  the  obliterating  process,  gradually 
lead  to  stenosis  of  the  orifices  of  the  hepatic  veins,  just  in  the  same  waj^ 
that  stricture  of  the  ileum  sometimes  occurs  at  the  point  where  Meckel's 
diverticulum  is  normally  obliterated.  A  more  closely  analogous  case  is 
to  be  found  in  the  stenosis  (or  coarctation)  of  the  aorta  at  the  point  where 
the  ductus  arteriosus  joins  the  aorta;  this  process  slowly  progresses  and 
eventually  leads  to  extreme  narroTving  or  even  complete  obliteration  of 
the  lumen  of  the  aorta.  It  seems  reasonable  to  imagine  that  a  similar 
train  of  results  may  follow  obliteration  of  the  ductus  venosus.  Moore, 
however,  beheves  that  congenital  influences  may  so  reduce  the  resistance 
of  the  mouths  of  the  hepatic  veins  as  to  enable  some  hsematogenous 
poison  to  induce  endoplilebitis. 

The  Hver  is  in  a  state  of  advanced  chronic  venous  engorgement  with 
dilatation  of  the  trunks  of  the  hepatic  veins  behind  the  stenosis.  Sec- 
ondary thrombosis  is  frecjuent. 

Symptoms. — The  symptoms  are  practically  the  same  as  those  referred 
to  in  the  section  on  Thrombosis  of  the  Hepatic  Veins.  Ascites  is  almost 
constant,  hsematemesis  rare,  and  jaundice  exceptional.  The  average 
age,  according  to  Craven  Moore,  is  about  twenty-ninfe  years,  and  the 
sexes  are  equally  affected. 

CHRONIC  PERIPHLEBITIS  AND   ENDOPHLEBITIS   OF   THE   HEPATIC 

VEINS. 

Spread  of  inflammation  around  the  inferior  vena  cava  to  the  hepatic 
veins  in  adherent  pericardium  may  result  in  periphlebitis  and  possibly 
slight  fibrosis  in  the  neighbourhood.  In  the  cases  that  I  have  examined, 
however,  there  has  been  no  extension  of  inflammation  from  the  walls 
of  the  veins  into  the  surrounding  liver  substance.     In  long-standing 

*  Rosenblatt:  Virchow's  Jahresbericht,  1867,  Bd.  i,  S.  226. 

t  Penkert :  Virchow's  Archiv,  Bd.  clxix. 

J  Craven  Moore's  (Medical  Chronicle,  July,  1902)  cases  were  tlio.se  of  Frerichs, 
(2),  Gee,  Rosenblatt,  Schuppel,  Hainske  (2),  Chiari  (3),  Leiclitenstern,  and  his  own. 
Some  of  these  cases  have  been  referred  to  under  otlier  causes  of  stenosis  of  the- 
hepatic  veins. 

§  Chiari:  Beitriige  z.  path.  Anat.  u.  z.  aUg.  Path.,  Bd.  xxvi. 


DISEASES    OF    THE    HEPATIC    VEIXS.  51 

backward  pressure  the  intima  of  the  hepatic  veins  may,  Hke  that  of  the 
inferior  vena  cava,  become  somewhat  thickened  and  opacjiie — a  slight 
degree  of  chronic  endophlebitis  due  to  increased  intravascular  pressure, 
and  the  veins  become  dilated.  Endophlebitis  may  spread  from  the  in- 
ferior vena  cava  in  cases  of  obliteration  of  that  vessel  into  the  hepatic 
veins,  and  may,  as  in  Dixon  Mann  and  Hall's  *  case,  give  rise  to  throm- 
bosis of  the  hepatic  veins. 

SUPPURATIVE  PHLEBITIS  OF  THE  HEPATIC  VEINS. 

Suppurative  phlebitis  is  more  likely  to  attack  the  hepatic  veins  than 
the  branches  of  the  portal  vein  in  hepatic  abscess,  since  the  latter 
are  surrounded  by  Glisson's  capsule,  while  the  hepatic  veins  and  their 
branches  are  not  protected  in  this  way.  TVlien  the  hepatic  veins  are 
thus  affected,  general  pysemia  is  more  hkely  to  occur  than  in  pylephlebitis, 
since  the  emboli  can  pass  more  readily  into  the  circulation. 

In  a  case  of  large  hepatic  abscess  in  a  man  aged  thirty-four  the  abscess  set 
up  thrombosis  in  the  right  hepatic  vein  which  produced  embohsm  of  the  right 
pulmonary  artery  and  suppurating  areas  in  both  lungs.  In  a  case  of  suppuration 
around  a  calculous  gall-bladder  recorded  by  West  t  the  abscess  opened  into  the 
hepatic  veins  and  produced  multiple  infarcts  in  the  limgs. 

In  a  case  of  proctitis,  due  to  a  bacillus  of  the  influenza  group,  Ophiils  |  found 
abscesses  in  the  submucous  coat  of  the  rectmn,  areas  of  necrosis  in  the  liver,  and 
suppurative  thrombosis  of  the  hepatic  veins  which  had  produced  secondary  foci 
in  the  right  lung.     The  portal  vein  was  quite  healthy. 

EMBOLISM  OF  THE  HEPATIC  VEINS. 

Embohsm  of  the  hepatic  veins  can  occur  only  when  the  embolus 
travels  against  the  blood-stream  and  enters  the  hepatic  A'eins  from  the 
inferior  vena  cava — in  other  words,  in  retrograde  embolism.  Retro- 
grade embolism  of  veins  is  verj^  rare;  when  it  occurs,  it  is  more  frequently 
seen  in  the  hepatic  veins,  since  the}"  are  not  protected  b}'  valves,  and  are 
so  close  to  the  heart  that  fragments  of  growth  or  thrombus  may  drop 
into  their  orifices  either  from  the  inferior  vena  cava  or.  from  the  heart 
and  superior  ^-ena  cava.  Welch  §  in  his  article  on  embolism  quotes 
examples  of  fragments  of  new-growth  being  found  in  the  hepatic  A'eins 
in  cases  where  the  primary  growths  were  in  the  abdomen  and  th}'roid 
gland. 

It  seems  probable  that  in  cases  of  cranial  suppuration  with  secondary 
abscesses  in  the  liver,  without  any  abscesses  in  the  lungs,  the  micro- 
organisms ma}^  drop  down  the  jugular  vein,  superior  vena  cava,  right 
auricle,  and  inferior  vena  cava  into  the  orifices  of  the  hepatic  veins,  and 
so  infect  the  hA^er.  The  production  of  retrograde  embolism  probably 
depends  on  the  temporary  stagnation  or  reversal  of  the  direction  of  the 
blood-flow.  Thus  if  a  thrombus  was  passing  up  the  inferior  cava  and 
a  violent  expiratory  effort  or  cough  occurred  at  the  moment  when  it 
was  opposite  the  openings  of  the  hepatic  veins,  the  embolus  might  be 
carried  into  the  liver. 

*  Dixon  Mann  and  W.  Hall:  Edinburgh  Med.  Jovu-n.,  Jul}',  1904,  p   .57. 

t  West,  S.:  Path.  Trans.,  vol.  xxxvii,  p.  281. 

t  Ophiils:  American  Journ.  of  Med.  Sciences,  1901,  p.  797. 

I  Welcli,  W.  H. :  Allbutt's  System  of  Medicine,  vol.  vi,  p.  232. 


THROMBOSIS  OF  THE  PORTAL  VEIN. 

Synonyms:  Pylethrombosis,  Pylephlebitis  Adhaesiva. 

In  this  condition  there  is  thrombosis  of  the  portal  vein  which  does 
not  go  on  to  suppuration. 

CAUSATION. 

In  considering  the  causes  of  thrombosis  of  the  portal  vein  it  will  be 
convenient  to  deal  first  with  thrombosis  depending  upon  inflammatory 
and  other  morbid  conditions  of  the  portal  vein,  and  then  to  consider  the 
influence  of  hepatic  cirrhosis,  intra-abdominal  malignant  disease,  tumors, 
adhesions,  and  traumatism,  in  the  production  of  portal  thrombosis. 

Inflammatory  Conditions  Causing  Portal  Thrombosis. — Throm- 
bosis of  the  portal  vein,  or,  as  it  may  in  this  particular  connexion 
be  more  appropriately  called,  adhesive  pylephlebitis,  occurs  as  a  pre- 
hminary  stage  in  the  course  of  suppurative  pylephlebitis.  By  extension 
from  adjacent  parts  inflammation  may  spread  to  the  walls  of  the  portal 
vein  and  set  up  thrombosis  which  does  not  necessarily  go  on  to  suppura- 
tion. This  may  occur  in  cholangitis,  in  pancreatitis,  in  peripancreatitis, 
in  hepatic  and  subphrenic  abscesses,  and  in  other  conditions.  As  a 
good  example  of  portal  thrombosis  in  an  early  stage  of  suppurative 
pylephlebitis  Rose  Bradford's  *  case  may  be  quoted : 

A  man  aged  twenty  died  from  intestinal  obstruction  due  to  suppurative  phlebitis 
of  the  superior  mesenteric  vein  regarded  as  secondary  to  suppuration  in  a  mesenteric 
gland.     The  portal  vein  was  blocked  by  recent  clot. 

Cholelithiasis,  by  setting  up  cholangitis  and  pericholangitis,  may  lead 
to  inflammation  of  the  walls  of  the  portal  vein  and  subsequently  to 
thrombosis. 

A  good  example  of  this  is  given  by  Rabe  :  f  In  a  man  aged  seventy-three  who 
died  with  ascites,  a  calculus  was  found  impacted  in  the  duodenal  end  of  the  bile-duct, 
causing  dilatation  of  the  duct  behind  this  point;  around  the  bile-duct  there  was 
fibrosis  which  involved  the  portal  vein.  The  walls  of  the  vein  were  thickened  and 
contained  firm  clot. 

Extension  of  inflammation  from  an  hepatic  abscess  is  a  rare  cause  of 
thrombophlebitis  of  the  portal  vein;  the  hepatic  veins,  being  unprotected 
by  the  sheath  of  Glisson's  capsule,  are  more  likely  to  be  affected. 

A  man  aged  twenty-seven,  who  had  contracted  dysentery  in  the  Boer  War  of 
1S99-1902,  was  brought  in  a  moribimd  state  into  St.  George's  Hospital.  At  the 
autopsy  there  was  acute  peritonitis  and  several  pints  of  turbid  fluid  in  the  ab- 
dominal cavity,  due  to  rupture  of  an  abscess  in  the  left  lobe  of  the  liver  into  the 
peritoneal  cavity.  There  was  a  firm  dry  clot  in  the  portal  vein,  wliich  might  have 
given  rise  to  the  ascites.  The  walls  of  the  portal  vein  were  greatly  thickened  and 
the  lymphatic  glands  in  the  portal  fissure  much  enlarged.  It  seemed  probable 
that  the  infection  had  spread,  at  any  rate  partly,  by  the  lymphatic  vessels  from  the 
abscess  to  the  trunk  of  the  portal  vein. 

*  Bradford,  J.  R. :  Trans.  Clinic.  Soc,  vol.  xxxi,  p.  203. 
t  Rabe:  Bull  Soc.  .-Vnat.  Paris,  1S9S,  p.  170. 
52 


THROMBOSIS   OF   THE    PORTAL    VEIN.  53 

Inflammation,  abscess,  or  infarction  of  the  spleen  may  set  up  throm- 
bosis of  the  splenic  vein,  which  by  extension  may  spread  into  the  portal 
vein. 

Simple  ulcer  of  the  stomach  must  be  a  very  rare  cause  of  portal  throm- 
bosis. Wickham  Legg  *  mentions  two  cases;  but  I  have  no  other  refer- 
ences. In  this  connexion  it  may  be  pointed  out  that  thrombosis  of  the 
gastric  veins  may  cause  ulceration  of  the  gastric  mucous  membrane.  I 
have  seen  this  in  a  case  where  suppurative  pylephlebitis  was  due  to 
appendicitis.  Indirectly  a  gastric  ulcer  may  cause  portal  thrombosis  by 
giving  rise  to  a  localized  abscess  in  the  neighbourhood.  I  have  seen 
portal  thrombosis  in  a  case  of  subphrenic  abscess  due  to  perforation  of 
a  gastric  ulcer. 

Probably  in  many  of  the  cases  that  appear  to  be  primary  thrombosis 
there  is  in  reality  microbic  infection  of  a  low  grade  of  virulence  present 
which  is  responsible  for  the  production  of  a  thrombus.  The  term  "adhe- 
sive pylephlebitis,"  formerly  used  to  designate  thrombosis  of  the  portal 
vein,  is  an  expression  of  the  view  originated  b}^  Hunter  and  Cruveilhier 
that  thrombosis  was  always  the  result  of  phlebitis.  Bacteriological 
examination  f  shows  that  many  thrombi  which  would  formerly  have 
been  regarded  as  marantic  contain  micro-organisms,  and  though  the 
presence  of  micro-organisms  does  not  necessarily  prove  that  they  played 
a  causal  part  in  the  production  of  thrombosis,  it  justifies  the  tendency 
to  return  to  the  point  of  view  of  Hunter  that  most  thromboses  are  secon- 
dary to  infection  of  the  wall  of  the  vein. 

Disease  of  the  Portal  Vein. — Chronic  phlehosclerosis,  which  is  prob- 
ably often  due  to  increased  blood-pressure  in  the  portal  vein,  plays  an 
important  part  in  producing  portal  thrombosis.  Though  generally  asso- 
ciated with  cirrhosis,  chronic  portal  phlebitis  may  occur  independently 
of  any  hepatic  disease.  It  is  quite  possible  that  similar  changes  in  the 
vein  waU  may  result  after  thrombosis  has  taken  place;  but  it  seems 
probable  that  phlehosclerosis  usually  precedes  and  disposes  to  portal 
thrombosis. 

Borrmann,J  who  has  insisted  on  this  sequence  of  events,  found  phlehosclerosis 
in  7  out  of  20  cases  of  portal  thrombosis. 

AVhen  the  change  is  of  old  standing,  calcification  of  the  wall  of  the 
vein  may  occur  and  calcareous  plates  or  spicules  ma}'  project  into  the 
lumen  of  the  portal  vein  and  induce  thrombosis. 

In  a  patient  of  Dr.  Ewart's,  on  whom  I  made  a  postmortem  examination  at 
St.  George's  Hospital,  the  dependence  of  thrombosis  on  calcification  of  the  wall  of 
the  portal  vein  seemed  clear.  A  man  aged  sixty-six  years,  addicted  to  some  alco- 
holic excess,  had  been  in  good  health  until  two  months  before  his  death,  wlien 
ascites  appeared.  He  was  thin,  but  there  had  been  no  meltena  or  hsematemesis. 
Paracentesis  was  required,  but  the  fluid  reaccumulated,  diarrhoea  set  in,  and  he 
became  delirious  and  finally  died  comatose.  At  the  autopsj^  there  were  pigmented 
scars  in  the  colon  as  if  from  old  dysentery,  but  no  ulceration.     There  was  localized 

*  Legg,  Wickham:  St.  Bartholomew's  Hosp.  Reports,  vol.  x,  p.  236. 
t  Vaquez :  These  de  Paris,  1890.     Bryant,  J.   H. :  Gu3^'s  Hosp.   Reports,  vol. 
Ivi,  p.  99. 

J  Borrmann:  Deutsch.  Archiv  f.  klin.  Med.,  Dec.  9,  1897. 


54 


DISEASES   OF   THE   LIVEE. 


fibrinous  peritonitis  around  the  site  of  the  trocar  punctures.  The  portal  vein  was 
much  thickened  and  showed  calcification,  and  there  was  a  softening  thrombus  in 
the  right  brancii  of  the  portal  vein.  The  splenic  vein  was  occluded  at  its  entry  into 
the  porta]  vein  and  contained  a  crumbling  thrombus  in  contact  with  an  area  of 
calcification  in  its  wall.  The  thrombosis  did  not  correspond  to  the  more  extensive 
changes  in  the  walls  of  the  portal  vein,  and  it  therefore  appeared  probable  that  the 
thrombosis  was  secondary  to  the  changes  in  the  portal  vein,  as  presiimably  the 
thrombosis  had  only  existed  since  the  ascites  developed,  viz.,  two  months.  The 
liver  was  atrophied,  weighing  32  ounces,  but  not  cirrhotic.  The  spleen  weighed 
18  ounces  and  on  section  appeared  fibrotic,  but  did  not   present    any   infarcts. 

Syphilitic  inflammation  of  the  portal  vein  may  probably  give  rise  to 
thrombosis  in  some  cases.     This  may  occur  in  both  the  hereditary  and 

the  acquired  form   of 
\  the  disease,  but  more 

exact  knowledge  is 
required  on  this  point. 
Cirrhosis  of  the 
Liver.  —  Thrombosis 
of  the  portal  vein  is 
most  often  found  to  be 
associated  with  por- 
tal cirrhosis.  Fagge,* 
indeed,  stated  that  he 
had  only  met  with  it 
in  that  disease  or  in 
association  with  peri- 
hep  atitis .  Although 
cirrhosis  is  the  most 
frequent  cause  of  por- 
tal thrombosis  it  does  not  appear  to  be  present  in  half  the  total 
cases  of  that  condition. 

In  60  cases  collected  from  various  sources,  including  most  of  Langdon  Brown's, 
there  were  22,  or  36.6  per  cent.,  due  to  cirrhosis.  These  22  cases  do  not  include 
cases  where  cirrhosis  and  intra-abdominal  malignant  disease  were  both  present, 
or  those  few  cases  where  the  observers  believed  cirrhosis  to  be  secondary  to  portal 
thrombosis. 

Portal  thrombosis  is  far  from  common  in  cirrhosis  of  the  liver. 

In  a  period  of  thirty-three  years  Langdon  Brown  f  found  that  in  334  autopsies 
performed  on  cases  of  hepatic  cirrhosis  at  St.  Bartholomew's  Hospital  10,  or  3.3 
per  cent.,  were  coinplicated  by  thrombosis  of  the  portal  vein. 

In  cirrhosis  of  the  liver  there  are  a  number  of  factors  favouring  portal 
thrombosis.  There  are  obstruction  to  the  passage  of  blood  through  the 
liver  and  stagnation  of  blood  in  the  vein,  while  the  increased  venous 
pressure  tends  to  set  up  endophlebitis  and  even  secondary  calcification 
of  the  walls  of  the  vein.  Further,  the  catarrhal  condition  of  the  intes- 
tinal tract,  so  common  in  portal  cirrhosis,  favours  microbic  invasion  of  the 
walls  of  the  tributaries  of  the  portal  vein.  In  cases  of  nodular  cirrhosis, 
or  cirrhosis  with  multiple  adenomata,  thrombosis  of  the  portal  vein  is 

*  H.  Fagge:  Principles  and  Practice  of  Medicine,  Ed.,  1886,  vol.  ii,  p.  297. 
t  Langdon  Brown :  St.  Bartholomew's  Hospital  Reports,  vol.  xxxvii,  p.62. 


Fig.  10.— The  Under  Surface  of  a  Cirrhotic  Liver,  show- 
ing Thrombosis  of  the  Portal  Vein.  (Drawn  by  Dr.  E.  A. 
AVilson.) 


THROMBOSIS    OF   THE    PORTAL    VEIN.  55 

relatively  common;  thus,  in  fifteen  cases  collected  by  LI  Powell*  there 
was  portal  thrombosis  in  nine.  The  contents  of  the  "adenomata"  may 
soften  down  from  necrosis  and  discharge  into  the  portal  vein,  thus  setting 
up  thrombosis.  On  the  other  hand,  thrombosis  of  the  portal  vein  may 
so  impair  the  nutrition  of  the  "adenomata"  as  to  set  up  fatty  degenera- 
tion and  necrosis. 

Intra-abdominal  Malignant  Disease. — After  cirrhosis  the  com- 
monest condition  associated  with  portal  thrombosis  is  malignant  disease 
either  in  the  liver  itself  or  elsewhere  in  the  abdominal  cavity.  In  sixty 
cases  of  portal  thrombosis  ten  were  associated  with  some  form  of  intra- 
abdominal malignant  disease. 

Malignant  Disease  of  the  Liver. — Carcinoma  of  the  liver  may  eat  its 
way  into  the  branches  of  the  portal  vein  and  induce  thrombosis;  this 
may  occur  either  in  primary  or  secondary  malignant  disease  of  the  organ, 
but  it  is  particularly  prone  to  occur  when  primary  carcinoma  supervenes 
in  a  liver  which  is  already  cirrhotic.  In  these  cases  the  contents  of  the 
portal  vein  may  be  composed  of  growth  as  well  as  of  blood-clot.  It  is 
only  a  step  from  cirrhosis  with  adenoma  to  carcinoma  with  cirrhosis, 
and  it  is  difficult  to  be  certain  in  many  of  the  published  cases  whether 
the  growth  was  still  adenomatous  or  had  become  malignant.  The  two 
conditions  further  show  their  close  resemblance  by  the  frequency  with 
which  portal  thrombosis  occurs  in  both. 

In  other  forms  of  intra-abdominal  disease,  such  as  carcinoma  of  the 
stomach,  pancreas,  colon,  etc.,  the  growth  may  involve  the  tributaries 
of  the  portal  vein,  spread  along  them,  and  set  up  secondary  thrombosis. 

Carcinoma  of  the  Stomach. — Malignant  disease  of  the  stomach  occa- 
sionally gives  rise  to  portal  thrombosis.  S.  and  S.  Fenwick  f  found  this 
complication  in  3  per  cent,  of  their  cases  of  gastric  carcinoma  and  con- 
sider that  this  is  probably  understating  the  incidence.  Gastric  cancer 
may  set  up  portal  thrombosis  in  several  ways;  the  growth  ma}^  enter 
the  gastric  veins  and  extend  directly  into  the  portal  vein  and  set  up 
secondary  thrombosis,  pass  up  the  lesser  omentum  by  continuity  and 
compress  and  involve  the  portal  vein,  or  by  means  of  secondary 
growths  in  the  portal  fissure  or  in  the  substance  of  the  liver  ma}^  com- 
press the  portal  vein. 

In  the  following  case  there  were  at  least  two  factors  favouring  thrombosis  of 
the  portal  vein.  A  woman  aged  sixty-five  years  died  in  St.  George's  Hospital  witli 
a  small  cirrhotic  liver  weighing  28  ounces  and  a  spheroidal  celled  carcinoma  near 
the  pylorus.  The  trunk  of  the  portal  vein  was  thiclcened  and  surrounded  by  adhe- 
sions. The  right  branch  of  the  portal  vein  was  thrombosed  and  there  was  an  ad- 
herent clot  at  the  entrance  of  the  splenic  vein. 

In  a  case  of  portal  throml)osi.s  secondary  to  gastric  carcinoma  Longcope  | 
found  infarcts  in  the  liver. 

Pressure  on  the  portal  vein,  by  tumors,  adhesions,  and  altered  condi- 
tions of  adjacent  viscera,  may  be,  but  is  not  necessarily,  accompanied 
by  thrombosis  of  the  portal  vein.     By  pressure  the  nutrition  of  the 

*  LI  Powell:  Unpublished  Tliesis  for  M.  B.  degree,  Cambridge,  1895. 

t  Cancer  and  Other  Tumours  of  the  Stomach,  p.  72. 

■|  Longcope:  University  of  Pennsjdvania  Med.  Bull.,  Aug.,  1901,  p.  22.3. 


56  DISEASES    OF   THE    LIVER. 

walls  of  the  vein  is  impaired,  microbic  infection  is  thus  favoured,  and 
stagnation  of  the  blood  is  induced — ^factors  which  all  dispose  to  throm- 
bosis. Pressure  may  be  exerted  on  the  portal  vein  in  a  number  of 
ways,  chiefly  by  malignant  disease  involving  the  adjacent  lymphatic 
glands  or  the  head  of  the  pancreas. 

yialignant  Disease  of  the  Pancreas. — In  41  cases  of  portal  thrombosis 
Langdon  Brown  found  that  the  condition  was  associated  with  malignant 
disease  of  the  pancreas  in  three  instances.  Sometimes  when  a  malignant 
growth,  which  compresses  the  portal  vein,  also  infiltrates  its  walls,  a 
finger-like  process  of  the  growth  may  extend  along  the  lumen  of  the 
vein  and  then  set  up  a  secondary  thrombosis.  This  very  rarely  happens 
in  mahgnant  disease  of  the  pancreas ;  it  is  chiefly  seen  in  mahgnant  dis- 
ease in  the  liver. 

Malignant  disease  of  the  glands  in  the  portal  fissure  secondarv'  to 
malignant  disease  of  the  stomach,  pancreas,  liver,  or  gaU-bladder  might 
compress  the  portal  vein.  Malignant  disease  of  the  liver  may  compress 
as  well  as  invade  branches  of  the  portal  vein,  and  set  up  thrombosis  which 
travels  distally  into  the  main  trunk.  Portal  thrombosis  has  been  recorded 
in  primary  carcinoma  of  the  bile-ducts.     (Bourgeret  and  Cossy.*) 

Chronic  Pancreatitis. — ^The  cicatricial  contraction  of  chronic  inflam- 
mation of  the  head  of  the  pancreas  may  greatly  constrict  the  superior 
mesenteric  vein  and  lead  to  thrombosis  which  eventually  extends  into 
the  portal  vein.  Barnard  f  met  with  a  case  of  this  kind.  Probably 
many  cases  of  chronic  pancreatitis  were  formerly  spoken  of  as  ''scirrhus" 
of  the  pancreas. 

The  traction  exerted  by  adhesions  due  to  gastric  or  duodenal  ulcers 
(Frerichs  %)  may  compress  the  portal  vein  and  in  rare  instances  induce 
thrombosis.  Similarly  haflammatorj^  adhesions  involving  the  mesenteric 
veins  may  start  thrombosis  which  may  extend  upwards  into  the  trunk 
of  the  portal  vein.  Cases  recorded  by  F.  Taylor  §  and  R.  Johnson  || 
illustrate  the  production  of  portal  thrombosis  in  this  way. 

Chronic  'peritonitis  in  rare  instances  may  be  the  only  other  morbid 
lesion  forthcoming,  and  so  appear  to  be  the  cause,  either  by  extension 
of  inflammation  to  the  waUs  of  the  portal  vein,  or,  in  verj'  rare  instances, 
by  constricting  or  compressing  the  vein. 

In  St.  Bartholomew's  Hospital  Museum  there  is  a  specimen  [No.  220.5  a]  of 
thrombosis  associated  -nnth  chronic  peritonitis;  the  hver  was  not  cirrhotic.  Frerichs 
quotes  some  similar  cases. 

The  mechanical  pressure  exerted  by  a  calculus  in  the  gall-bladder, 
or  more  frequently  in  the  ducts,  on  the  portal  vein  may  give  rise  to  simple 
thrombosis.  This  is  more  hkely  to  occur  when  the  calculus  is  in  the 
common  duct,  where  it  is  in  close  contact  with  the  portal  vein. 

*  Bourgeret  and  Cossy:  Bull.  Soc.  Anat.  Paris,  1873,  p.  347. 
t  Barnard,  H.  L. :  Vide  Langdon  Brown,  St.  Bartholomew's  Hosp.  Reports,  vol. 
xxxvii,  p.  87. 

%  Frerichs :  Diseases  of  the  Liver,  vol.  i,  p.  1 172. 
§  Taylor,  F.:  Trans.  Path.  Soc,  vol.  xxxii,  p.  21 
il  Johnson,  Pt. :  Trans.  Clinic.  Soc,  vol.  xxxi,  p.  212. 


THROMBOSIS   OF   THE    PORTAL   VEIX.  0/ 

Cases  are  recorded  by  Leudet,  Geigel,  Naiinjoi,*  Westenhoffer.f  Korte.t  Naiinyn 
also  describes  a  case  where  a  calcvdus  in  the  cystic  duct  compressed  and  gave  rise 
to  portal  thrombosis,  and  refers  to  a  case  of  Klesser's  where  a  calculus  in  the  same 
position  compressed  one  branch  of  the  portal  vein.  Donkin  §  met  ^^^th  portal 
thrombosis  due  to  pressure  exerted  by  several  calculi  iu  the  gall-bladder  on  the 
vein. 

Gummatous  in-jiamnnation  in  the  portal  fissure  is  a  rare  cause  of  throm- 
bosis of  the  portal  vein.  It  is  possible  that  aneurysm  of  the  abdoininal 
aorta  or  of  the  hepatic  artery  may  press  on  the  portal  vein  and  induce 
thrombosis. 

Traumatism  may  be  followed  by  portal  thrombosis.  Welch  ||  men- 
tions a  case  where  symptoms  strongly  suggesting  pylethrombosis  fol- 
lowed a  blow  on  the  abdomen;  but  recovery  took  place.  Pitt**  described 
a  man  who  after  a  fall  on  his  side  vomited  and  became  collapsed ;  he  was 
found  to  have  a  strangulated  scrotal  hernia;  at  the  operation  the  bowel 
was  found  to  be  bruised.  Death  occurred  five  days  later  and  throm- 
bosis of  one  of  the  intrahepatic  branches  of  the  portal  vein  was  found. 
As  an  example  of  post-operative  thrombosis  Delatour's  If  case  of  throm- 
bosis of  the  splenic  vein  after  splenectomy,  extending  into  the  portal 
vein,  may  be  mentioned.  Traumatism  involved  in  volvulus  or  in  kinking 
of  the  mesenter}^  may  be  the  starting-point  of  thrombosis  in  the  portal 
area.     Langdon  Brown  refers  to  an  example  of  this  kind. 

Thrombosis  of  the  portal  vein  may  be  secondaiy  to  thrombosis  of  the 
hepatic  veins. 

At  the  post-mortem  examination  of  a  woman  aged  fifty-two  who  died  in  St. 
George's  Hospital  in  1898  there  was  marked  ascites  with  very  little  chronic  peritonitis. 
The  intestines  were  full  of  blood  and  deeply  congested;  no  enlargement  of  the 
cutaneous  veins  over  the  abdomen  or  of  those  of  the  oesophagus  or  retroperitoneal 
space.  The  inferior  vena  cava  showed  a  decolorised  parietal  clot  close  to  the  opening 
of  the  hepatic  veins;  the  right  hepatic  vein  was  blocked  with  decolorised  clot;  the 
left  was  normal.  The  inferior  vena  cava  was  not  obstructed  and  there  was  no 
clot  elsewhere  in  its  course.  The  portal  and  splenic  veins  were  blocked  by  more 
recent  clot.  The  liver  was  much  atrophied,  markedly  nutmeg,  and  somewhat  fatty, 
but  not  cirrhotic  to  the  naked  eye.  Microscopically  there  was  extensive  atrophy 
of  the  liver  cells,  but  they  were  not  necrosed  or  destroyed  as  they  are  in  acute 
yellow  atrophy.  The  fibrous  tissue  around  the  portal  spaces  was  prominent  from 
the  atrophy  of  the  liver  cells,  but  there  was  no  definite  evidence  of  cirrhosis.  The 
spleen  weighed  9  oimces.  There  were  numerous  cutaneous  and  visceral  haemor- 
rhages. |t 

Puerperal  eclampsia  has  been  thought  b}^  Schmorl  §§  to  induce  portal 
thrombosis.  This  may  be  the  result  of  degenerative  changes  in  the  liver 
giving  rise  t-o  discharge  of  necrotic  hepatic  cells  and  tissue  fibrinogens 
into  the  portal  vein. 

In  a  number  of  cases  there  is  no  local  cause  or  associated  morbid 
change,  such  as  cirrhosis  or  inflammation,  to  account  for  portal  throm- 

*  Naunyn :  Cholelithiasis,  p.  133. 

t  Westenhoffer:  La  Semaine  M^dicale,  1903,  p.  32.  J  Korte:  Ibid. 

§  Donkin :  Medical  Press  and  Circular,  1868,  vol.  ii,  p.  390. 
II  Welch,  W.  H.:  Allbutt's  Svstem,  vol.  vi,  p.  220. 
**  Pitt,  G.  N. :  Trans.  Path.  Soc,  vol.  xlvi.  p.  74. 
tf  Delatour:  Annals  of  Surgery,  vol.  xxi,  p.  24. 
ij  Rolleston:  Trans.  Path.  Soc.,  vol.  1,  p.  148. 
§§  Schmorl:  Quoted  by  AVelch,  Allbutt's  System,  vol.  vi,  p.  219. 


58  DISEASES    OF   THE    LIVER. 

bosis.  In  some  of  these  cases  it  is  associated  \Yith  thrombosis  elsewhere 
in  the  body,  and  therefore  ahnost  certainly  depends  on  a  widespread 
change  in  the  blood  of  either  a  chemical  or  infective  nature.  It  is  anal- 
ogous to  the  thrombosis  sometimes  seen  in  marasmus  and  in  anaemias. 
The  altered  blood  condition  must  favour  infection,  and  the  intestinal 
tract  would  appear  to  be  so  eminently  favoural^le  to  the  passage  of  micro- 
organisms into  the  tributaries  of  the  portal  vein  that  it  is  surprising  that 
portal  thrombosis  is  so  comparatively  infrequent.  I  have  myself  on 
two  occasions  seen  portal  thrombosis  associated  with  thrombosis  in  the 
iliac  veins.  Langdon  Brown  found  that  in  33  cases  6  were  associated 
with  thrombosis  elsewhere. 

It  is  curious  that  nothing  is  known  as  to  the  occurrence  of  portal 
thrombosis  in  connexion  with  diseases  such  as  gout,  influenza,  pneu- 
monia, ty]3hoid  fever,  etc.,  which  lead  to  thrombosis  elsewhere  in  the 
body.  It  is  specially  noticeable  that  thrombophlebitis  of  the  portal 
vein  does  not  occur  in  or  after  enteric  fever. 

Sex. — More  cases  occur  in  males  than  in  females.  In  62  cases, 
38  were  males  and  24  females;  the  preponderance  of  males  depends  on 
the  greater  frequency  of  hepatic  cirrhosis  in  that  sex.  Cirrhosis  of  the 
liver  was  present  in  18  out  of  the  38  males  and  in  only  4  of  the  24  female 
cases.  Intra-abdominal  malignant  disease  accounted  for  8,  or  exactly 
one-third  of  the  cases  of  portal  thrombosis  in  women. 

Age. — In  61  cases  the  average  age  w^as  forty-four  years.  The  ex- 
tremes were  eighty  years  in  a  man  and  five  years  in  a  girl.*  In  the  two 
sexes  the  average  ages  were  44.8  years  among  the  males  and  41  years 
among  the  females.  This  again  corresponds  with  the  shghtly  earlier 
age  at  W'hich  cirrhosis  is  fatal  in  women.  There  were  ten  patients  under 
thirty  years  of  age,  equally  divided  among  the  two  sexes;  four  were 
under  twenty  years  of  age— three  females  and  one  male.  The  average 
age  of  portal  thrombosis  is  thus  more  than  twelve  years  above  the  average 
age  [31.6  years]  in  suppurative  pylephlebitis.  The  explanation  of  this 
is  to  be  found  in  the  fact  that  the  two  conditions — hepatic  cirrhosis  and 
intra-abdominal  malignant  disease — w^hich  most  frequently  cause  portal 
thrombosis  are  commoner  after  forty  years  of  age,  while  appendicitis, 
which  is  the  most  prolific  source  of  suppurative  pylephlebitis,  is  essen- 
tially a  disease  of  young  persons. 

DISTRIBUTION  OF  THE  THROMBOSIS  ON  THE  PORTAL  VEIN. 

The  thrombosis  varies  considerably  in  its  distribution.  It  may  be 
extensive  and  spread  throughout  the  portal  vein,  its  tributaries  and 
branches.  Usually  it  is  more  limited;  it  may  occupy  the  main  trunk 
of  the  portal  vein  and  one  or  both  of  its  branches  in  the  liver,  or  it  may 
obstruct  the  trunk  and  one  or  more  of  its  tributaries,  while  in  other 
instances  thrombosis  may  be  confined  to  one  of  its  intra-hepatic  branches 
or  one  of  its  tributaries.  The  clot  obstructing  a  tributary,  such  as  the 
splenic  vein,  may  just  project  into,  but  not  obstruct,  the  blood-flow 
*  Taylor,  F, :  Trans.  Path.  Soc  ,  vol.  \\\ii,  p.  61. 


THROMBOSIS    OF  THE   PORTAL   VEIN.  59 

through  the  main  trunk  of  the  portal  vein;  in  many  instances  the  clot 
extends  from  the  tributaries  upwards  into  the  portal  vein.  In  other 
instances  the  clotting  may  begin  in  the  portal  vein  and  subsequently 
spread  into  the  peripheral  tributaries.  Thrombosis  may  be  confined 
entirely  to  the  tributaries  of  the  portal  vein — the  splenic,  superior  and 
inferior  mesenteric  veins — or  to  its  intra-hepatic  branches.  Though 
this  can  hardly  be  called  portal  thrombosis,  it  is  difficult  to  separate 
thrombosis  of  the  main  trunk  of  the  portal  vein  from  thrombosis  of  its 
branches. 

MORBID  ANATOMY. 

The  thrombosed  vein  is  distended  with  clot,  and  thus  differs  from 
the  more  or  less  collapsed  condition  of  the  portal  vein  when  containing 
ordinary  post-mortem  blood-clot.  Distal  to  the  obstructing  thrombus  the 
vein  may  be  considerably  dilated  or  even  sacculated;  this  may  also  occur 
in  the  splenic  vein.  The  vein  wall  is  usually  thickened,  sometimes  con- 
siderably so,  from  chronic  phlebosclerosis,  a  condition  analogous  to 
arteriosclerosis,  which  Borrmann  considers  may  be  responsible  for  throm- 
bosis. The  wall  of  the  vein  sometimes  contains  calcareous  plates,  a 
further  stage  of  chronic  phlebosclerosis.  In  other  instances  the  vein 
wall  is  swollen  from  recent  inflammation.  In  cases  where  the  patient 
lives  for  a  long  time  after  the  onset  of  thrombosis  the  portal  vein  may 
be  reduced  to  a  mere  cord  of  fibrous  tissue.  In  such  cases  a  collateral 
circulation  is  developed  and  quite  a  plexus  of  veins  may  be  found  in  the 
position  of  the  portal  vein.  It  is  very  possible  that  in  some  cases  thick- 
ening and  calcification  of  the  walls  of  the  portal  vein  are  results  of  throm- 
bosis with  partial  canalization  and  organization  of  the  blood-clot. 

The  character  of  the  clot  varies  according  to  its  age:  it  may  be  c[uite 
recent  and  not  very  firixily  adherent  to  the  vein  wall,  or  it  may  be  granular, 
decolorized,  or  even  laminated.  In  some  instances  the  lumen  of  the 
vein  is  not  obliterated,  the  clot  being  only  parietal.  As  has  already 
been  mentioned,  the  thrombosis  may  be  parietal  in  one  part  of  the 
portal  vein  and  completely  obstruct  the  lumen  in  another,  or  the  central 
part  of  the  clot  may  be  canalized.  When  the  central  part  of  the  thrombus 
softens  down,  the  condition  approaches,  if  it  does  not  merge  into,  sup- 
purative pylephlebitis.  The  thrombus  may  obstruct,  without  spreading 
into,  the  orifice  of  one  of  the  tributaries  of  the  portal  vein;  this  is  not 
uncommon  at  the  junction  of  the  splenic  vein  with  the  trunk  of  the  portal 
vein. 

The  Liver. — The  liver  may  present  conditions  that  have  caused  or 
favoured  the  occurrence  of  thrombosis  in  the  portal  vein,  such  as  portal 
cirrhosis,  nodular  cirrhosis,  primary  or  secondary  malignant  disease,  or 
abscess.  The  liver  may  show  changes  depending  on  and  secondary  to 
portal  thrombosis.  Thus,  the  hepatic  artery  may  be  enlarged  in  order 
to  compensate  for  obstruction  to  the  advent  of  blood  to  the  liver  by 
means  of  the  portal  vein.  Thrombosis  of  the  portal  vein  may  be  asso- 
ciated with  a  fatty  and  necrotic  condition  of  the  "hobnails"  of  a  cirrhotic 
liver,  and  it  may  reasonably  he  l)elieved  tliat  portal  thrombosis,  by  cutting 


60  DISEASES   OF  THE   LI^^R. 

off  the  blood-supply,  has  brought  about  this  change.  It  is,  however,  pos- 
sible that  the  converse  occurs,  and  that  a  softened  hobnail  may,  by  dis- 
charging into  a  branch  of  the  portal  vein,  start  thrombosis. 

Infarcts,  though  rare  in  the  hver,  are,  when  present,  associated  in  a 
fair  percentage  of  the  cases  with  portal  thrombosis.  They  are,  however, 
very  far  from  being  a  necessary  sequence  of  that  condition.  Some  other 
factor,  such  as  obstruction  of  the  hepatic  artery  or  a  toxic  condition  of 
the  blood,  is  necessary  before  infarction  occurs  in  portal  thrombosis. 
{Vide  page  104.)  The  softening  and  necrosis  of  cirrhotic  hobnails  in 
portal  thrombosis  might  be  compared  with  the  production  of  an  anaemic 
infarct  in  an  other^dse  healthy  liver  under  similar  conditions.  In  portal 
thrombosis  the  infarcts  are  usually  red  or  hsemorrhagic,  and  in  only  a 
few  instances  anaemic. 

Frerichs  *  describes  local  atrophy  and  depressions,  sometimes  leading  to  a 
lobulated  condition  of  the  liver,  as  a  result  of  obstruction  of  individual  branches 
of  the  portal  vein.  It  is  possible  that  in  an  early  stage  of  these  cases  of  atrophy 
there  was  an  infarct. 

In  some  cases  where  the  portal  vein  has  been  thrombosed  for  some 
considerable  time  the  Hver  may  show  ver}'  little  change,  or  may  merely 
be  fatty. 

In  a  remarkable  case  recorded  by  Langdon  Bro-«Ti  f  symptoms  of  portal  ob- 
struction had  existed  for  twenty  years,  and  indeed  this  diagnosis  had  been  made 
early  in  the  patient's  illness  by  the  late  Sir  William  Jenner.  The  portal  vein  was 
represented  by  a  fibrous  cord  mth  a  minute  lumen.  The  liver  was  described  as 
natural  though  pale.  In  a  case  of  much  the  same  kind  recorded  by  Cruveilhier  j 
the  liver  was  mialtered.  In  other  instances  the  liver  is  small,  atrophied,  and  shows 
a  little  replacement  fibrosis.  In  a  case  regarded  as  primary  thrombosis  of  the 
portal  vein  by  Dickinson  §  in  a  woman  aged  twenty-one,  the  liver,  though  fatty, 
presented  no  signs  of  cirrhosis  and  weighed  only  28  ounces.  A  similar  case  was 
recorded  bj'  Peacock.  ||  In  a  case  under  Dr.  Penrose's  care,  which  I  examined 
after  death,  the  liver  weighed  46  ounces  and  appeared  atropliied  to  the  naked  eye. 
Microscopicall}^  there  was  no  evidence  of  cirrhosis,  though  the  fibrous  tissue  around 
the  portal  areas  was  very  prominent.  I  have  foimd  exactlj'^  the  same  appearances 
in  two  other  cases  examined  postmortem  and  microscopically. 

It  has  been  thought  by  West  **  and  Goodhart  ff  that  thrombosis  of 
the  portal  vein  may  give  rise  to  portal  cirrhosis  in  a  previously  healthy 
liver.  There  is  ample  evidence  that  this  need  not  occur;  on  the  other 
hand,  some  atrophy  of  the  Hver  cells  with  fibrous  replacement  is  not 
uncommon,  and  this  relative  fibrous  increase  might  have  been  regarded 
as  cirrhosis  of  slight  degree. 

Fibrosis  of  the  liver  was  produced  in  dogs  by  Solo-nieff  J  J  as  a  result  of  gradual 
thrombosis  of  the  portal  vein.  This  might  possibly  have  been  due  to  some  extension 
of  inflammation  into  the  liver  along  the  portal  vein,  or  have  been  a  replacement 
fibrosis  associated  with  atrophy  of  the  liver  ceUs  from  diminished  blood-supply. 

*  Frerichs :  Diseases  of  the  Liver,  vol.  ii,  p.  396.  Translated  by  New  Sydenham 
Soc. 

t  Langdon  Bro-mi :  St.  Bartholomew's  Hospital  Reports,  vol.  xxxvii,  p.  64. 

I  Cruveilhier:  Atlas  d'Anat.  Pathol.,  livraison  xvi,  PI.  6. 
§  Dickinson:  Trans.  Path.  Soc,  vol.  xiv,  p.  6.3. 

II  Peacock:  Trans.  Path.  Soc,  vol.  xxiv,  p.  122. 
**  West,  S. :  Trans.  Path.  Soc,  vol.  xxix,  p.  106. 
tt  Goodhart:  Trans.  Path.  Soc,  vol.  xl,  p.  134. 

it  Solowieff :  Virchow's  Archiv,  Bd.  ixii.  S.  195,  1875. 


THROMBOSIS   OF   THE   PORTAL   VEIN.  61 

Bermant's  *  experimental  researches  support  Solowieff's  views  as  to  cirrhosis  being 
produced  by  portal  obstruction,  while  Cohnheim  and  Litten  f  came  to  a  diametrically 
opposite  conclusion. 

To  sum  up  the  late  effects  of  portal  thrombosis  on  the  liver,  there 
may  be  no  alteration  except  slight  fatty  change;  there  may  be  atrophy 
of  the  liver  with  some  fibrous  replacement,  but  there  is  very  little  reason 
to  believe  that  genuine  cirrhosis  is  produced  in  this  way. 

Spleen. — Enlargement  of  the  spleen  is  almost  constant  when  the 
trunk  of  the  portal  vein  is  completely  occluded  by  a  thrombus.  Langdon 
Brown  estimates  that  it  is  enlarged  in  70  per  cent,  of  the  cases.  Enlarge- 
ment may  be  reduced  by  copious  ascites  or  gastro-intestinal  haemorrhages 
or  prevented  by  firm  perisplenic  adhesions  or  chronic  capsulitis. 

In  a  case  under  my  care  of  thrombosis  of  the  portal  vein  in  cirrhosis  associated 
with  rapid  and  excessive  ascites  the  spleen  only  weighed  4  ounces. 

On  the  other  hand,  there  may  be  no  splenic  enlargement  with  a 
parietal  thrombosis  of  the  portal  vein  or  where  the  mesenteric  veins  only 
are  obstructed.  Very  great  enlargement  of  the  spleen  follows  complete 
thrombosis  of  the  splenic  vein;  it  may  weigh  20  or  30  ounces  and  may 
show  infarcts,!  either  anaemic  or  hsemorrhagic.  In  connection  with  the 
association  of  infarcts  and  thrombosis  of  the  splenic  vein  it  should  be 
remembered  that  an  infarct  due  to  arterial  embolism  may  induce  throm- 
bosis, possibly  by  the  liberation  of  tissue  fibrinogens. 

Intestines. — When  there  is  extensive  thrombosis  of  the  mesenteric 
veins  there  may  be  hsemorrhagic  infarction  going  on  to  gangrene  in  part 
of  the  small  intestine,  usually  in  the  middle  of  the  jejunum.  The  fact 
that  the  middle  of  the  jejunum  is  more  often  affected  than  the  rest  of  the 
intestine  is  due  to  this  part  of  the  bowel  being  entirely  dependent  for 
its  blood-supply  on  the  superior  mesenteric  artery  and  unable  to  draw 
any  blood  from  other  sources,  such  as  the  parietal  veins  around  the 
duodenum  and  caecum.  §  A  good  example  of  hsemorrhagic  infarction  of 
9  inches  of  the  jejunum  due  to  this  cause  is  in  St.  Bartholomew's  Hos- 
pital Museum  (1956  g). 

I  have  seen  secondary  ulceration  of  the  stomach  occur  from  portal 
thrombosis.  When  the  portal  vein  has  been  obstructed  for  some  con- 
siderable time,  the  small  veins  in  the  intestines,  or  more  rarely  in  the 
stomach,  may  be  considerably  dilated.  A  varicose  vein  in  the  stomach 
may  become  eroded  and  give  rise  to  fatal  haemorrhage. 


CLINICAL  PICTURE. 

Onset. — In  the  presence  of  cirrhosis  of  the  liver  or  intra-abdominal 
disease  there  may  be  nothing  to  mark  the  occurrence  of  portal  thrombosis, 
especially  when  ascites  is  already  present.  In  latent  cirrhosis  or  other 
cases  where  the  patient  has  been  in  good  or  in  fair  health  the  onset  may 

*  Bermant  (1897) :  Quoted  by  Welch,  Allbutt's  System,  vol.  vi,  p.  221. 
t  Cohnheim  and  Litten:  Virchow's  Archiv,  Bd.  Ixvii,  S.  153,  1876. 
t  RoUeston:  Trans.  Path.  Soc,  vol.  xliii,  p.  49. 
§  Barth :  Soc.  med.  des  Hop.  Paris,  Oct.  28,  1897. 


62  DISEASES    OF   THE    LIVER. 

be  sudden  and  marked  by  the  rapid  development  of  ascites  or  by  pro- 
fuse hsematemesis.  In  34  cases  analyzed  by  Langdon  Brown  the  onset 
was  gradual  in  14  and  acute  in  20. 

Symptoms  and  Signs. — The  chnical  manifestations  of  portal  throm- 
bosis present  a  certain  amount  of  variation  which  may  roughly  be  corre- 
lated with  the  situation  and  extent  of  the  thrombosis  in  the  portal  area. 
Thus,  if  the  portal  vein  alone  is  involved,  the  most  prominent  symptom 
is  that  of  obstruction  to  the  passage  of  blood  through  the  liver,  viz., 
ascites,  while  hgematemesis  may  also  occur.  If  the  thrombus  occludes 
the  proximal  end  of  the  splenic  vein  where  it  joins  the  portal  vein,  en- 
largement of  the  spleen  and  hsematemesis  may  be  expected.  Thrombosis 
of  the  mesenteric  veins  is  associated  with  intestinal  obstruction,  diarrhoea, 
melsena,  and  collapse. 

Arranged  in  the  order  of  their  frequency  and  importance,  the  chief 
clinical  features  of  portal  thrombosis  are:  ascites,  enlargement  of  the 
spleen,  gastro-intestinal  haemorrhages,  abdominal  pain,  symptoms  of 
intestinal  obstruction,  diarrhoea,  and  manifestations  of  toxaemia  re- 
sembling those  in  the  late  stages  of  cirrhosis,  and  not  unlike  uraemia. 
It  will  be  seen  that  thrombosis  of  the  portal  vein  may  present  the  aspect 
of  cirrhosis  of  the  liver,  of  a  gastro-intestinal  disorder,  or  may  combine 
the  features  of  these  two  groups. 

Ascites  is  the  most  frequent  cUnical  manifestation.  In  61  coUected 
cases  it  was  present  in  40,  or  65.6  per  cent.  It  may  be  absent  in  acute 
cases  where  death  rapidly  results  from,  gastro-intestinal  haemorrhage,  or 
where  the  mesenteric  veins  are  chiefly  involved  and  the  symptoms 
suggest  intestinal  obstruction.  Copious  gastro-intestinal  haemorrhage 
or  diarrhoea  may  prevent  the  development  of  ascites.  In  the  rare  cases 
where  life  has  been  prolonged  for  years  there  may  be  no  ascites,  pre- 
sumably from  compensation  brought  about  by  a  free  collateral  anasto- 
mosis. Stress  was  laid  by  Frerichs  on  the  rapid  development  of  ascites 
and  on  its  reaccumulating  directly  after  paracentesis  as  an  important 
diagnostic  sign  of  portal  thrombosis,  but  it  must  be  admitted  that  this 
is  not  of  much  value,  inasmuch  as  the  same  phenomena  may  occur  in 
cirrhosis  and  occasionally  in  ascites  due  to  other  causes,  e.  g.,  tuberculous 
peritonitis. 

Enlargement  of  the  Sple-en. — The  spleen  is  ^^er}^  frequently  found 
enlarged  after  death,  but  is  not  palpable  in  all  these  cases  during  life. 
Since  most  statistics  refer  to  the  size  of  the  spleen  as  determined  after 
death,  a  much  lower  estimate  than  70  per  cent.,  the  percentage  arrived 
at  by  Langdon  Brown  by  adding  his  41  cases  to  Frerichs'  and  to  25 
collected  by  Crof ton- Atkins,  must  be  made  of  the  existence  of  a  palpable 
spleen  intrxi  vitam.  The  enlargement  may  be  masked  by  ascitic  or 
tympanitic  distension  of  the  abdomen.  Enlargement  may  be  observed 
to  diminish  after  copious  gastro-intestinal  haemorrhage.  Very  consider- 
able enlargement  should  suggest  the  possibility  of  hsematemesis  or 
melaena  due  to  a  thrombus  obstructing  either  the  splenic  vein  or  its 
junction  with  the  portal  vein. 

Gastro-intestinal  sympioms  are  somewhat  varial)le  and  are  related 


THROMBOSIS    OF    THE    PORTAL    VEIX.  63 

to  thrombosis  involving  the  trunks  or  orifices  of  the  gastric  and  mesenteric 
veins,  rather  than  to  thrombosis  of  the  trunk  of  the  portal  vein  in  the 
hilum  of  the  liver.  G astro-intestinal  hsemorrhage  was  noted  in  27  out 
of  61  collected  cases,  or  in  44.2  per  cent.  Hsematemesis  and  intestinal 
hsemorrhage  may  be  due  to  venous  oozing  or  to  definite  ulceration  from 
necrosis  of  the  mucosa  induced  by  thrombosis  of  the  gastric  or  mesenteric 
veins.  When  the  mesenteric  veins  are  thrombosed,  haemorrhagic  infarc- 
tion may  occur  and  give  rise  to  paralysis  of  the  bowel  with,  hsemorrhagic 
effusion  into  its  lumen.  Gastro-intestinal  haemorrhage  ma}''  be  the  initial 
symptom;  this  was  so  in  7  out  of  20  cases  of  acute  onset  collected  by 
Langdon  Brown.  Hsematemesis  and  melsena  may  be  frec^uently  repeated 
and  rapidly  prove  fatal.  On  the  other  hand,  in  cases  that  survive  for 
a  number  of  years  haemorrhages  may  recur  from  time  to  time  during  the 
course  of  the  disease  in  spite  of  a  very  considerable  collateral  circulation. 
Diarrhoea. — Frerichs  found  that  diarrhoea  was  present  in  25  out  of 
28  cases,  while  in  Langdon  Brown's  41  cases  diarrhoea  only  occurred  in 
11.  The  motions  are  watery  and -may  be  inixed  with  blood.  Diar- 
rhoea is  probably  due  to  increased  venous  pressure  and  concomitant 
failure  of  nutrition  in  the  mucous  membrane  of  the  bowel.  There  may 
be  a  somewhat  sudden  onset  of  acute  intestinal  symptoms,  due  to  hsem- 
orrhagic infarction  and  paralysis  of  part  of  the  small  intestine.  Portal 
thrombosis  may  thus,  like  acute  pancreatitis,  simulate  acute  intestinal 
obstruction  due  to  some  mechanical  cause. 

In  a  case  of  Pearce  Gould's,*  where  the  superior  mesenteric  vein  was  thrombosed 
and  the  superior  mesenteric  artery  much  narrowed,  there  was  a  palpable  abdominal 
tumor  shortly  before  death,  which  was  formed  by  the  adherent  coils  of  the  lower 
part  of  the  ileum  extensively  infiltrated  with  blood. 

As  a  rule,  in  thrombosis  of  the  mesenteric  veins  the  onset  of  symp- 
toms of  intestinal  obstruction  is  gradual,  while  in  thrombosis  of  the 
corresponding  artery  the  symptoms  come  on  acutely.     (Makins.f) 

Dilatation  of  the  Superficial  Abdominal  Fews.— Enlargement  of  the 
subcutaneous  veins  around  the  umbilicus,  like  that  in  ordinary  cirrhosis, 
is  noted  in  less  than  one-third  of  the  cases  of  portal  thrombosis.  It  has 
been  thought  that  its  rapid  development  is  an  indication  of  portal  throm- 
bosis, but  no  weight  can  be  laid  on  this,  or  indeed  on  the  presence  or 
absence  of  dilated  veins  around  the  umbilicus. 

Jaundice  may  be  due  to  the  same  cause  that  gi^'es  rise  .to  portal 
thrombosis,  but  does  not  depend  on  it  and  usually  does  not  occur  in 
uncomplicated  cases. 

In  41  cases  it  was  present  in  13  (Langdon  Brown).  It  may  be  due  to  mahgnant 
disease,  i.  e.,  carcinoma  of  the  head  of  the  pancreas,  compressing  or  obstructing 
both  the  portal  A-ein  and  the  bile-duct.  In  only  one  of  Langdon  Brown's  cases 
was  it  thought  that  the  thrombosed  vein  pressed  on  the  common  bile-duct. 

The  urine  is  diminished  in  amount.  This  may  be  explained  as  due 
to  the  lowered  blood-pressure,  since  experimental  ligature  of  the  portal 
vein  is  followed  by  a  great  fall  in  arterial  tension.     There    are    other 

*  Gould,  A.  P. :  Lancet,  1902,  vol.  1,  p.  121. 

t  ^lakins,  G.  H. :  Brit.  Med.  Journ.,  1S9S,  vol.  i,  p.  1137. 


64  DISEASES   OF  THE   LIVER. 

factors,  such  as  loss  of  blood,  diarrhoea,  and  diminished  absorption  of  fluid, 
that  would  also  tend  to  produce  a  scanty  excretion  of  urine.  The  urine 
is  high  coloured  and  lithatic.  Alimentary  glycosuria  has  been  thought 
to  be  constantly  present,  and  its  absence  to  be  good  evidence  that  a 
suspected  case  is  not  one  of  portal  thrombosis.  Sugar,  if  absorbed  from 
the  intestinal  tract,  must  pass  by  collateral  channels  straight  into  the 
general  circulation;  since  it  manifestly  cannot  reach  the  liver  by  means 
of  the  portal  vein.  The  absorption  from  the  intestines  is  greatly  ob- 
structed and  it  is  very  doubtful  whether  this  test  is  of  much  value.  (For 
consideration  of  this  point  see  p.  230.) 

It  was  certainly  absent  one  day  before  death  in  a  patient,  under  the  care  of 
my  colleague,  Dr.  Penrose,  with  simple  portal  thrombosis,  probably  secondary 
to  thrombosis  of  the  hepatic  veins;  I  have  never  observed  it. 

In  a  case  of  cirrhosis  with  thrombosis  of  the  portal  vein  Boinet  * 
observed  paralysis  of  the  legs;  he  also  produced  paralysis  of  the 
hind  limbs  in  animals  by  aseptic  ligature  of  the  portal  vein. 

In  some  cases  the  symptoms  are  those  of  toxaemia  resembling  uraemia, 
and  probably  due  to  hepatic  insufficiency.  The  symptoms  are  therefore 
the  same  as  in  the  terminal  stage  of  portal  cirrhosis. 

I  have  seen  widespread  cutaneous  and  visceral  haemorrhages  in  portal  throm- 
bosis. 

In  experimental  ligature  of  the  portal  vein  toxic  symptoms,  such  as  paraplegia, 
low  temperature,  and  drowsiness,  develop;  there  is  also  a  marked  fall  of  arterial 
blood-pressure  which  may  be  associated  with  the  great  engorgement  of  the  portal 
system.  Castaigne  and  Bender  f  refer  death  in  experimental  ligature  of  the  portal 
vein  to  this  factor  and  not  to  toxsemia. 

DIAGNOSIS. 

This  is  very  difficult,  and  it  is  only  seldom  that  a  correct  opinion  is 
arrived  at  during  life.  The  sudden  onset  of  ascites  or  of  haematemesis 
and  their  recurrence,  accompanied  by  considerable  splenic  enlargement, 
might  suggest  it.  But  since  these  symptoms  are  much  the  same  as  those 
of  cirrhosis,  with  which  portal  thrombosis  is  so  often  associated,  it  is  diffi- 
cult to  differentiate  between  portal  thrombosis  and  cirrhosis.  Cirrhosis 
is  so  common,  while  portal  thrombosis  is  so  comparatively  rare,  that 
in  any  given  case  the  probabilities  are  rather  in  favour  of  the  former,  even 
though  the  onset  of  symptoms  is  sudden  and  severe. 

The  sudden  onset  of  ascites  in  a  case  of  cirrhosis  led  me  on  one  occasion  to 
diagnose  pylethrombosis,  but  the  cause  was  tuberculous  peritonitis. 

In  some  cases  of  gastric  ulcer  profuse  gastro-intestinal  haemor- 
rhage with  collapse  may  suggest  portal  thrombosis.  Difficulty  is  likely 
to  occur  only  when  the  gastric  ulcer  is  acute  and  occurs  in  an  adult  male 
or  in  a  woman  who  has  never  had  any  signs  of  gastric  ulcer  and  is  con- 
siderably past  the  age  at  which  it  is  commonly  seen. 

Very  profuse  hsematemesis  and  melsena  in  a  soldier,  aged  thirty-five  years,  coming 
on  suddenly  at  Pretoria  and  accompanied  by  a  low  temperature,  led  me  to  an  erro- 

*  Boinet:  Quoted  by  Gorget,  Rev.  de  M4d.,  1897,  p.  539. 

t  Castaigne  and  Bender:  Archiv  de  M6d.  Experim.,  Nov.,  1899. 


THRO:\IBOSIS    OF   THE    PORTAL    VP:iN.  65 

neous  diagnosis  of  portal  tlirombosis;  at  tlie  autopsy  tliere  was  acute  "diphtheritic" 
dysentery  with  an  ulcer  of  similar  nature  in  the  stomach.* 

In  splenic  anaemia  the  spleen  is  very  considerably  enlarged,  there  is 
ansemia  of  the  chlorotic  type,  with  a  diminished  number  of  leucocytes, 
while  recurrent  gastro-intestinal  hsemorrhages  may  occur.  The  disease 
is  essentially  chronic  while  thrombosis  of  the  portal  vein  is  usually  rapid. 
But  in  some  instances  of  portal  thrombosis,  especially  when  the  splenic 
vein  is  occluded,  the  spleen  is  greatly  enlarged  and  there  may  be  periodic 
gastro-intestinal  hsemorrhages  for  many  years,  with  fairly  good  health 
in  the  intervals. 

Thus,  Langdon  BroA\'n  t  rejiorted  the  case  of  a  woman  \vho  had  had  hoemate- 
mesis  at  intervals  of  ten  months  for  twenty  years,  and  in  whom  the  portal  and 
splenic  veins  were  found  occluded. 

Such  cases  are,  however,  most  exceptional. 


PROGNOSIS. 

The  diagnosis  being  so  beset  with  difficulties  the  practical  application 
of  prognosis  is  very  limited,  but  there  is  no  doubt  that  the  prognosis  is 
infinitely  better  than  in  pylephlebitis.  It  is  probable  that  if  the  process 
of  portal  thrombosis  is  gradual,  so  that  a  compensatory  circulation  can 
to  some  extent  be  developed  before  the  obstruction  becomes  absolute, 
the  patient  has  a  much  better  chance  of  surviving. 

If  recovery  from  the  acute  symptoms  occurs,  the  patient  may  live 
many  years,  even  though  the  main  trunk  of  the  portal  vein  is  obstructed. 
Thus,  Langdon  Brown,  Osler,t  Rogers,  §  and  others  have  recorded  cases 
where  life  was  prolonged  for  many  years.  In  these  cases  the  develop- 
ment of  a  collateral  circulation  to  some  extent  compensates  for  the 
portal  obstruction.  There  is,  however,  usually  only  a  partial  return  to 
health,  as  from  time  to  time  hsematemesis  recurs  and  relieves  the  en- 
gorgement, while  a  very  profuse  gastro-intestinal  haemorrhage  or  a  suc- 
cession of  haemorrhages  may  prove  fatal.  It  is  also  possible  that  the 
process  of  thrombosis  may  recur  in  the  vessels  forming  the  compensatory 
circulation. 

TREATMENT. 
Hsematemesis  and  ascites  should  be  treated  on  the  ordinary  lines 
as  in  cirrhosis-.  When  portal  thrombosis  is  suspected,  the  coagulation 
time  and  the  amount  of  calcium  salts  of  the  blood  should  be  determined 
by  A.  E.  Wright's  \\  method,  and  if  the  coagulability  of  the  blood  and 
the  amount  of  calcium  salts  are  both  found  to  be  increased,  citric  acid 
in  30-grain  doses  should  be  given  three  times  a  day  in  order  to  prevent 

*  The  Imperial  Yeomanry  Hospitals  in  South  Africa,  vol.  iii,  ]>.  193.  Medical 
and  Surgical  Reports. 

t  Langdon  Brown:  St.  Bartholomew's  Hospital  Reports,  vol.  xxxvii,  ]\  155 

X  Osier,  W. :    Journ.  Anat.  and  Phys.,  vol.  xvi,  p.  20S. 

§  Rogers,  B.  M.  H. :  Bristol  IMcdico-chirurg.  Journ.,  June,  1899. 

II  Wright,   A.   E.,   and  Knapp,   H.   II.:  Lancet,   1902,  vol.   ii;  Medico-cliirurg. 
Trans.,  vol.  Ixxxvi,  p.  1. 
5 


66  DISEASES    OF   THE    LIVER. 

the  process  of  thrombosis  extending.  The  rationale  of  giving  citric  acid 
is  to  "decalcify"  the  blood  and  so  reduce  its  coagulability.  It  is  im- 
portant that  the  blood  should  be  tested  before  giving  citric  acid,  since  in 
some  cases  of  cirrhosis,  which  is  the  morbid  lesion  most  frequently  asso- 
ciated with  portal  thrombosis,  the  alkahnity  and  coagulating  power  of 
the  blood  are  diminished,  and  no  good,  and  possibly  harm,  would  result 
from  citric  acid.  "V\Tien  there  is  a  history  of  syphilis,  iodides  and  mer- 
cury may  be  given  on  the  chance  that  there  may  be  a  gumma  pressing 
on  the  portal  vein  or  S3^philitic  change  attacking  the  walls  of  the  vein. 

The  operation  of  promoting  vascular  adhesions  around  the  liver 
would  theoretically  be  an  ideal  form  of  treatment  for  portal  thrombosis, 
but  there  would  probably  be  practical  difficulties  in  performing  it.  Hem- 
orrhage would  be  likely  to  occur  from  the  engorged  vessels,  and  there  is 
the  further  danger  that  an  extension  of  the  thrombotic  process  might  be 
induced  by  the  necessary  manipulation  of  the  peritoneum.  This  opera- 
tion was  performed  in  one  case,  but  without  benefit.     (Langdon  Brown.) 


SUPPURATIVE  PYLEPHLEBITIS. 

Synonyms  :  Portal  Pysemia,   Porto-pvEemic  Liver  Abscess  (Davidson). 

Suppurative  inflammation  may  involve  the  portal  vein  together  with 
some  of  its  tributaries  and  the  terminal  branches  in  the  liver;  thus,  in 
appendicitis  there  may  be  continuous  suppurative  pylephlebitis  involving 
the  superior  mesenteric  vein  and  the  trunk  and  the  intra-hepatic  branches 
of  the  portal  vein.  Usually  it  is  less  extensive  and  may  l^e  limited  to 
the  extra-hepatic  or  to  the  intra-hepatic  branches.  When  the  branches 
inside  the  liver  are  alone  affected,  the  resulting  condition  is  practically 
the  same  as  multiple  abscesses  due  to  infective  embolism  of  the  branches 
of  the  portal  vein.  The  only  difference  between  the  two  is  one  of  degree, 
viz.,  more  continuous  purulent  inflammation  of  the  intra-hepatic  branches 
of  the  portal  vein  in  intra-hepatic  pylephlebitis,  while  in  multiple  abscess 
the  branches  of  the  portal  vein  may  be  healthy  for  most  of  their  extent. 
Since  the  clinical  features  of  multiple  hepatic  abscesses  due  to  intestinal 
infection  are  much  the  same  as  those  of  pylephlebitis,  the  description  of 
the  latter  will  suffice  for  a  detailed  account  of  multiple  hepatic  abscesses. 
Suppurative  pylephlebitis  is  not  a  common  disease ;  it  is  much  less  often 
seen  than  multiple  liver  abscesses  due  to  infective  emboli  conveyed  by 
the  portal  A'ein. 

The  infrequency  of  pylephlebitis  is  shoMii  by  the  following  statistics.  In 
twenty  years  only  11  cases  were  met  with  at  Guy's  Hospital  (Bryant*);  and  in 
thirty-three  years  only  12  were  found  at  St.  Bartholomew's  Hospital  out  of  9494 
postmortem  examinations,  or  in  0.12  per  cent.  (Langdon  Brown  f). 

CAUSATION. 

Suppurative  infection  of  the  portal  vein  is  generally  secondar}-  to 
gastro-intestinal  lesions,  such  as  ulceration  and  suppuration. 

Thus,  in  64  cases  of  pylephlebitis  tabulated  by  Langdon  Brown,  45,  or  70.3 
per  cent.,  were  associated  with  gastro-intestinal  lesions;  of  the  remaining  19,  no 
cause  at  all  was  forthcoming  in  7;  4  were  due  to  gall-stones;  2  were  associated 
Avith  empyema;  and  6  with  other  forms  of  intra-abdominal  suppuration. 

As  might  naturally  be  expected  from  analogy,  infection  of  the  portal 
vein  is  most  readily  produced  by  a  collection  of  pus  confined  under  con- 
siderable tension.  Thus,  a  localized  abscess  in  connexion  with  appen- 
dicitis is  a  relatively  frequent  cause  of  suppurative  pylephlebitis,  while 
diffuse  inflammation  of  the  peritoneum,  though  it  may  be  a  result,  is  not 
by  itself  a  causal  factor.  In  some  cases  pylephlebitis  may  be  secondary 
to  suppuration  in  the  substance  of  the  liver,  for  example,  in  single  or 

*  Bryant,  J.  H. :  Guy's  Hospital  Reports,  vol.  liv. 

t  r^angdon  Brown,  W.  L. :  St.  Bartholomew's  Hospital  Reports,  vol.  xxxvii,  p.  95. 

67 


68  DISEASES    OF   THE    LITER. 

''tropical"  abscess.  Suppuration  in  the  gall-bladder  and  bile-ducts 
may  also  cause  infective  pylephlebitis.  A  septic  wound  of  the  main 
trunk  of  the  portal  vein  is  hardly  likely  to  cause  pylephlebitis,  as  rapid 
death  from  haemorrhage  would  probably  follow.  But  an  exploring 
syringe  might  infect  some  of  the  intra-hepatic  branches  of  the  portal 
vein  and  so  set  up  pylephlebitis.  '  In  a  few  carefully  examined  cases  no 
inlet  for  the  infection  is  found  in  the  area  of  the  portal  vein. 

In  a  case  of  suppuratiA'^e  pylephlebitis  in  which  the  primary  disease  was  an 
empyema  rupturing  into  the  lung,  Bryant  could  find  no  lesion  of  the  alimentary 
canal,  but  he  considered  the  possible  explanation  either  that  p3rogenetic  cocci 
in  swallowed  pus  were  absorbed  from  the  stomach  and  thus  reached  the  portal 
vein,  or  that  exploratory  punctures  had  passed  through  the  empyema  into  the 
liver  and  thus  directh'  infected  it. 

Possibly  in  some  of  the  cases  where  no  definite  source  of  inlet  is  found 
in  the  intestinal  tract  the  cause  may  have  been  pyorrhoea  alveolaris  and 
the  associated  swallowing  of  pus  and  micro-organisms.  The  pyogenetic 
micro-organisms  could  pass  through  microscopic  lesions  in  the  stomach 
into  the  portal  vein. 

Appendicitis  is  the  most  frequent  cause  of  suppurative  pylephlebitis 
and  multiple  liver  abscesses.  This  association  has  been  emphasized  Dy 
the  term  "appendicular  liver"  (Dieulafoy  *).  In 64  cases  of  suppurative 
pylephlebitis  collected  by  Langdon  Brown,  the  appendix  was  the  source 
of  infection  in  27,  or  42.2  per  cent.  But  appendicitis  is  luckily  not  often 
followed  by  suppurative  pylephlebitis. 

In  257  cases  of  perforative  appendicitis  Fitz  f  found  suppurative  pylephlebitis 
in  11  cases,  and  in  1189  cases  of  appendicitis  operated  upon  in  the  Mount  Sinai 
Hospital,  New  York,  there  were  only  9  cases  (Gerster  |),  or  0.75  per  cent.,  which 
is  a  little  higher  than  Treves'!  estimate  of  0.5  per  cent. 

Infection  of  the  portal  vein  is  more  likely  to  occur  when  an  abscess 
has  formed  around  the  appendix  and  the  pus  is  under  pressure.  Some- 
times, however,  the  morbid  process  in  the  appendix  has  begun  to  subside 
when  the  body  of  a  patient  with  pylephlebitis  is  examined.  Pylephlebitis 
may  occur  after  the  appendix  has  been  removed,  infection  of  the  mesen- 
teric veins  having  already  taken  place. 

In  a  boy  under  the  care  of  my  colleague,  Mr.  Pendleburj',  in  St.  George's 
Hospital,  the  appendix  was  removed  on  May  16  and  the  temperature  remained 
normal  until  June  13,  1904,  when  it  rose  and  a  rigor  occurred.  The  temperature 
contmued  raised  until  death,  on  July  8.  There  Avas  extensive  suppurative  pyle- 
jDhlebitis. 

Impaction  of  a  pin  in  the  vermiform  appendix  is  a  rare  accident,  but  it  appears 
that  Avhen  it  does  occur  tliere  is  a  great  likelihood  of  intra-hepatic  suppuration; 
in  8  out  of  Mitchell's  ||  33  cases  of  impacted  pins  in  the  appendix  there  was  some 
form  of  intra-hepatic  suppuration,  in  most  instances  multiple  or  pylephlebitic 
abscesses. 

*  Dieulafoy:  Clinique  Medicale  d'Hotel  Dieu,  1898.  Manuel  de  Patliologie 
Interne,  t.  ii,  p.  785,  1901. 

t  Fitz:  Trans.  Assoc.  American  Physicians,  lS8(i. 

t  Gerster:  Medical  Record  (N.  Y.),  June  27,  1903,  p.  1005. 

§  Treves,  F. :  Alllnitt's  System,  vol.  iii,  p.  927. 

II  Mitchell:  Johns  Flopkins  Hospital  Bull,  1899,  p.  35. 


SUPPURATIVE  PYLEPHLEBITIS.  69 

Gastric  ulcer  is  very  rarely  the  starting-point  of  suppurative  pyle- 
phlebitis. Cases  have  been  recorded  by  Carrington,*  Bristowe,!  Hart,J 
West,  §  and  others,  and,  in  all,  there  are  under  ten  on  record. 

Hart's  case  was  specially  interesting  inasmuch  as  it  was  complicated  l)y  a  left 
pyopneumothorax.  In  several  of  the  other  cases  pylephlebitis  was  associated  with, 
and  probably  the  result  of,  localized  suppuration  set  up  by  the  gastric  ulcer.  Tn 
Carrington's  case  a  gastric  ulcer  had  eroded  the  substance  of  the  liver  and  set  up 
local  suppuration. 

Gastric  Carcinoma. — Suppurative  pylephlebitis  very  seldom  follows 
cancer  of  the  stomach.  It  may  in  rare  instances  be  due  to  infection 
from  a  sloughing  mass  of  carcinoma  in  the  stomach,  but  this  is  even  rarer 
than  in  simple  ulcer.  Legg||  has  reported  a  case  in  carcinoma  of  the 
pylorus. 

Duodenal  ulcer  is  a  most  exceptional  cause  of  suppurative  pylephleb- 
itis; Warfwinge  **  and  Bryant  ff  have  reported  cases. 

Intestinal  Ulceration. — The  two  common  forms  of  ulceration  of  the 
small  intestine,  typhoid  and  tuberculous,  very  seldom  set  up  pylephlebitis. 
Possibly  this  is  in  some  degree  accounted  for  by  the  open  condition  of 
the  ulcers,  which  allow  free  drainage  and  discharge  into  the  bowel.  When 
the  inflammatory  process  is  more  circumscribed  in  the  walls  of  the  bowel, 
as  in  amoebic  dysentery,  the  radicles  of  the  portal  vein  are  in  greater 
danger  of  infection. 

Keen,l|  in  his  exhaustive  treatise  on  the  surgical  complications  of  tj^Dhoid  fever, 
only  refers  to  five  cases  of  pylephlebitis.     Osler§  §  has  seen  only  one  case. 

It  is  even  rarer  then  than  solitary  hepatic  abscess  after  typhoid  fever. 

Dysentery  very  seldom  gives  rise  to  suppurative  inflammation  of  the 
trunk  of  the  portal  vein.  Bryant  records  one  case.  Infective  emboli, 
however,  may  give  rise  to  multiple  hepatic  abscess  both  in  amoebic  and 
in  bacillary  dysentery. 

Penetration  of  the  Mesenteric  Veins  by  Infecting  Foreign  Bodies. 
— This  is  extremely  rare;  though  a  closely  allied  condition,  pins  perforat- 
ing the  vermiform  appendix,  is  a  less  infrequent  antecedent  of  suppura- 
tive pylephlebitis. 

Lambron  1!  ||  published  a  case  where  a  fish-bone  passed  from  the  stomach  into 
the  superior  mesenteric  vein  and  set  up  pylephlebitis. 

S.  Phillips  ***  has  described  suppuration  in  the  spleen  and  pyleplileljitis  due  to 
bristles  in  the  inferior  mesenteric  vein. 

*  Carrington :  Guy's  Hospital  Reports,  vol.  xli. 
t  Bristowe,  J.  S. :  Trans.  Path.  Soc,  vol.  ix,  p.  279. 
j  Hart,  S. :  Med.  and  Surg.  Reports,  Presbyterian  Hosp.,  1900,  p.  150. 
§  West,  S. :  Trans.  Path.  Soc,  vol.  xli,  p.  14G,  1S90. 
II  Legg,  W. :   St.  Bartholomew's  Hos;:).  Reports,  vol.  x,  p.  2.39. 
**  Warfwinge:  (Quoted  by  Bernard:  Gaz.  d.  Hop.,  Aug.  14,  1897.)     Sclunidt's 
Jahrb.,  1882,  Bd.  cxcv,  S.  130. 

tt  Bryant:  Guy's  Hosp.  Reports,  vol.  liv. 

jt  Keen,  W.  W. :  Su^gical  Complications  and  Sequels  of  Typlioid  Fever,  1S9S, 
p.  247. 

§§  Osier,  W. :  Studies  in  Tvphoid  Fever.  Johns  Hopkins  Hospital  Reports, 
No.  3,  p.  381. 

II II  Lambron:  Archiv.  gen.  de  M^d.,  1842,  p.  129. 
***  Phillips,  S:  Trans.  Clin.  Soc,  vol.  xxviii,  p.  222. 


70  DISEASES    OF   THE    LIVER. 

The  following  pelvic  conditions  occasionally  give  rise  to  suppurative 
pylephlebitis:  Operations  on  the  rectum  for  piles,  fissure,  and  stricture; 
carcinomatous  and  other  forms  of  rectal  ulceration;  suppuration  in  con- 
nexion with  the  female  genital  organs,  such  as  suppurating  ovarian  cysts, 
pyosalpinx.     (De  Silva,*  Bryant.) 

Suppuration  of  the  umbilical  vein  in  the  newly  born  may  extend  into 
the  liver  and  give  rise  to  pylephlebitis.  Cantlie  f  states  that  this  condi- 
tion is  extremely  common  in  Hongkong. 

Suppurative  and  gangrenous  pancreatitis  may  be  associated  with 
suppurative  pylephlebitis.  Etienne  J  has  insisted  on  the  spread  of 
inflammation  from  the  pancreas  to  the  portal  vein  and  the  production 
of  suppurative  pylephlebitis. 

A  man  aged  forty  was  in  St.  George's  Hospital  under  the  care  of  my  colleague, 
Mr.  Turner,  in  1899,  with  whom  I  often  saw  the  patient.  On  admission  there  was 
a  fluctuating  abscess  in  tlie  epigastrium  which  was  at  once  opened,  and  found  not 
to  be  connected  with  the  Uver,  but  to  come  from  the  region  of  the  pancreas.  The 
patient  improved  for  a  time,  but  fever  and  rigors  occurred;  empyema  on  the  left 
side  and  shght  jaundice  followed.  At  the  autopsy  the  pancreas  was  gangrenous, 
there  pylephlebitis  and  pus  were  found  in  the  intrahepatic  branches  of  the  portal 
vein. 

It  may,  however,  be  very  difficult  to  decide  whether  the  supjouration 
in  the  pancreas  is  the  cause  or  the  result  of  pylephlebitis.  Wlien  there 
is  some  other  available  cause  for  pylephlebitis,  such  as  appendicitis, 
suppuration  in  the  pancreas  must  be  regarded  as  secondary;  but  when 
suppurative  pancreatitis  and  pylephlebitis  are  the  only  lesions  present, 
it  is  often  difficult  to  determine  which  occurred  first. 

Suppurating  Mesenteric  Glands  and  Suppuration  between  the 
Layers  of  the  Mesentery. — Frerichs  §  describes  cases,  but  it  is  open  to 
discussion  whether  the  glandular  affection  may  not,  at  least  in  some 
instances,  be  secondary  to  the  suppurative  pylephlebitis.  In  other 
cases  the  suppuration  in  the  portal  vein  and  in  the  mesenteric  glands 
may  be  both  concomitant  results  of  some  intestinal  or  appendicular 
ulcer  that  has  been  overlooked  or  has  healed. 

Abscess  of  the  Spleen. — Cases  have  been  recorded  by  Frerichs,  || 
Law,**  and  Langdon  Brown.  It  is  probable  that  in  some  instances  the 
splenic  abscess  is  in  reality  secondary  to  pylephlebitis  and  not  the  primary 
cause.  It  seems  more  probable  that  perisplenic  or  subdiaphragmatic 
abscess  on  the  left  side  may  be  a  primary  source  of  infection  for  pyle- 
phlebitis, as  the  pus  is  then  under  some  pressure.  It  is  possible  that 
infective  endocarditis  by  septic  embolism  of  the  branches  of  the  splenic 
artery  may  lead  to  sloughing  infarcts  of  the  organ,  and  so  to  suppurative 
thrombosis  of  the  splenic  vein  and  pylephlebitis. 

Suppuration  in  the  Liver. — As  a  result  of  infection  spreading  from  a 
large  solitary  abscess  or  from  a  suppurating  hydatid  cyst  secondary 

*  De  Silva:  Ceylon  Med.  Joum.,  July,  1890. 
t  Cantlie,  J. :  Encyclopasdia  Medica,  vol.  vii,  p.  41. 
X  Etienne:  Archiv.  de  M^d.  experiment,  et  d'anat.  path.,  March,  189S. 
§  Frerichs:  Diseases  of  Liver.     New  Sydenham  Soc,  vol.  ii,  p.  421. 
II  Frerichs:  Diseases  of  Liver,  New  Svdenham  Soc,  vol.  ii,  p.  418. 
**  Law:  Dublin  Quarterlv  Journal,  1851,  p.  238. 


SUPPURATIVE    PYLEPHLEBITIS.  71 

pylephlebitis  may  be  set  up.  A  suppurating  hydatid  is,  however,  much 
more  often  the  cause  of  suppurative  inflammation  of  the  bile-ducts  than 
of  the  portal  vein,  but  may  give  rise  to  both.  Suppurative  cholangitis 
is  frequently  complicated  by  an  extension  of  the  inflammatory  process 
to  the  intra-hepatic  branches  of  the  portal  vein,  and  it  is  highly  probable 
that  the  infection  may  spread  by  the  lymphatics.  In  most  cases  where 
suppurative  pylephlebitis  complicates  suppurative  cholangitis  it  is  evi- 
dently secondary  and  not  nearly  so  widespread.  But  this  tendency  to 
pyleplilebitis  in  suppurative  cholangitis  makes  the  latter  disease  even 
more  formidable. 

Gall-stones.— The  usual  mechanism  by  which  cholelithiasis  sets  up 
multiple  liver  abscesses  is  by  suppurative  cholangitis;  the  multiple  ab- 
scesses are  then  in  connexion  with  the  bile-ducts.  Gall-stones  in  the 
ducts  may,  however,  induce  pylephlebitis,  either  by  direct  spread  of 
inflammation  from  the  ducts  to  the  walls  of  the  veins  or  through  the 
lymphatic-  or  blood-vessels.  In  rare  cases  a  fistulous  passage  between  a 
suppurating  bile-duct  and  the  portal  vein,  or  one  of  its  branches,  may 
be  the  method  by  which  gall-stones  in  the  ducts  may  set  up  pylephlebitis; 
in  exceptional  instances  the  gall-stone  may  pass  into  the  portal  vein. 
It  is  often  stated  that  three  calculi  were  found  in  the  portal  vein  of 
Ignatius  Loyola,  but  this  historically  interesting  case  has  been  disputed 
by  Thuclichum  and  GaUiard.* 

The  lymphatics  may  become  inflamed  in  cases  of  cholangitis,  and  in 
this  way  suppuration  may  extend  along  the  portal  spaces.  The  suppura- 
tion may  then  extend  to  the  portal  vein,  and  the  pylephlebitis  may  super- 
vene on  cholangitis.  This  sequence  of  events  probably  occurred  in  a 
man  aged  forty-four  whose  case  was  described  by  Strangeways  Pigg 
and  myself. t  In  this  case  there  was  no  evidence  of  gall-stones;  but  if 
it  occurs  in  non-calculous  cholangitis,  it  may  presumably  also  occur  in 
the  calculous  form.  The  infection  may  pass  from  the  ducts  by  the  small 
veins  of  the  bile-ducts,  which  open  into  the  branches  of  the  portal  vein. 
Bright  X  recorded  a  case  of  calculous  cholangitis  in  which  pjdephlebitis 
was  probably  produced  in  this  way.  An  abscess  due  to  cholecystitis 
may  erode  the  portal  vein,  discharge  into  it,  and  set  up  pylephlebitis 
and  multiple  suppurating  foci  in  the  liver  (Bristowe  §) . 

In  some  instances  it  is  ver}^  difficult  to  make  out  how  cholelithiasis 
gives  rise  to  suppuratii^e  pylephlebitis.  A  calculus  may  give  rise  to 
cholangitis  and  infection  may  spread  to  the  portal  vein  and  so  set  up 
pylephlebitis,  but  the  calculus  in  the  meanwhile  may  be  passed  and  the 
cholangitis  may  disappear. 

The  following  case  illustrates  the  difficulties  that  may  arise:  A  man  aged  fifty- 
one  was  admitted  to  St.  George's  Hospital  with  a  history  of  recent  gall-stone  colic; 
he  was  apparently  going  on  fairly  well  until  he  was  suddenly  seized  witli  abdominal 
pain  and  collapse.  I  saw  him  when  in  extremis  and  thought  that  probably  per- 
foration of  an  abdominal  viscus  had  taken  place.     At  the  autopsy  there  was  no 

*  GaUiard:  M^decine  Modcrne,  Nov.  20,  1895. 

t  RoUeston  and  Strangeways  Pigg:  Journ.  Path,  and  Bacteriol.,  vol.  v,  p.  221, 
1898.  X  Bright,  R. :  Guy's  Hosp.  Reports,  vol.  i,  p.  632,  1830. 

§  Bristowe,  J.  S. :  Trans.  Path.  Soc,  vol.  ix,  p.  285. 


72  DISEASES    OF   THE    LIVER. 

perforation  of  the  viscera  or  peritonitis,  but  there  was  suppurative  pj'lephlebitis 
without  any  definite  cause.  The  larger  bile-ducts  were  carefully  examined  and  no 
ulceration  or  calculi  were  found  in  them;  the  gall-bladder  contained  two  calculi. 

ETIOLOGY. 

Sex. — The  condition  is  commoner  in  males  than  in  females,  probably 
in  accordance  with  the  greater  frequency  of  appendicitis  in  the  male  sex. 
In  72  cases,  51  were  males  and  21  females. 

Age. — The  disease  usually  occurs  earlier  in  life  than  portal  throm- 
bosis; this  may  be  correlated  with  the  fact  that  it  is  most  frequently 
secondary  to  appendicitis.  When  it  occurs  later  in  life  it  may  be  due  to 
gall-stones  or  to  malignant  or  other  forms  of  ulceration  of  the  colon. 

In  56  cases  the  average  age  was  31.6  years;  of  these,  39  were  males,  with  an 
average  age  of  thirty-one  years,  and  17  females,  with  an  average  age  of  thirty-two 
years.  Langdon  Brown  found  that  half  the  cases  occur  between  the  ages  of  twentj^ 
and  twenty-nine. 

MORBID  ANATOMY. 

The  portal  vein  or  its  branches  contain  pus  and  broken-down  blood- 
clot;  sometimes  there  is  merely  pus,  in  other  instances  there  is  much 
blood-clot  and  but  little  pus,  the  infection  and  softening  of  the  thrombus 
being  only  in  an  early  stage.  The  vein  walls  are  swollen,  acutely  in- 
flamed, and  from  the  resulting  softening  the  vessels  dilate,  there  is  endo-, 
meso-,  and  periphlebitis;  the  walls  may  thus  melt  awa}^  in  the  suppura- 
tive process.  As  a  result  of  the  inflammation  of  the  wall  of  the  vein, 
blood-clot  forms  and  becomes  adherent  to  the  intima.  The  clot  softens 
down  and  a  mixture  of  pus,  clot,  and  blood  results.  This  sanious  pus 
may  be  of  a  reddish  tint,  but  from  changes  in  the  hgemoglobin  to  some- 
thing like  hsematin,  the  pus  frecpently  has  a  dirty  brown  color.  The 
suppuration  may  extend  through  the  walls  of  the  vein  and  lead  to  an 
abscess  outside  the  vein;  thus  in  some  cases  of  pylephlebitis  there  is  an 
abscess  behind  the  pancreas;  this,  though  sometimes  described  as  a 
cause,  is  usually  a  result,  of  pylephlebitis. 

As  a  very  rare  accident  in  pylephlebitis  Hodenp^'l's  *  case  may  be  referred  to. 
A  young  man  aged  twenty-five  died  from  rupture  of  the  portal  vein,  the  abdominal 
cavity  being  filled  with  pus.     The  pylephlebitis  was  due  to  streptococcal  infection. 

The  extent  of. the  vein  affected  may  vary  very  greatly;  a  localized 
part  of  the  portal  vein  or  one  of  its  branches  may  be  found  full  of  pi's 
and  shut  off  from  the  remainder  of  the  vein  by  a  partition  of  firm  clot. 
Thus,  when  the  trunk  of  the  portal  vein  is  suppurating  the  splenic  vein 
is  sometimes  cut  off  from  the  infective  process  by  a  firm  clot  at  its  junction 
with  the  portal  vein.  Occasionally  there  may  be  two  foci  of  suppuration, 
one  near  the  periphery,  the  other  in  the  intra-hepatic  branches  of  the 
portal  vein,  while  the  intervening  parts  of  the  A^ein  are  healthy  Tn 
such  cases  the  intra-hepatic  focus  is  due  to  emboli  derived  from  the  other 
focus  of  suppuration. 

The  liver  is  nearly  always  involved,  either  by  an  extension  to  it  of 
*  Hodenpyl:  Medical  Record  (N.  Y.),  July  23,  1S9S. 


SUPPURATIVE    PYLEPHLEBITIS.  73 

the  suppurative  inflammation  of  the  portal  vein,  or  by  secondary  abscesses 
due  to  emboli  from  the  portal  vein.  In  very  rare  cases,  of  which  I  have 
examined  one,  the  liver  may  show  no  signs  of  acute  inflammation;  this, 
however,  was  a  case  where  suppurative  inflammation  had  only  recently 
supervened  on  thrombosis  of  the  vein. 

The  liver  is  nearly  always  enlarged  and  ma}^  be  double  its  natural 
weight.  There  is  usually  perihepatitis  due  to  extension  of  inflammation 
to  the  capsule,  which  commonly  leads  to  adhesions  to  the  diaphragm. 
The  surface  of  the  organ  is  usually  smooth,  but  abscesses  may  project 
somewhat  from  the  surface  and,  if  seen  during  the  course  of  an  operation, 
ma}^  suggest  multiple  new-growth.  Over  these  abscesses  there  may  be 
a  thin  layer  of  recent  and  adherent  lymph.  The  liver  has  a  mottled 
appearance;  the  abscesses,  or  the  areas  where  suppuration  is  about  to 
take  place,  are  of  a  palish-yellow  colour.  Before  abscess  formation 
occurs  coagulation  necrosis  of  the  liver  cells  may  render  parts  of  theliver 
firm  and  like  nodules  of  secondary  carcinoma.  On  section  multitudes 
of  small  abscesses,  varying  in  size  from  a  millet-seed  to  a  walnut,  may  be 
seen,  due  to  the  suppurating  portal  canals  being  cut  transversely.  If 
the  course  of  the  portal  canals  be  followed,  suppuration  is  seen  to  spread 
out  from  the  portal  fissure  into  the  liver  like  the  branches  of  a  tree. 
There  is  often  dark-green  staining  of  the  portal  canals  from  decomposi- 
tion. One  lobe  or  only  a  limited  part  of  a  lobe,  or  again  the  whole  liver, 
may  show  abscesses.  The  left  lobe  escapes  more  often  than  the  right. 
From  the  coalescence  of  a  number  of  originally  separate  abscesses  a  large 
(areolar)  abscess  may  be  formed.  In  other  instances  the  abscesses  are  so 
close  to  each  other  that  a  honeycombed  condition  of  part  of  a  lobe  results. 

The  abscesses  due  to  pylephlebitis  may  resemble  at  first  sight  some 
cases  of  suppurative  cholangitis  with  abscesses  in  the  liver.  A  careful 
examination  of  the  bile-ducts  and  portal  vein  and  their  branches  inside 
the  liver  should  therefore  always  be  made  in  any  case  of  doubt.  Simi- 
larly any  difficulty  in  differentiating  between  tuberculous  abscesses  in 
connexion  with  the  bile-ducts  and  pylephlebitis  can,  if  necessary,  be 
settled  by  microscopic  examination.  Multiple  pysemic  abscesses,  due 
to  emboli  conveyed  by  the  hepatic  artery,  are  small  and  hardly  ever 
resemble  pylephlebitis.  The  condition  of  multiple  abscesses,  due  to 
embolism  of  the  portal  vein  from  some  foci  in  its  tributaries,  only  differs 
from  pylephlebitis  in  the  absence  of  extensive  phlebitis  of  the  portal  vein; 
in  other  respects  the  two  conditions  are  practically  identical. 

Leakage  or  rupture  of  the  small  abscesses  on  the  surface  of  the  liver 
will  set  up  peritonitis,  either  general  or  local,  such  as  a  subphrenic  ab- 
scess. When  the  diaphragm  is  previously  adherent  to  the  liver  extension 
of  infection  may  set  up  pleurisy,  empyema,  or  suppuration  in  the  lower 
lobe  of  the  lung,  usually,  of  course,  on  the  right  side.  Abscesses  on  the 
under  surface  of  the  liver  may  give  rise  to  pei'ihepatic  or  subhepatic 
collections  of  pus. 

Histology. — Microscopically  the  portal  vein  is  filled  with  fibrin  and 
leucocytes,  its  walls  are  infiltrated  with  small  round  cells,  and  may  be 
destroyed.     In  the  liver  the  portal  space  is  similarly  affected  and  small 


74  DISEASES    OF   THE    LIVER.. 

cell  infiltration  extends  between  the  lobules  and  around  the  intralobular 
branches  of  the  vein.  The  liver  cells  at  the  periphery  of  the  lobules  are 
compressed  and  become  elongated  and  look  somewhat  hke  oval  connec- 
tive-tissue cells;  the  small  cell  infiltration  spreads  between  the  liver  cells, 
which  undergo  degenerative  changes.  Micro-organisms  are  seen  in  the 
vessels  and  between  the  ceUs. 

Bacteriology. — Streptococci,  staphylococci,  diplococci,  and  Bacillus 
coli  communis  in  pure  cultures  have  been  met  -v^dth.  In  dysenteric 
cases  the  Amoeba  coU  and  other  micro-organisms,  and  in  cases  after 
typhoid  fever  the  Bacillus  typhosus,  have  been  found.  Mixed  infections 
are  not  uncommon. 

In  Norris'*  case  two  anaerobic  micro-organisms,  a.  streptococcus  resembling  ttie 
Micrococcus  foetidus  and  a  new  bacillus,  were  regarded  as  tlie  cause  of  suppuration. 

The  spleen. — There  is  usually  some  enlargement,  which  may  be 
explained  as  due  to  the  general  septic  or  toxic  condition.  In  cases 
where  the  splenic  vein  is  occupied  by  suppurating  clot  or  where  the 
junction  of  that  vein  with  the  trunk  of  the  portal  vein  is  excluded  the 
spleen  may  be  very  large  from  venous  obstruction.  Abscesses  are  some- 
times found  in  the  spleen,  and  may  either  be  part  of  suppurative  pyle- 
phlebitis or  its  starting-point. 

Peritonitis  is  common;  according  to  Bryant,  it  occurs  in  50  per  cent. 
of  the  cases.  It  may  be  due  to  rupture  of  the  pylephlebitic  abscesses  on 
the  surface  of  the  liver  and  may  be  general  or  localized.  Peritonitis 
is  also  frequent  around  the  primary  lesion,  such  as  appendicitis,  pyo- 
salpinx,  etc. 

The  pancreas  is  usually  healthy;  it  has  occasionally  been  found  to 
contain  abscesses,  probably  as  a  result  of  suppurative  phlebitis  of  the 
splenic  vein  spreading  into  its  pancreatic  tributaries.  An  abscess  behind 
the  pancreas  and  around  the  portal  vein  is  sometimes  seen  as  a  result  of 
suppurative  pylephlebitis.  In  some  instances  an  abscess  due  to  sup- 
purative pancreatitis  may  be  the  cause  of  suppurative  inflammation 
of  the  portal  vein. 

Pleura. — The  right  pleura  is  seldom  healthy;  there  may  be  recent 
pleurisy,  with  or  without  a  serous  or  purulent  effusion.  Inflammation 
readily  spreads  through  the  diaphragm  from  the  hver.  Rupture  of  a 
pysemic  abscess  in  the  lung  may  set  up  an  empyema  or  even  a  pyo- 
pneumothorax. 

Lungs. — ^The  right  lung  may  show  collapse  and  hypostatic  congestion 
of  the  base;  abscesses  with  surrounding  pneumonic  consoHdation  may 
be  due  to  direct  extension  through  the  diaphragm,  or  in  rare  instances 
to  general  pyaemia,  some  pylephlebitic  abscesses  having  discharged  into 
the  hepatic  veins. 

Pylephlebitis  with  multiple  small  abscesses  in  the  liver  may  give  rise 
to  general  hsemic  infection  and  secondary  abscesses  in  other  organs. 
According  to  Langdon  Brown,  this  occurs  in  40  per  cent,  of  the  cases. 
Reference  may  be  made  to  two  cases  of  secondary  cerebral  suppuration. 

*  Norris:  Joum.  of  Medical  Research,  July,  1901. 


SUPPURATIVE  PYLEPHLEBITIS.  /O 

Thus,  in  an  undoubted  case,  recorded  by  Norman  Moore,*  of  pylephlebitis  due 
to  appendicitis,  there  were  numerous  small  abscesses  in  the  brain;  and  in  Cassirer'sf 
case  the  symptoms  were  tliose  of  a  cerebral  lesion,  the  cause — a  fish-bone  in  the 
appendix — being  only  found  at  the  autopsy. 


CLINICAL  PICTURE. 

The  onset  of  symptoms  is  more  often  sudden  than  gradual.  In  43 
cases  analyzed  by  Langdon  Brown  the  onset  was  acute  in  27,  gradual  in 
15.  It  may  be  ushered  in  by  rigors,  but  usually  abdominal  pain  is  the 
earliest  symptom.  The  initial  symptoms  may  be  those  of  the  disease- — 
most  often  appendicitis — causing  the  pylephlebitis.  Thus,  pain,  vomit- 
ing, and  abdominal  distension  may  be  the  first  indications  that  any- 
thing is  amiss.  In  a  tjq^ical  case  there  should  be,  first,  evidence  of  the 
primary  cause,  such  as  appendicitis;  secondly,  the  development  of  a 
pysemic  state;  and,  thirdly,  evidence  that  the  liver  is  involved.  (Tav- 
lor.t) 

Course. — After  the  onset  the  patient  passes  into  a  "septic"  state 
resembling  pygemia;  rigors  may  be  present  at  first,  but  usually  dis- 
appear later.  After  a  time  most  cases  show  signs  of  hepatic  disease  in 
pain,  enlargement,  and  tenderness;  the  septic  condition  continues,  and 
signs  suggesting  empyema,  pneumonia  of  the  right  lung,  or  peritonitis 
may  develop.  Gradually  increasing  weakness  often  passing  into  coma 
precedes  death. 

Duration. — There  is  considerable  variation  in  the  duration  of  the 
disease.  The  average  of  the  cases  collected  by  Langdon  Brown  §  was 
forty-seven  days,  the  shortest  being  three  days.  In  an  exceptional  case 
of  Goodhart's,  ||  where  partial  recovery  was  taking  place,  the  disease 
lasted  two  hundred  and  ninety-six  days. 

Signs. — ^The  patient  has  an  abdominal  facies,  looks  sallow,  ill,  and 
anxious,  and  has  a  raised  temperature.  The  type  of  fever  varies  very 
widely;  it  may  be  continuous,  intermittent,  or  remittent.  Towards 
the  close  it  may  be  subnormal;  it  is  interesting  in  this  connexion  to 
remember  Hanot's  view  that  in  infections  with  the  colon  bacillus  the 
temperature  is  depressed.  The  pulse  is  soft,  compressible,  and  rapid 
(100  to  140).  The  respirations  are  quickened.  When  the  disease  has 
lasted  some  time  there  will  be  wasting  and  great  prostration. 

Rigors  are  seen  in  a  majority  of  the  cases. 

In  42  cases  Brown  found  them  in  29,  or  69  per  cent. ;  in  Bryant's  series  they 
were  present  in  half  the  cases. 

The  rigors  occur  during  the  earlier  part  of  the  illness  and  tend  to 
disappear  in  the  later  stages.  They  are  followed,  as  in  tropical  abscesses 
and  in  malaria,  by  profuse  sweating,  but  are  uncontrolled  by  quinine. 

Jaundice  occurs  in  less  than  half  the  cases  and  is  often  quite  slight, 

*  Norman  Moore:  Trans.  Path.  Soc,  vol.  xxxiii,  p.  186. 

tCassirer:  Medical  Press,  Oct.  30,  1901. 

%  Taylor,  F. :  Guy's  Hospital  Reports,  vol.  Ivi,  p.  109. 

§  Lancdon  I')rown :  St.  Bartholomew's  Hospital  Reports,  vol.  xxxvii. 

]|  Goodhart:  Trans.  Path.  Soc,  vol.  xxxii,  p.  1.37. 


76  DISEASES    OF   THE    LIVER. 

transient,  or  only  noted  late  in  the  course  of  the  disease,  and  can  be  ex- 
plained as  due  to  the  general  toxsemia.  In  some  cases  it  is  marked  and 
may  be  due  to  cholangitis,  concomitant  obstruction  of  the  bile-duct  by 
calculi,  or  to  pressure  of  an  abscess  on  the  common  bile-duct. 

In  44  cases,  tabulated  by  Langdon  Brown,  there  was  jaundice  in  19;  in  four 
of  these  it  was  very  shght  or  transient,  while  in  five  it  was  an  initial  sign. 

CHnically  the  liver  can  be  felt  to  be  enlarged  in  more  than  half  the 
cases;  Frerichs  says  in  75  per  cent.,  Bryant  in  60  per  cent.,  and  Langdon 
Brown,  who  collected  a  larger  number  of  cases,  in  57.  per  cent.,  of  the 
cases.  The  enlargement  is  usually  uniform,  but  in  a  few  instances 
elevations,  due  to  projecting  abscesses,  are  distinctly  palpable.  The 
enlarged  liver  may  reach  down  to  the  umbiHcus  and  may  lead  to  upward 
displacement  of  the  diaphragm,  and  thus  to  collapse  of  the  lower  lobe  of 
the  right  lung  and  even  to  displacement  of  the  apex  of  the  heart.  A 
friction  rub  from  inflammation  of  its  peritoneal  surface  may  be  heard 
over  the  liver.  Pain  and  tenderness  in  the  hepatic  region  are  generally 
met  with,  but  they  may  be  absent.  Local  tenderness,  which  is  some- 
times present  when  the  liver  cannot  be  felt  to  be  enlarged,  is  more  valu- 
able as  evidence  of  hepatic  suppuration  than  pain  referred  to  the  right 
hypochondrium. 

Enlargement  of  the  spleen  is  sometimes  obser^'ed;  in  33  cases  it  was 
noted  in  9  (Langdon  Brown).  "\ATien  there  is  very  considerable  enlarge- 
ment, hsematemesis  should  be  expected;  as  the  size  of  the  spleen  may 
be  due  to  obstruction  of  the  splenic  vein,  which  w^ould  also  lead  to 
engorgement  of  the  cardiac  end  of  the  stomach  by  interfering  T^dth  the 
return  of  blood  through  the  vasa  brevia  veins. 

Vomiting  is  often  met  with  early  in  the  course  of  the  disease.  It  was 
present  in  24  out  of  42  cases  collected  by  Langdon  Brown,  being  an 
initial  symptom  in  11.  It  is  not  so  much  a  sign  of  pylephlebitis  as  of  the 
disease,  such  as  appendicitis,  responsible  for  suppurative  inflammation 
of  the  portal  vein. 

In  rare  instances  a  gastric  ulcer  may  be  secondary  to  pylephlebitis 
and  even  go  on  to  perforation. 

In  a  man  aged  fifty-four  examined  by  me  in  1897,  with  suppurative  pylephlebitis 
secondary  to  appendicitis,  there  was  perforative  peritonitis  due  to  rupture  of  a 
gastric  ulcer,  which,  in  its  turn,  was  evidently  due  to  thrombosis  of  a  gastric  vein. 

DiarrJma  is  fairly  common,  occurring  in  about  half  the  cases.  Blood 
is  occasionally  seen  in  the  stools.  Constipation  is  rarely  noticed.  Hic- 
cough may  be  a  troublesome  feature. 

Tympanitic  distension  of  the  abdomen  may  occur  from  peritonitis  and 
will  obscure  enlargement  of  the  liver  and  spleen. 

Ascites  is  rare.  It  is  more  likely  to  occur  in  cases  that  last  a  consid- 
erable time,  and  Avhere  suppuration  supervenes  on  thrombosis  of  the 
portal  vein.  Although  clinically  ascites  is  seldom  seen,  there  may  be  a 
small  amount  of  ascitic  effusion,  due  to  local  acute  i)eritonitis  over  the 
abscesses  in  the  liver. 

Thoracic  Signs. — There  maybe  an  audil)le  friction  I'lil)  over  the  right 


SUPPURATIVE  PYLEPHLEBITIS.  77 

side  of  the  chest  from  extension  of  inflammation  tlirough  the  cHaphragm 
to  the  pleura.  The  pressure  exerted  b}-  the  enlarged  Yixer  may  lead  to 
bulging  of  the  chest  wall  and  to  collapse  of  the  lung,  imitating  i)leurisy 
with  effusion.  In  some  cases  there  may  actually  be  a  purulent  effusion 
into  the  pleura  or  the  lung  may  contain  abscesses.  It  is  not  to  be  won- 
dered at  that  such  cases  may  be  diagnosed  as  empyema  or  septic  pneu- 
monia. 

Blood. — There  is  some  degree  of  secondary  angemia,  especially  in 
prolonged  cases.  In  the  reported  cases  leucocytosis  is  not  mentioned  as 
a  rule,  but  it  would  naturally  be  expected.  It  was  present  in  3  out  of 
4  cases  referred  to  by  Langdon  Brown;  and  in  4  cases,  associated  with 
appendicitis,  French  *  found  marked  leucocytosis  (24,000)  in  one  and 
in  the  others  counts  of  18,000,  12,000,  and  10,500.  Micro-organisms 
may  be  found  in  the  blood  when  pyjemia  has  developed,  but  this  only 
occurs  near  the  end  of  the  case. 

Urine. — Albuminuria  is  sometimes  found  and  is  due  to  septic  absorp- 
tion. When  there  is  jaundice  bile-pigment  will  be  found  in  the  urine. 
Indicanuria  mav  be  present,  and  excessive  urobilin  has  been  observed. 
(Goodfellow.t)  "^ 

Termination. — Towards  the  end  the  patient  passes  into  a  semi- 
comatose condition  of  stupor.  Death  may  occur  from  peritonitis,  from 
coma  and  increasing  weakness,  or  in  rare  instances  suddenly  from  col- 
lapse after  sudden  hsematemesis  or  melaena. 


DIAGNOSIS. 

A  septic  or  pysemic  state  with  evidence  that  the  liver  is  affected,  in 
a  patient  who  has  had  appendicitis  or  some  other  intra-abdominal  condi- 
tion known  to  cause  pylephlebitis,  forms  the  broad  outline  of  the  disease. 
Enlargement  and  tenderness  of  the  liver,  with  pain,  fever,  and  a  pysemic 
state,  not  due  to  any  other  cause,  should  suggest  suppurative  pylep.  Jeb- 
itis.  Pyaemia  from  bone  and  ear  disease  and  infective  endocarditis 
must  be  excluded.  But  a  diagnosis  is  not  always  possible,  and  since 
hepatic  enlargement  is  absent  or  is  not  detected  in  a  certain  proportion 
of  cases  of  pylephlebitis,  there  may  be  nothing  to  direct  attention  to 
the  liver.  The  difficulty  of  diagnosis  is  shown  by  the  fact  that  in  20 
cases  examined  after  death  at  Guy's  Hospital  a  correct  diagnosis  during 
life  was  only  arrived  at  in  two  instances  during  life.  J 

Differential  Diagnosis. — In  tropical  abscess  there  is  not  such  rapid 
emaciation  and  prostration  as  in  pylephlebitis,,  fluctuation  may  be  felt, 
a  history  of  past  dysentery  rather  than  of  appendicitis  should  be  forth- 
coming, and  the  spleen  is  not  enlarged,  as  it  may  be  in  pylephlebitis. 
In  many  cases  it  is  impossible  to  be  certain  whether  there  is  a  single 
abscess  deeply  situated  in  the  liver  or  pylephlebitis  with  multiple  hepatic 
abscesses.     As  mentioned  above,  the  history  of  pre-existing  dysenterj^ 

*  French,  H.  S. :  Medico-Chir.  Trans.,  vol.  Ixxxvii. 

t  Goodfellow:  Medical  Chronicle,  vol.  xxxvii,  p.  2SS,  1903. 

J  Bryant,  J.  H. :  Guy's  Hospital  Reports,  xo\  liv. 


/8  DISEASES    OF   THE    LIVER. 

is  generally  in  favour  of  a  single  abscess,  but  it  must  be  remembered 
that  dysentery  may  be  followed  b}^  multiple  abscesses  in  the  Uver  like 
those  of  pylephlebitis;  this  was  notably  the  case  in  the  dysenter}^  seen 
in  South  Africa  during  the  Boer  War  of  1899-1902. 

In  hepatic  suppuration  secondar}"  to  appendicitis  multiple  foci  of 
suppuration  are  the  rule,  but  in  exceptional  instances  a  large  areolar 
abscess,  probabty  due  to  the  union  of  originaUy  independent  abscesses, 
results.  In  a  given  case  with  hepatic  enlargement,  fever,  rigors,  and 
pain,  the  question  whether  the  condition  is  one  of  multiple  abscesses, 
pjdephlebitis,  or  a  single  abscess  is  a  very  difficult  one  to  decide,  and 
probably  the  patient  should  be  given  the  benefit  of  the  doubt  and  abdom- 
inal exploration  be  undertaken.  CEdema  of  the  chest  waU  or  definite 
fluctuation  justifies  a  diagnosis  of  a  large  and  probably  single  abscess. 

In  suppurative  cholangitis  jaundice  is  commoner,  appears  earlier,  and 
is  more  prominent  than  in  pylephlebitis.  Splenic  enlargement  may 
occur  in  both,  but  is  more  likely  to  be  marked  in  pylephlebitis.  A 
history  of  cholelithiasis  and  biliary  colic  is  in  favour  of  suppurative 
cholangitis. 

Typhoid  Fever. — In  typhoid  fever  the  agglutination  (Widal's)  reac- 
tion with  typhoid  bacilli  should  be  present,  while  rigors  and  jaundice, 
though  not  unknoT\Ti,  are  decidedly  rare.  A  positive  agglutination  reac- 
tion may  occur  in  pyleplilebitis  when  the  patient  has  had  tj-'phoid  fever 
some  time  previously. 

In  a  woman  aged  twenty-eight,  who  died  of  pylephlebitis  under  Dr.  F.  Taylor's  * 
care,  there  was  a  positive  agglutination  reaction  with  typhoid  bacilH  although  she 
had  not  had  tj'phoid  fever. 

Pyleplilebitis  may  closely  resemble  typhoid  fever,  especially  when 
there  is  blood  in  the  stools:  in  such  cases  the  absence  of  the  agglutination 
reaction  and  of  Ehrlich's  diazo  reaction  in  the  urine  would  help  to  ehmi- 
nate  tj^hoid  fever.  Bryant  lays  stress  on  the  difference  between  the 
pulse,  temperature,  and  respiration  rates  in  pyleplilebitis  and  in  t^^hoid 
fever;  the  pulse  rate  is  low  (80)  in  enteric,  high  (140)  in  pylephlebitis. 

In  infective  endocarditis  murmurs  are  occasionally  absent  and  the 
aspect  of  the  case  is  one  of  pyaemia  of  obscure  origin;  in  such  cases,  when 
accompanied  by  enlargement  of  the  fiver  and  spleen,  the  resemblance  to 
pylephlebitis  may  be  considerable.  In  the  majority  of  cases  of  infective 
endocarditis,  however,  there  is  evidence  of  cardiac  disease,  and  there  is 
little  difficult}^  in  distinguishing  between  it  and  pylephlebitis. 

In  chronic  cases  of  malarial  infection  the  enlarged  and  sometimes  very 
tender  liver  and  the  raised  temperature  associated  with  shivering  and 
sweating  may  lead  to  considerable  difficulty  in  diagnosis.  Malaria 
should  be  recognized  by  the  presence  of  the  parasite  in  the  blood  and 
improvement  under  quinine,  while  the  patient's  condition  is  not  so  bad 
as  in  pylephlebitis. 

Intra-thoracic  conditions,  such  as  pleural  effusion,  empyema,  pul- 
monary abscess  or  pneumonia,  ma}'  be  diagnosed  as  the  sole  condition, 

*  Taylor,  F. :  Guy's  Hospital  Reports,  vol.  Ivi,  p.  109. 


SUPPURATIVE    PYLEPHLEBITIS.  79 

from  physical  signs  depending  on  the  spread  of  inflammation  from  the 
liver  in  pylephlebitis.  In  the  same  way  a  subdiaphragmatic  abscess 
may  be  recognized,  while  its  imderh-ing  cause — multiple  pylephlebitic 
abscesses — is  unsuspected. 

Malignant  disease  of  the  liver  may  imitate  pylephlebitis  when  fever 
and  rigors  accompany  rapid  increase  of  the  malignant  gro^^•th.  A  case 
of  secondary  endothelioma  of  the  liver  resembling  pylephlebitis  is  de- 
scribed in  the  heading  of  the  diagnosis  of  malignant  disease  of  the 
liver. 

In  cases  of  acute  cirrhosis  the  enlarged  and  tender  liver  and  the  pres- 
ence of  fever  may  imitate  pylephlebitis.     (Carrington.*) 

PROGNOSIS. 

Since  diagnosis  is  difficult,  more  cases  are  recognized  on  the  post- 
mortem table  than  during  life,  and  grave  doubt  must  exist  as  to  the 
nature  of  cases  regarded  as  suppurative  pylephlebitis  which  have  re- 
covered without  any  laparotomy  and  examination  of  the  liver.  It  is  in 
the  highest  degree  improbable  that  widespread  suppuration  of  the  portal 
vein  would  be  followed  by  recovery,  and  the  general  consensus  of  opinion 
is  that  the  disease  is  uniformly  fatal.  Conceivabl}^  this  verdict  may 
require  some  modification  in  the  light  of  more  frequent  observations  of 
the  state  of  the  liver  as  seen  in  the  course  of  exploratory  laparotomies. 
In  isolated  cases  recovery  has  occurred  where  multiple  abscesses  were 
thought  to  exist,  but  some  question  must  arise  whether  suppurative 
inflammation  of  the  portal  vein  was  actually  present  in  these  instances. 

Treves  t  opened  the  abdomen  of  a  girl  aged  fifteen  with  pylephlebitis  after 
appendicitis  and  observed  appearances  pointing  to  abscesses  in  the  liver;  the 
patient  recovered.  West  J  recorded  recovery  after  multiple  abscess  secondary  to 
appendicitis  had  been  opened.  In  a  boy  aged  eighteen  years  who  died  after  ten 
months'  illness  there  was  occlusion  of  the  portal  vein  and  scars  with  caseous  centres 
in  the  liver;  this  case  was  regarded  by  Goodhart  §  as  suggesting  that  suppurative 
pylephlebitis,  due  to  appendicitis,  had  ended  in  cicatrization.  Death  was  due  to 
suppuration  connected  with  ulceration  and  perforation  of  the  descending  colon, 
possibly  secondary  to  portal  obstruction,  and  lardaceous  disease. 

Possibly  some  cases  recover  that  are  not  sufficiently  well  marked  to 
be  recognized,  but  there  is  no  avoiding  the  conclusion  that  the  prognosis 
can  hardly  be  worse  than  in  this  disease. 

TREATMENT. 

When  the  disease  is  recognized  treatment  is  usually  confined  to 
relieving  pain  and  other  symptoms.  Langdon  Brown  and  Gerster|l 
have  employed  antistreptococcic  serum  without  any  good  results.  Its 
use  is  perhaps  worth  trying  on  the  chance  that  the  infection  of  the  portal 

*  Carrington:  Guy's  Hospital  Reports,  Series  iii,  vol.  xxvii,  1884. 

t  Treves:  Allbutt's  System,  vol.  iii,  p.  927.     Brit.  Med.  Journ.,  1894,  vol.  i. 

t  West,  S. :  Trans.  Clinic.  Soc,  vol.  xvii,  126. 

§  Goodhart.  Trans.  Path.  Soc,  vol.  xxxii,  p.  1.37. 

il  Gerster:  Medical  Record  (N.  Y.),  Jime  27,  1903. 


80  DISEASES    OF   THE    LIVER. 

vein  is  a  j)iire  streptococcal  one,  but  in  most  cases  there  is  a  mixed  in- 
fection. In  the  future  it  is  probable  that  treatment  with  l^oly^'alent 
sera,  viz.,  from  animals  immune  against  various  strains  of  micro-organ- 
isms of  the  same  and  of  different  species  (streptococci,  Bacillus  coli), 
may  be  emploj^ed.  Since  it  is  difficult  or  impossible  to  be  sure  that 
symptoms  of  pyaemia  wdth  hepatic  enlargement  after  appendicitis  are 
not  due  to  a  single  abscess,  operative  interference  gives  the  patient  a 
chance  of  recovery.  Further,  it  is  possible  that  success  might  follow 
the  opening  and  draining  of  several  abscesses,  as  in  West's  case.  "VSTien 
operation  is  undertaken,  the  liver  should  be  freely  exposed.  Aspiration 
through  the  abdominal  wall  is  not  only  fallacious,  but  may  be  dangerous. 
Prophylactic  treatment  is  most  important,  and  consists  in  the  early 
and  radical  removal  of  conditions,  such  as  appendicitis,  hkely  to  induce 
suppurative  pylephlebitis.  During  such  operations  removal  of  any 
suppurating  veins  in  the  immediate  neighbourhood  is  an  important  step 
in  preventing  the  spread  of  infection  from  the  intestinal  branches  to  the 
trunk  of  the  portal  ^'ein.  This  was  carried  out  in  two  cases  of  appen- 
dicitis which  recovered  (Gerster).  It  is  also  important  not  to  disturb 
the  parts  unnecessarily,  so  as  to  avoid  detaching  a  thrombus  and  pro- 
ducing embolism  of  the  intra-hepatic  branches  of  the  portal  vein. 


OTHER  AFFECTIONS   OF   THE   PORTAL  VEIN. 

Embolism;  Endophlebitis;  Calcification;  Parasites. 

EMBOLISM. 

Embolism  of  the  intra-hepatic  branches  of  the  portal  vein  is  freciuent 
in  suppurative  inflammation  of  the  intestinal  tributaries  of  the  portal 
vein  and  accounts  for  multiple  abscesses  in  the  liver  after  appendicitis, 
etc.  In  most  cases  the  emboli  are  small  and  do  not  themselves  attract 
attention.  Similarly  embolism  plays  an  important  part  in  the  produc- 
tion of  secondary  gro^\i:hs  in  the  liver  in  carcinoma  of  the  stomach  and 
intestine.  Sometimes  large  embolic  masses  of  clot  may  1_^e  found  in  the 
main  intra-hepatic  branches  of  the  portal  vein. 

In  17  cases  of  infarcts  in  the  liver  Chiari  =*=  found  that  15  were  due  to  embolism 
of  the  portal  vein,  the  emboli  being  derived  from  thrombosis  in  its  peripheral  tribu- 
taries, such  as  the  hfemorrhoidal,  gastric,  splenic   and  mesenteric  veins. 

ENDOPHLEBITIS. 

Acute  inflammation  of  the  portal  vein  is  practically  the  same  as 
pylephlebitis.  Chronic  endophlebitis  of  the  portal  vein  is  not  inicom- 
monly  associated  with  hepatic  cirrhosis,  and  may  be  explained  as  the 
result  of  increased  blood-pressure  in  the  vein,  combined  perhaps  with 
degeneration  and  hypei-plastic  changes  due  to  the  action  of  toxic  bodies. 
There  is  a  certain  amount  of  chronic  endophlebitis  of  the  portal  vein  in 

*  Chiari :  Zeitschrift  f.  Heilkunde,  Bd.  xix,  S.  475. 


OTHER   AFFECTIONS    OF   THE    PORTAL    VEIX.  81 

long-standing  backward  pressure  from  tricuspid  regurgitation,  in  mitral 
disease,  and  in  obstructive  pulmonary  diseases,  such  as  emphysema. 
According  to  Borrmann,*  syphilitic  disease  of  the  liver  may  extend  into 
the  portal  vein  and  set  up  syphilitic  endophlebitis  of  its  walls.  But  in 
a  certain  number  of  cases  the  endophlebitis  is  primar}'  and  the  liver 
merely  shows  a  secondary  atrophy.  The  essential  cause  of  the  chronic 
inflammatory  change  in  the  vein  is  somewhat  obscure,  and  has  been 
referred  to  a  number  of  causes.  Possibly  syi^hilis  may  play  a  part  in 
some  cases,  but  of  this  there  is  no  convincing  proof.  In  general  paralysis 
of  the  insane,  Avhich  is  regarded  by  Bruce  f  and  Ford  Robertson  %  as  a 
chronic  toxaemia  of  intestinal  origin,  chronic  endophlebitis  has  been 
described  by  Angiolella.  §  Inflammation  may  also  spread  into  the  vem 
walls  from  chronic  peritonitis. 

In  splenic  anaemia  endothelial  hyperplasia  may  spread  from  the 
l^lood  sinuses  in  the  spleen  into  the  splenic  and  portal  veins;  as  a  result 
of  these  changes  the  terminal  cirrhosis  of  the  liver  in  splenic  anaemia 
(Banti's  disease)  has  been  explained.  Chronic  endophlebitis  may  lead 
to  calciflcation  and  to  thrombosis;  the  latter  result  is  a  fact  of  practical 
importance. 

CALCIFICATION. 

This  is  a  seciuel  of  long-standing  endophlebitis  and  is  analogous  to 
secondary  calcification  in  endarteritis.  It  is  probably  much  commoner 
than  is  usually  thought.  I  have  seen  it  microscopically  in  cases  where 
there  was  not  sufficient  infiltration  to  attract  attention  in  the  postmortem 
room.  Its  occurrence  has  been  known  for  a  long  time.  FrerichsU 
gives  Cjuite  a  number  of  references  to  "ossification"  or  calcification  of 
the  portal  vein.  The  calcareous  plates  or  spicules  may  project  into  the 
lumen  of  the  portal  vein  and  set  up  thrombosis.  But  calcification  ma}- 
be  very  extensive  without  any  trace  of  thrombosis,  and  it  must  not  be 
assumed,  as  Lancereaux  **  does,  that  calcification  of  the  wall  of  the 
portal  vein  is  merely  the  result  of  thrombosis  of  the  vein  and  of  sub- 
sec}uent  changes. 

A  marked  degree  of  chronic  endophlebitis  with  calcification  of  the  splenic  and 
portal  veins  occurred  in  a  man  aged  fifty -three  who  died  in  St  George's  Hospital 
after  a  surgical  operation  for  hydrocele.  The  splenic  vein  was  greatly  dilated  and 
the  splenic  artery  was  very  calcareous  and  had  three  aneurysms  on  it.  The  spleen 
was  much  enlarged  (42  ounces)  and  fibrotic.  The  liver  (37  ounces)  was  scarred, 
and  to  the  naked  eye  suggested  syphilis,  but  microscopically  it  .showed  multiloljular 
cirrhosis  of  old  standing  and  no  evidence  of  syphilis.  The  colon  showed  extensive 
ulceration,  possibly  of  vascular  origin,  but  there  was  no  thrombosis  in  any  of  the 
branches  of  the  mesenteric  arteries  or  in  any  part  of  the  portal  vein  or  its  branches.ft 

*  Borrmann :  Deutsche  Archiv  f.  klin.  Med.,  1897. 
t  Bruce,  L.  C. :  Brit.  Med.  .Journ.,  1901,  vol.  i,  p.  1600. 
t  Ford  Robertson:  Brit.  Med.  .Journ.,  1901,  vol.  i,  p.  1602. 
§  Angiolella:  II  Manicomio  Modema,  1894,  1895.     Quoted  by  Ford  Robertson. 
II  Frerichs :  Diseases  of  the  Liver,  vol.  ii,  p.  402.     Translated  by  New  Svdenham 
Soc. 

**  Lancereaux:  Traite  de.s  Maladies  du  Foie  et  du  Pancreas,  p.  571,  1899. 
tt  Trevor,  R.  S.:  Trans.  Path.  Soc,  vol.  liv,  p.  302. 
6 


82  DISEASES   OF   THE   LIVER. 

PARASITES  IN  THE  PORTAL  VEIN. 
Bilharzia  hajmatobia,  endemic  in  Egypt,  Natal,  Mauritius,  and  Syria, 
may  be  found  in  the  trunk  of  the  portal  vein  or  in  its  hsemorrhoidal 
tributaries,  while  the  walls  may  contain  the  ova.  The  liver  may  show 
shght  cirrhosis,*  but  there  are  no  symptoms  associated  with  the  presence 
of  the  worms  or  their  ova  in  the  portal  vein.  The  hver  fluke  (Distomum 
hepaticum)  was  described  in  a  case  quoted  by  Budd  t  as  being  found  in 
the  portal  vein,  but  it  is  conceivable  that  a  dilated  bile-duct  was  mistaken 
for  the  vein. 

*Symmers:   Journ.  Path,  and  Bacteriol.,  vol.  ix,  p.  237. 
tBudd:  Diseases  of  the  Liver,  1857. 


MORBID  CONDITIONS   OF   LYMPHATIC   VESSELS   AND 

GLANDS. 

MORBID  CONDITIONS  OF  THE  LYMPHATIC  VESSELS. 

Comparative!}'  little  is  known  on  this  subject,  and  primary  affections 
of  the  lymiDhatics  of  the  liver  are  not  recognized.  That  the  lymphatics 
must  frequently  suffer  when  the  portal  spaces  are  affected  by  morbid 
processes  such  as  inflammation  and  tuberculosis  is  clear,  and  there  is 
evidence  that  this  is  so  in  the  enlargement  of  the  lymphatic  glands  in 
the  portal  fissure. 

Pericholangitis  is  very  closely  connected  with,  if  indeed  it  is  not  prac- 
tically synonymous  with,  lymphangitis  of  the  portal  spaces.  Thus,  the 
glands  in  the  portal  fissure  are  enlarged  in  hjq^ertrophic  biliary  cirrhosis, 
tuberculous  cavities  in  the  liver,  cholangitis,  and  pylephlebitis,  all 
of  which  are  inflammatory  lesions  involving  the  tissues  and  the 
portal  canals  around  the  bile-duct  and  portal  vein.  In  a  case  of  splenic 
anaemia  in  which  the  spleen  showed  most  extensi^-e  endothelial  prolifera- 
tion Bovaird  *  figures  a  similar  endothelial  proliferation  in  the  lymphatic 
vessels  of  the  portal  spaces. 

New-growth  may  sometimes  be  seen  working  its  way  into  the  liver, 
against  the  lymph-stream,  along  the  lymphatics  of  the  portal  fissure ;  more 
commonly  the  glands  in  the  portal  fissure  become  infected  secondarily  to 
a  groT\i;h  in  the  liver,  the  infecting  cells  travelling  in  the  normal  direction 
along  the  lymphatic  vessels.  Distension  of  the  Ij-mphatic  vessels  in  the 
portal  spaces  is  occasionally  due  to  obstruction;  it  has  also  occurred 
from  torsion  of  the  bile-duct  in  hepatoptosis.  In  diabetic  lipaemia  I  have 
seen  the  lymphatics  of  the  portal  spaces  graphically  mapped  out  by  the 
contained  fat.  Maresch  f  has  described  a  pedunculated  lymphangioma 
which  was  removed  from  the  right  lobe  of  the  liver  of  a  girl  aged  five 
years. 

THE  LYMPHATIC  GLANDS  IN  THE  PORTAL  FISSURE. 

Any  enlargement  of  these  glands  is  of  importance  inasmuch  as  pres- 
sure may  thus  be  exerted  on  the  bile-ducts  and  jaundice  set  up.  Thus 
it  has  been  thought,  but  probably  without  sufficient  reason,  that  the 
jaundice  occasionally  seen  in  the  roseolous  stage  of  syphilis  may  be  due 
to  swelling  of  the  glands  in  the  portal  fissure.  Enlargement  of  the  portal 
glands  may  occur  in  lardaceous  disease  and  leukemia,  but  carmot  be 
credited  with  producing  jaundice  or  ascites  liy  compression  of  the  bile- 
duct  or  portal  vein. 

Enlargement  of  the  portal  lymphatic  glands  may  be   due  to  \ari- 

*  BoA'aird:  American  Journ.  of  Med.  Sciences,  vol.  cxx,  p.  SOL 
t  Maresch :  Zeitschrift  f.  Heilkunde,  Bd.  xxiv,  S.  39,  1903. 

83 


34  DISEASES    OF   THE    LIVER. 

ous  conditions,  chiefly  inflammatory,  inside  the  hver,  such  as  abscess, 
pylephlebitis,  suppurative  cholangitis,  tubercle,  h}i3ertrophic  biliary 
cirrhosis,  and  primary  carcinoma.  As  already  mentioned,  new-growth 
may  extend  into  the  portal  fissure  along  the  lymphatic  vessels  against 
the  flow  of  lymph,  and  occasionally  infikration  of  the  portal  lymphatic 
glands  may  be  secondary  to  carcinoma  in  the  peritoneal  cavity,  and  may 
give  rise  to  jaundice. 


CHRONIC  VENOUS  ENGORGEMENT  OF  THE  LIVER. 

Synonyms:   Nutmeg  Liver,  Cardiac  Liver,  Cyanotic  Atrophy,  Hepatic  Asystole. 

The  term  red  atrophy  has  been  applied  to  the  small  mitmeg  liver 
seen  in  long-standing  cases  of  backward  pressure,  but  is  unfortunate  in 
that  it  may  lead  to  confusion  with  an  entirety  different  condition,  viz., 
the  red  atrophy  seen  in  acute  (yellow)  atrophy.  An  old  and  now  for- 
gotten name  for  the  condition  of  the  liver  was  hypertrophy  of  the  white 
substance.* 

Though  this  is  not  a  primary  morbid  condition  of  the  liver,  it  may 
be  convenient  to  describe  it  in  considerable  detail.  Chronic  venous 
engorgement  of  the  liver  is  practically  always  secondary  to  obstructive 
heart  or  lung  disease,  and  the  symptoms  due  to  the  hepatic  condition 
are  added  to  those  of  the  primary  disease.  Hanot  f  has  suggested 
the  term  hepatic  asystole  for  those  cases  in  which  the  hepatic  symptoms 
are  more  prominent  than  those  of  the  primary  cardiac  disease. 

ETIOLOGY. 

Cardiac  Lesions. — Obstructive  or  regurgitant  mitral  disease,  and 
some  diseases  of  the  myocardium,  such  as  dilatation  of  the  left  ventricle 
due  to  alcoholic  excess,  give  rise  to  backward  pressure,  tricuspid  regurgi- 
tation, and  chronic  hepatic  engorgement.  When  tricuspid  stenosis  is 
present,  it  is  practically  always  secondary  to  mitral  stenosis;  in  th^e 
cases  the  hepatic  engorgement  is  extremely  marked.  Mitral  stenosis 
is  of  all  connnon  cardiac  lesions  the  most  effective  in  producing  chronic 
venous  engorgement  of  the  liver. 

Lung  Lesions. — Obstruction  to  the  passage  of  blood  through  the 
pulmonary  artery  and  its  branches  in  the  lungs  gives  rise  first  to  hyper- 
trophy of  the  right  ventricle,  but  eventually  this  compensation  becomes 
strained,  the  right  ventricle  dilates,  and  tricuspid  incompetence  results. 
This  train  of  events  most  often  follows  chronic  bronchitis  and  emphysema, 
the  pneumokonioses,  and  sometimes  chronic  interstitial  pneumonia.  It 
is  remarkable  that  in  ordinary  pulmonary  tuberculosis  chronic  venous 
engorgement  is  not  more  often  seen.  My  own  experience  is  that  it  is 
rare  to  see  it  in  cases  of  chronic  pulmonaiy  tuberculosis,  but  Gilbert  and 
Weil, J  in  a  study  of  25  livers,  found  that  in  6  the  naked-eye  appearances 
were  those  of  a  typical  nutmeg  liver,  and  that  in  5  more  the  microscop- 
ical appearances  were  undoubted.  Possibly  those  cases  where  it  occurs 
are  complicated  by  alcoholic  dilatation  of  the  heart. 

Other  Factors. — It  is  possible  that  a  tumor  or  aneurysm  may  press 

*  Compare  llf>i)e:  Principles  and  Illustrations  of  Morbid  Anatomv,  p.  102,  1834. 
t  Hanot:  Bull,  de  la  Soc.  Med.  d.  H.jp.,  1S95,  p.  409. 

I  Gilbert  and  Weil:  Archiv  de  Med.  expi^riment.  et  d'.\nat.  path.,  tome  xiv,  p. 
729,  Nov.,  1902. 

85 


86  DISEASES    OF   THE    LIVER; 

on  the  small  segment  of  the  mferior  vena  cava  between  the  entrance  of 
the  hepatic  veins  and  its  termination  in  the  right  auricle;  but  it  is  ex- 
tremely rare  for  an  intra-thoracic  gro-v\-th  to  obstruct  the  inferior  cava. 
I  have  seen  nodules  of  secondar}^  groT\i;h  on  the  diaphragm  in  close  con- 
tact with  the  inferior  cava.  In  thrombosis  and  in  stricture  of  the  orifices 
of  the  hepatic  veins  {vide  p.  49)  a  nutmeggy  condition  of  the  liver  may 
be  produced.  Obstruction  of  the  inferior  vena  cava  vhere  it  receives 
the  two  hejoatic  veins  may  have  the  same  result. 

Butin  a  marked  example  of  obliteration^of  the  inferior  vena  cava  recorded  by 
Oslei,*  in  which  the  orifices  of  the  hepatic  veins  were  ven'  greatly  narrowed,  the 
hver  was  cirrhotic  rather  than  nutmeggy. 

Inside  the  liver  the  pressure  of  mahgnant  growths  or  hydatid  cysts 
may  lead  to  local  areas  of  chronic  venous  engorgement.  It  is  possible 
that  marked  displacement  of  the  heart  in  pleural  or  pericardial  effusion, 
by  producing  kinking  of  the  inferior  A'ena  cava,  might  lead  to  venous 
stasis  in  the  hepatic  veins  of  the  li^-er  as  well  as  in  the  other  tributaries 
of  the  inferior  cava.  It  has  been  suggested  that  pericardial  adhesions 
may  lead  to  torsion  of  the  uif erior  vena  cava  and  so  to  chronic  venous 
engorgement.  It  has  been  thought  that  any  pre-existing  morbid  condi- 
tion of  the  liver,  such  as  may  result  from  alcohohsm,  biliary  calculi,  or 
malaria,  renders  the  organ  more  prone  to  suiter  from  the  effects  of  back- 
ward pressure  in  any  given  case  of  tricuspid  incompetence. 

HORBID  ANATOMY. 

Adhesions  between  the  upper  surface  of  the  liver  and  the  diaphragm 
are  frequently  seen.  They  are  the  legacies  of  past  attacks  of  acute 
perihepatitis  which  are  not  uncommonly  due  to  the  spread  of  inflamma- 
tion through  the  diaphragm  from  acute  pleurisy  or  pericarditis.  The 
upper  surface  of  the  right  and  left  lobes  often  shows  a  depression  cor- 
responding to  an  liA^Dertrophied  and  dilated  heart.  The  peritoneum 
covering  this  depressed  area  is  often  thickened  and  opaque  as  the  result 
of  increased  and  long-continued  friction.  In  cases  of  universal  chronic 
perihepatitis  or  ''iced  liver"  {vide  p.  170)  there  is  usually  chronic  venous 
engorgement,  but  this  condition  should  be  kept  distinct  from  uncompli- 
cated nutmeg  liver,  in  which  there  is  no  general  perihepatitis. 

Size. — After  death  the  liver  is  sometimes  larger  than  natural,  but 
is  smaller  than  in  life.  During  life  the  hver  is  distensible  and  may  xaxj 
in  size  very  considerably  within  short  periods  as  the  result  of  alterations 
in  the  amount  of  backward  pressure.  After  death,  when  rigor  mortis  has 
set  in,  coagulation  of  the  protoplasm  of  the  Hver  cells  gi^•es  a  firmness 
to  the  organ  which  does  not  represent  its  condition  in  life. 

Sir  Lauder  Bruntonf  found  that  if  artificial  circulation  be  kept  up  through  the 
portal  A'ein  of  an  animal  just  killed,  the  liver  -R-ill  enlarge  and  diminish  in  response 
to  variations  in  the  pressm-e  exerted,  almost  as  if  it  were  a  sponge,  and  much  in  the 
same  way  as  it  does  in  cases  of  pulsating  livers. 

*  Osier:  Joum.  Anat.  and  Phj^siol.,  vol.  xiii,  p.  291. 

t  T.  Lauder  Brunton  in  Murchison's  Diseases  of  the  Liver,  3d  edition,  1S85, 
p.  134. 


CHRONIC   YEXOUS    EXG0RGE:\IEXT    OF   THE   LIVER.  87 

In  the  later  stages  the  Uver  becomes  smaller;  this  is  associated  with, 
and  most  probably  due  to,  atrophj^  of  the  liver  cells  and  not  to  the  con- 
traction of  the  fibrous  tissue  in  the  portal  spaces,  as  suggested  by  Legg.* 
The  liver  is  of  a  darkish  purple  colour  externall}'  and  is  rather  firmer 
than  natural.  Dilated  veins  ma}'  be  seen  on  the  surface,  and  no  doubt 
their  prominence  is  largel}'  due  to  atrophj-  of  the  surrounding  liver  tissue. 
As  a  rule,  the  surface  of  the  organ  shows  depressed  lines  of  atroph}', 
and  may  thus  become  slightly  uneven,  suggesting  to  the  naked  eye  early 
cirrhosis.  The  characteristic  mottling  is  generally  not  well  seen  exter- 
nally. If  there  has  been  long-standing  ascites,  the  serous  covering  of 
the  Uver  will  be  thickened  or  opaque. 

On  section  the  organ  contains  an  unusual  amount  of  l)lood  and 
presents  the  characteristic  "nutmeggy"  appearance,  which  depends  on 
the  fact  that  the  sublobular  and  intralobular  vehis  are  dilated  and  appear 
as  dark  purple  spots  or  streaks  according  as  they  are  cut  transversely 
or  longitudinally,  while  the  other  parts  of  the  lobules,  being  stained  with 
bile  or  infiltrated  with  fat,  are  paler  than  natural.  This  contrast  between 
the  deeply  coloured  and  the  pale  areas  resembles  the  section  of  a  nutmeg. 
In  a  tjqDical  case  the  centre  of  the  lobule  appears  as  a  dark  spot;  this  is 
surrounded  by  a  whitish-j^eUow  margin  clue  to  fatt}'  and  slightly  bile- 
stained  liver  cells.  In  other  cases  there  is  a  coarse  nutmeg  appearance 
due  to  alternation  between  areas  of  engorgement  and  areas  sho-^dng  fatt}^ 
change  and  bile  staining.  The  hepatic  veins  are  dilated  and  larger  than 
natural  and  their  waUs  are  thicker  and  more  opaque;  this  phlebosclerosis 
is  evidently  the  result  of  chronic  engorgement  and  is  accompanied  by 
atrophy  and  condensation  of  the  hepatic  tissue  immediately  around  the 
vein  walls. 

Opponet,  in  a  thesis  f  on  hepatic  asystole,  puts  forward  the  \dew  that  the  in- 
cidence of  hepatic  manifestations  in  a  case  of  heart  disease  is  determined  by  a  pecu- 
liar arrangement  of  the  hepatic  veins  at  their  entry  into  the  inferior  vena  cava;  this 
anatomical  disposition  he  regards  as  congenital  and  as  fairly  common.  It  seems, 
however,  more  natural  to  regard  the  size  and  manner  of  the  openings  of  the  hepatic 
veins  into  the  inferior  vena  cava  as  the  results  of  backward  pressure. 

In  backward  pressure  in  the  inferior  vena  cava  the  main  stress  usually 
falls  on  the  legs;  occasionally,  however,  the  renal  veins  are  chiefly  in- 
volved, as  shown  by  persistent  albuminuria  "udthout  any  corresponding 
nephritis  on  histological  examination,  while  in  cases  of  hepatic  asj'stole 
the  hepatic  veins  suffer  chiefly.  In  backward  pressure  the  brunt  may 
fall  on  any  one  of  these  three  branches  of  the  inferior  vena  cava. 

Occasionally  a  liver  which  is  the  subject  of  chronic  venous  engorge- 
ment is  also  distinctly  cirrhotic.  Thus,  a  patient  with  cirrhosis  may  die 
with  alcoholic  dilatation  of  the  heart  or  with  backward  pressure  from 
cardiac  failure  due  to  other  causes.  The  two  conditions,  nutmeg  and 
cirrhotic  livers,  are  both  common  and  sometimes  coincide,  but  chronic 
venous  engorgement  alone  does  not  cause  real  cirrhosis.  This  is  my  firm 
conviction  from  an  examination  of  a  large  number  of  livers  both  post- 
mortem and  microscopically. 

*  Legg:    Med.-Chirurg.  Trans.,  vol.  Iviii,  p.  3.52.  f  f'^iri'?;  1S05. 


88  DISEASES    OF   THE    LIVER. 

The  Question  of  "  Cardiac  Cirrhosis." — The  question  whether 
chronic  venous  engorgement  per  se  leads  to  cirrhosis  of  the  liver  has 
given  rise  to  very  considerable  discussion,  for  a  fuU  account  of  which 
the  reader  should  consult  Piery's  thesis.*  In  1840  Becquerel  t  consid- 
ered that  chronic  venous  engorgement  was  the  cause  of  half  the  number 
of  cases  of  cirrhosis  examined  by  him;  his  view  was  supported  by 
Rokitansky,J  Henle,  §  and  others.  It  is  possible,  as  suggested  by  Wick- 
ham  Legg,  that  at  this  time  cirrhotic  and  nutmeg  livers  were  not  differ- 
entiated from  each  other.  In  1845  Budd  ||  and  in  1848  Handfield  Jones 
definitely  separated  cirrhosis  and  chronic  venous  engorgement  from  each 
other  and  stated  that  chronic  venous  engorgement  did  not  give  rise  to 
cirrhosis. 

Considerable  discussion  has  ranged  as  to  the  locality  of  increased 
fibrosis  in  cardiac  cirrhosis.  Rokitansky,  and  Sabourin**  described  it  as 
centrilobular,  while  English  obsen^ers — Handfield  Jones,tt  Green,t| 
and  Legg  §  § — considered  that  it  was  perilobular  but  not  genuine  multi- 
lobular cirrhosis.  Xumerous  obserA^ations  prove  that  chronic  venous 
engorgement  of  the  liver  may  exist  for  prolonged  periods  mthout  pro- 
ducing any  fibrosis  at  all,  or  only  a  slight  fibrosis,  as  seen  iTiicroscopicaU}', 
which  can  be  satisfactorily  accounted  for  by  atrophy  of  the  liver  ceUs 
and  secondary"  fibrous  replacement.  The  firm  appearance  of  most  nut- 
meg livers  often  suggests  concomitant  fibrosis  which  can  only  be  dis- 
proved when  a  microscopic  examination  is  made.  The  rather  widespread 
belief  that  chronic  venous  engorgement  induces  cirrhosis  is  chiefly  based 
on  naked-eye  obser^-ation  uncorrected  by  a  further  microscopic  examina- 
tion. Parmentier  experimentally  produced  chronic  venous  engorgement 
of  the  liver  in  animals  bj'  setting  up  tricuspid  regurgitation,  and  found 
that  fibrosis  did  not  follow. 

In  the  rather  exceptional  instances  where  more  fibrosis  is  found,  some 
other  factor,  such  as  continued  gastro-intestinal  catarrh  or  considerable 
alcoholic  stimulation  during  the  course  of  chronic  valvular  disease,  may 
be  invoked.  It  is  noteworthj"  that  in  chronic  venous  engorgement  the 
resistance  of  the  Hver  is  necessarily  reduced  and  that  the  organ  is  there- 
fore more  likely  to  be  affected  by  poisons  than  in  health.  It  would  thus 
be  reasonable  to  expect  to  find  cirrhosis  secondary,  not  to  chronic  venous 
engorgement  pure  and  simple,  but  to  factors  such  as  alcoholism,  auto- 
intoxication from  intestinal  fermentation  (dyspeptic  or  Budd's  cirrhosis), 
or  actual  bacterial  infection.  Pier}",  who  has  paid  much  attention  to 
the  pathogeny  of  so-called  "cardiac  cirrhosis,"  believes  that  tuberculosis 
and  acute  rheumatism  may  also  be  responsible  for  hepatic  cirrhosis  in 

*  Piery:    Archiv  general  de  Med.,  tome  cIxxxaI,  p.  582,  1900. 

t  Becquerel:   Ibid.,  1840,  t.  viii,  p.  40. 

t  Rokitanskv:    Handb.  der  path.  Anat.,  1842,  Bd.  iii,  S.  347. 

§  Henle:    Zeitsch.  f.  int.  Med.,  1844. 

II  Budd:    Diseases  of  the  Liver,  184.5,  p.  118. 
**Sabourin:    Rev.  de  Med.,  1SS3,  p.  523  . 
ft  Handfield  Jones:   Med.  Gaz.,  vol.  vii,  1848,  p.  1033. 
Ji  Green:    Introduction  to  Pathology,  1871,  p.  244. 
§§  Legg,  AVickham:   Medico-Chirurg.  Trans.,  vol.  Iviii,  1875,  p.  345. 


CHRONIC    VENOUS    ENGORGEMENT    OF   THE    LIVER. 


89 


patients  with  heart  disease.  StiU,  Avith  aU  these  different  ways  in  which 
cirrhosis  may  become  implanted  on  a  nutmeg  liver,  the  association  of 
well-marked  cirrhosis  with  chronic  venous  engorgement  is  infrequent. 

Comparison  of  Passive  Engorgement  in  the  Liver  and  Lung. — In 
comparing  the  effects  of  backward  pressure  on  the  liver  with  those  on 
the  lung  it  is  seen  that  both  these  organs  have  a  double  blood-supply, 
the  portal  vein  and  the  hepatic  artery  in  the  one  case,  and  the  pulmonary 
and  bronchial  arteries  in  the  other.  While  pulmonary  apoplexies  are  of 
frequent  occurrence,  the  structure  of  the  liver  does  not  allow  extensive 
extravasation  of  blood  into  the  bile-ducts,  for  hsemorrhage  into  the  bile- 
capillaries  and  ducts  would  constitute  the  exact  counterpart  of  pulmonary 
apoplexies.  Comparatively  large  areas  of  haemorrhage  into  the  liver 
substance  occur,  however,  in  chronic  venous  engorgement  and  can  be 
seen  microscopically  to  be 
more  than  engorgement. 
Bonome  *  has  described 
hsemorrhagic  infarcts  in  nut- 
meg liver. 

Microscopic  Appear- 
ances.— The  intralobular 
vein  is  dilated  and  its  cap- 
illaries are  two  or  three 
times  larger  than  natural 
and  full  of  red  blood-cor- 
puscles. This  dilatation  is 
at  first  limited  to  the  cen- 
tral zone,  but  in  the  more 
advanced  stages  spreads 
into  the  intermediate  zone 
towards  the  peripheral  zone. 
The  liver  cells  are  com- 
pressed by  the  engorged 
capillaries  and  present 
varying  degrees  of  distor- 
tion.    Partly  as  the   result 

of  constant  pressure,  partly  from  impaired  nutrition,  due  to  an  im- 
perfect supply  of  oxygen,  which  necessarily  follows  on  the  stagnation 
of  venous  Blood,  they  atrophy  and  may  show  degenerative,  especially 
fatty,  changes.  The  liA'er  cells  contain  pigment — hsematoidin — deriA'ed 
from  haemoglobin  which  differs  from  the  iron-containing  pigment  (hsemo- 
siderin)  deposited  in  the  peripheral  zone  of  the  lobule  in  pernicious 
ansemia,  in  not  striking  a  blue  colour  with  dilute  hydrochloric  acid  and 
ferrocyanide  of  potassium  (Perl's  test).  This,  of  course,  is  because 
hsematoiclin  is  iron-free. 

In  the  peripheral  part  of  the  lobule  the  Yixcr  cells  tend  to  undergo 
varying  degrees  of  fatty  degeneration  and  may  contain  large  globules  of 
fat.     This  fatty  change  is  not,  however,  universally  met  with.     In  the 
'■^-  Bonome:    Rev.  general,  de  path,  intern.,  1900,  p.  70. 


Fig.  11.— Photomicrograph  of  Liver  in  Chkonic 

Venous  Engorgement. 
Shows  dilatation  of  capillaries  aiul  compressed  liver  cells. 
Portions  of  several  lobules  are  seen.     Some  of  the  blood  has 
fallen  out  of  part  of  the  section.     (Photomicrograph  by  S. 
Cj.  Penny,  I'^sq.) 


90 


DISEASES    OF   THE    LIVER. 


more  affected  parts  (the  centres  of  the  lobules)  the  liver  cells,  being 
compressed  by  the  dilated  capillaries,  undergo  atrophy  and  allow  the 


Fig.  12.— Photomiceograpii  of  Cheoxic  Venous  Engorgement. 
Same  section  as  the  foregoing;  under  a  high  power  shows  great  dilatation  of  blood-capillaries  and  dis- 
torted liver  cells.     (S.  G.  Penny,  Esq.) 


Fig.  13.— Photomicrograph  of  Liver  showing  Second.'VRY  Infiltration  with  Sphe- 
roidal-celled Carcinoma  and  Local  Chronic  Venous  Engorgement.  Low  Power.  (S.  G. 
Penny,  Esq.) 

vascular  channels  to  come  into  contact,  so  that  a  nseA^oid  or  angiomatous 
appearance  is  produced.     In  these  areas  the  blood-channels  are  separated 


CHRONIC  VENOUS  ENGORGEMENT  OF  THE  LIVER.        91 

from  each  other  by  connective-tissue  cells  (Kupffer's  cells).  Some  lobules 
are  unaffected  by  the  general  venous  engorgement,  and  their  liver  cells 
are  either  normal  or  hj^ertrophied.  There  may  be  compensatory  hyper- 
plasia,* such  as  is  seen  in  a  more  advanced  degree  in  nodular  cirrhosis. 

Jacobif  and  EarlJ  have  recorded  cases  of  chronic  venous  engorgement  of  the 
liver  in  which  there  were  multiple  adenomata  of  liver  cells,  which  did  not  show  the 
effects  of  chronic  venous  engorgement. 

The  atrophy  of  the  liver  cells  allows  the  existing  fibrous  tissue  to 
become  more  prominent  and  to  increase  in  bulk  to  &ome  extent ;  in  other 
words,  the  process  of  fibrous  replacement.  The  increase  in  fibrous  tissue 
is  seen  both  around  the  portal  spaces  and  also  to  a  lesser  degree  in  the 
walls  of  and  around  the  intralobular  veins  (centrilobular  cirrhosis).  Its 
characters  are  sporadic  or  irregular  distribution  and  absence  of  active 
hyperplasia.  It  is,  therefore,  mainly  a  fibrous  replacement  and  not  an 
active  proliferation.  This  accounts  for  the  apparent  increase  in  the 
amount  of  fibrous  tissue  seen  in  a  nutmeg  liver.  As  mentioned  above, 
nutmeg  livers  not  infrequently  have  a  naked-eye  appearance  that  sug- 
gests cirrhosis,  but  microscopic  examination  shows  very  little  fibrosis, 
and  that  of  a  sporadic  character  in  no  way  comparable  to  cirrhosis. 
Atrophy  of  the  liver  cells  and  replacement  fibrosis  are  most  advanced 
under  the  capsule  of  the  liver;  macroscopically  this  subcapsular  fibrosis 
closely  resembles  chronic  perihepatitis.  Microscopically,  however,  the 
capsule  is  seen  to  be  unaffected.     (Vide  Fig.  15.) 

The  morbid  anatomy  of  the  other  abdominal  organs  is  that  seen  in 
the  backward  pressure  of  mitral  or  obstructive  lung  disease  and  need  not 
be  described  in  detail.  The  spleen  is  firm,  deeply  engorged,  but  not  in- 
creased in  weight.  This  is  shown  by  Kelynack's  §  figures  of  the  weight 
of  the  spleen  in  56  cases  of  nutmeg  liver  due  to  cardiac  disease  and  un- 
complicated by  any  febrile  or  septic  process,  in  which  the  average  weight 
of  the  spleen  was  7.3  ounces,  or  just  about  the  normal.  The  pancreas 
may  be  enlarged  from  fibrosis  and  may  even  be  palpable  during  life.  || 
It  may,  however,  be  of  normal  size.** 


CLINICAL  PICTURE. 
Symptoms. — There  is  a  feeling  of  tightness,  heaviness,  and  discomfort 
in  the  right  hypochondrium,  which  is  markedly  tender  on  pressure.  It 
may  be  noted  in  passing  that  the  tenderness  of  an  enlarged  liver  in  alco- 
holic cirrhosis,  which  is  usually  explained  as  being  due  to  active  fibrous 
hyperplasia,  may  be  due  to  chronic  venous  engorgement,  the  result  of 
alcoholic  dilatation  of  the  heart.     The  general  tenderness  of  a  chronically 

*Letulle:    Anatomie  Pathologique,  vol.  i,  1897. 

t  Jacobi,  A.:   Trans.  Association  American  Physicians,  vol.  xii,  p.  500. 
JEarl:  Lancet,  1902,  vol.  ii,  p.  1464. 
§  Kelynack:    Birmingham  Med.  Review,  Feb.,  1S97. 
II  Hale  White:   International  Clinics,  Series  iv,  p.  90,  1S9G-97. 
**  Lefas:   Archiv  g(5ndral  de  M6d.:  tome  clxxxv,  p.  539,  1900. 


92  DISEASES    OF   THE    LIVER. 

engorged  liver  probably  depends  on  the  distension  and  stretching  of 
the  capsule  of  the  organ.  Very  marked  tenderness  accompanied  by 
pain,  which  is  independent  of  palpation,  is  due  to  concomitant  perihep- 
atitis and  may  be  accompanied  by  friction.  Mackenzie*  points  out 
that  the  tenderness  which  is  usually  assumed  to  be  in  the  hver  is  often 
in  the  abdoininal  walls,  and  that  this  can  be  sho"\\Ti  by  the  fact  that  the 
area  of  tenderness  is  generally  more  extensive  than  would  correspond  to 
the  liver  and  that  the  abdominal  wall  is  tender  when  it  is  carefully 
lifted  up. 

Chronic  portal  engorgement  gives  rise  to  impairment  or  loss  of  appe- 
tite, dyspepsia,  flatulence,  tympanites,  and  favours  gastro-intestinal 
catarrh.  Constipation  and  irregularity  of  the  bowels  with  perhaps  diar- 
rhoea are  part  and  parcel  of  this  same  condition;  together  they  lead 
to  considerable  distension  of  the  abdomen.  The  digestive  disturbance, 
brought  on  by  chronic  venous  engorgement  of  the  liver  and  portal  system, 
interferes  with  assimilation,  and  the  patients  are  thin,  though  this  may 
be  somewhat  masked  by  oedema;  in  children  groT\-th  is  interfered  with 
and  very  considerable  wasting  may  be  iDrought  about.  Hsematemesis 
is  usually  said  to  occur,  but  I  have  not  seen  it  in  uncomplicated  cases 
of  nutmeg  liver. 

In  a  case  of  mitral  stenosis  t  '^'ith  thrombosis  of  the  splenic  "\-ein  hsematemesis 
occmred,  but  was  e\ddently  due  to  the  extreme  venous  congestion  of  the  vasa  brevia 
of  the  stomach  which  open  into  the  splenic  vein. 

Dyspnoea  on  exertion,  and  in  advanced  cases  orthopncea,  clue  to  the 
primary  cardiac  lesion  or  to  concomitant  ascites,  are  common.  It  is 
possible  that  dyspnoea  in  some  instances  may  be  due  to  hepatic  insuffi- 
ciency, and,  like  the  ursemic  form,  toxsemic. 

Physical  Signs.— The  skin  over  the  malar  bones  is  much  congested 
and  of  a  high  colour,  while  the  lips,  eai's,  and  skin  elsewhere  may  show 
cyanosis.  The  forehead  and  especially  the  temples  have  a  shghtly 
icteric  tint.  The  contrast  between  these  two  tints  of  the  skin  produces 
a  facial  aspect  which  is  ver}^  characteristic  of  advanced  mitral  disease. 
The  slight  icteric  tinge  is  probably  due  to  a  low  grade  of  catarrhal  inflam- 
mation of  some  of  the  small  intra-hepatic  bile-ducts,  but  it  is  possible 
that  it  may  be  mechanical  and  due  to  oedematous  sweUing  of  the  mucous 
membrane  of  the  bile-ducts.  In  some  instances  ordinar}'  catarrhal  jaun- 
dice depending  on  the  spread  of  gastro-duodenal  inflammation  to  the 
biliary  papilla  super\-enes  in  the  course  of  the  disease. 

The  liver  is  nearly  always  enlarged,  and  can  be  felt  two  or  three  fingers' 
breadths  below  the  costal  arch  in  the  right  nipple  hne.  Its  size  varies 
with,  and  is  a  fair  indication  of,  the  condition  of  the  right  side  of  the 
heart.  It  diminishes  when  backward  pressure  is  relieved  and  is  affected 
in  a  similar  manner  by  free  purgation.  The  surface  of  the  liver  is  smooth 
to  the  touch  and  firm.  When  the  engorgement  is  marked,  the  liver  is 
tender  from  distension ;   the  tenderness,  like  the  increased  size,  is  a  good 

*  Mackenzie,  J.:    The  Studv  of  the  Pulse,  p.  221,  1902. 
t  Green,  T.  H.:    Brit.  Med."  Journ.,  1899,  vol.  ii,  p.  1415. 


CHRONIC   VENOUS   ENGORGEMENT    OF   THE    LIVER.  93 

index  of  increased  backward  pressure.     In  a  small  percentage  of  cases 
the  liver  can  be  felt  b}^  the  hand  to  pulsate  with  each  beat  of  the  heart. 

In  235  cases  of  tricuspid  regurgitation  analyzed  by  Pitt  *  pulsation  was  present 
in  15,  and  in  87  cases  of  tricuspid  stenosis  in  S. 

When  one  hand  is  placed  over  the  liver  and  the  other  is  pressed  into 
the  right  loin,  the  liver  can  be  felt  to  expand  and  diminish  like  an  accor- 
dion. This  shows  that  the  pulsation  is  not  a  transmitted  impulse,  but 
is  clue  to  the  liver  being  injected  with  blood  at  each  beat  of  the  heart. 
The  left  lobe  pulsates  more  than  the  right,  as  the  blood  regurgitates  into 
it  more  readily. 

Pulsation  may  also  be  communicated  to  the  liver  from  a  hypertrophied  and 
labouring  right  ventricle,  the  liver  receiving  a  jog  with  each  beat  of  the  heart,  the 
left  lobe  being  chiefly  affected;  in  rare  instances  pulsation  is  transmitted  from  an 
abdominal  or  even  an  hepatic  aneurysm. 

J.  Mackenzief  has  made  an  exhaustive  study  of  hepatic  pulsation  by  means 
of  the  polygraph,  a  modification  of  the  cardiograph.  The  following  are  some  of 
his  conclusions:  Pulsation  of  the  liver  only  occurs  in  valvular  disease,  but  is  very 
commonly  detected  by  this  instrument,  though  not  by  the  hands.  When  once  the 
liver  has  begun  to  pulsate,  it  probably  always  continues  to  do  so  till  death.  Pul- 
sation of  the  liver  may  be  synchronous  with  the  systole  of  the  ventricles  or  of  the 
auricles,  and  corresponds  with  the  rhythm  of  venous  pulsation  in  the  neck.  Pul- 
sation of  the  liver  synchronous  with  contraction  of  the  auricle  is  generally  associated 
with  tricuspid  stenosis  and  may  be  confused  with  pulsation  communicated  to  the 
liver  from  a  vigorously  contracting  heart. 

If  pressure  in  an  upward  direction  is  made  on  the  liver,  the  jugular 
veins  in  the  neck  jnay  be  observed  to  swell  up.  The  incompetency  of 
the  valves  at  the  origin  of  the  jugular  veins  allows  the  column  of  blood 
in  the  inferior  vena  cava,  right  auricle,  and  superior  vena  cava  to  be 
displaced  upwards. 

The  enlarged  liver  may  push  the  diaphragm  up  and  by  encroaching 
on  the  thorax  lead  to  some  collapse  of  the  base  of  the  right  lung.  Dulness, 
absence  of  breath-sounds  and  of  vocal  vibrations  at  the  base  of  the  right 
lung  behind  are  not  uncommon  in  cases  of  advanced  mitral  disease, 
and  may  be  due  to  collapse  of  the  lower  lobe  of  the  lung  or  to  a  pleural 
effusion. 

Chronic  venous  engorgement  of  the  liver  necessitates  chronic  portal 
obstruction;  ascites  may  thus  be  set  up,  and  if  of  long  duration  is  found 
to  be  associated  with  a  certain  amount  of  chronic  peritonitis.  Whether 
the  latter  is  set  up  by  the  ascites  or  whether  the  ascites  is  the  result 
of  the  chronic  peritonitis  brought  about  by  chronic  portal  and  peritoneal 
engorgement  is  open  to  discussion.  Probably  most  observers  would  con- 
sider the  chronic  peritonitis  the  primary  and  important  factor.  Ascites 
occurs  in  more  than  half  the  cases  of  tricuspid  regurgitation,  but  is  less 
frequent  than  oedema  of  the  feet. 

Thus,  in  235  cases  of  tricuspid  reflux  collected  by  Pitt,t  oedema  was  noted  in 
200  and  ascites  in  140.  So  far  as  these  figures  go  it  might  appear  that  ascites  is  only 
part  of  an  ascending  oedema.     Dr.  Pitt  has  kindly  provided  me  with  a  further 

*  Pitt,  G.  N.:   Allbutt's  System  of  Medicine,  vol.  vi,  p.  16. 

t  Mackenzie:    A  Study  of  the  Pulse,  p.  220,  1902. 

t  Pitt,  G.  N.:   Allbutt's  System  of  Medicine,  vol.  vi,  p.  16. 


94  DISEASES   OF   THE   LIVER. 

analysis  which  showed  that  oedema  and  ascites  occurred  together  in  124  cases, 
oedema  alone  in  76,  ascites  alone  in  only  14,  and  neither  in  21.  This  tends  to  sup- 
port the  view  that  the  ascites  of  nutmeg  liver  is  part  of  a  general  oedema. 

This  form  of  ascites  resembles  that  of  chronic  peritonitis  in  persisting 
and  recurring,  and  in  not  being,  Hke  the  ascites  of  cirrhosis,  a  close 
forerunner  of  death.  The  fluid  is  straw-coloured,  as  a  rule,  but  has  been 
known  to  be  chyliform. 

Dry  pleurisy  may  occur  or  signs  of  pleural  effusion  at  the  right  base; 
these  may  be  explained  as  the  result  of  pulmonary  apoplexy,  which  is 
commoner  in  the  lower  lobe  of  the  right  lung.  On  the  other  hand,  the 
upward  pressure  of  the  enlarged  liver  may  simulate  closely  a  small 
effusion. 

The  Urine. — The  amount  of  urine  is  diminished  from  chronic  venous 
engorgement  of  the  kidneys,  but  as  the  result  of  treatment  with  digitalis 
and  other  cardiac  tonics,  the  amount  of  urine  may  be  far  above  the  nor- 
mal for  a  time.  In  cases  where  chronic  venous  engorgement  of  the  liver  is 
marked  the  urine  is  concentrated,  of  a  high  specific  gravity,  high  coloured, 
and  on  cooHng  deposits  urates.  It  contains  urobilin  and  in  some  instances 
hsematoporphyrin,*  but  unless  there  is  definite  jaundice  bile-pigment  is 
usually  absent.  In  some  instances  there  is  albuminuria;  its  occurrence  is 
variable  and  does  not  necessarily  depend  on  gross  structural  change. 
In  cases  where  backward  pressure  falls  on'  the  renal  veins  in  a  marked 
degree  the  nutrition  of  the  renal  epithelium  may  be  sufficiently  impaired 
to  allow  of  albuminuria.  Alimentary  glycosuria  is  quite  exceptional  and 
probably  depends  on  concomitant  pancreatic  change  rather  than  on 
hepatic  insufficiency.  The  excretion  of  urea  varies  with  the  amount  of 
urine ;  diminution  in  its  amount  has  been  correlated  with  hepatic  insuffi- 
ciency. 

There  is  delay  in  absorption  of  liquid  from  the  intestines,  and  accord- 
ingly the  amount  of  urine  excreted  during  digestion,  instead  of  being 
larger  than  that  excreted  during  fasting,  the  normal  relationship,  is  less 
(Gilbert  and  Lereboulletf).  This  has  been  tested  by  giving  meals  with 
eight-hour  intervals  and  collecting  the  urine  every  four  hours.  The  term 
opsiuria  has  been  applied  to  this  condition  (Lecerf|). 

Complications. — Well-marked  jaundice  may  be  produced  by  exten- 
sion of  catarrhal  gastritis  to  the  duodenum,  and  so  to  the  biliary  papilla 
and  lower  end  of  the  common  bile-duct.  In  rare  instances  jaundice  may 
be  a  terminal  event  due  to  acute  infection  falling  on  the  liver  and  setting 
up  icterus  gravis. 

In  chronic  venous  congestion  of  the  liver  there  are  several  factors 
favouring  the  development  of  auto-intoxication. 

(I)  In  the  liver  itself.  Owing  to  malnutrition  the  antitoxic  or  poison- 
stopping  function  of  the  liver  cells  is  impaired  or  arrested.  Toxic  bodies 
derived  from  the  alimentary  canal  therefore  tend  to  pass  into  the  general 
circulation  and  affect  the  nervous  centres. 

*Garrod,  A.  E.:    Lancet,  1900,  vol.  ii,  p.  1327. 

t  Gilbert  and  Lereboullet:   Soc.  de  biolog.,  Paris,  Mar.  9,  1901. 

JLecerf:  These,  Paris,  1901. 


CHRONIC    VENOUS    ENGORGEMENT    OF    THE    LIVER.  95 

(II)  Owing  to  portal  stagnation  the  processes  of  digestion  are  inter- 
fered with  and  more  toxic  material  is  carried  to  the  liver,  which  is,  as 
has  already  been  said,  unable  to  cope  with  even  the  normal  amount. 

(III)  Chronic  venous  engorgement  of  the  renal  veins  leads  to  dimin- 
ished urinary  excretion. 

Course. — ^The  course  of  the  disease  depends  on  the  condition  of  the 
heart,  and  may,  like  it,  improve  periodically  only  to  relapse  again.  The 
hepatic  enlargement  tends  to  increase  during  each  recurrence,  though,  as 
already  pointed  out,  the  liver  gets  somewhat  atrophied  towards  the  end 
of  a  case.  According  to  Mackenzie,  pulsation  when  it  appears  remains 
to  the  end. 

Termination. — Death  is  commonly  due  to  gradually  increasing 
cardiac  failure  or  to  some  terminal  or  secondary  infection,  usually  of 
other  parts  of  the  body,  such  as  pneumonia,  pleurisy,  etc.  The  infection, 
however,  may  attack  the  liver  itself,  and  thus  give  rise  to  icterus  gravis 
either  with  a  high  or  with  a  low  temperature.  In  such  cases  diarrhoea 
and  vomiting  are  the  early  symptoms;  jaundice,  haemorrhages,  and  dry 
tongue  develop  and  finally  coma  precedes  death.  A  slighter  degree  of 
the  terminal  infection  may  show  itself  by  acute  perihepatitis. 

DIAGNOSIS. 

"Wlien  the  cardiac  lesion  is  manifest,  there  will  be  no  difficulty;  but 
in  the  class  of  cases  termed  by  Hanot  hepatic  asystole,  where  attention 
is  focused  on  the  liver,  the  condition  may  appear  to  be  primarily  hepatic 
and  be  thought  to  be  cirrhosis,  or,  when  the  liver  is  large  and  ver}^  tender, 
malignant  disease. 

With  regard  to  the  diagnosis  from  cirrhosis,  it  is  noteworthy  that  the 
abdominal  wall  does  not  show"  the  dilated  veins  seen  in  many  cases  of 
hepatic  cirrhosis,  and  that  there  is  no  enlargement  of  the  spleen,  while 
the  symptoms  improve  on  cardiac  tonics.  Examination  of  the  heart  and 
lungs  should  alw^ays  be  made  in  any  case  of  cirrhosis,  and  the  existence 
of  definite  signs  of  mitral  disease  should  lead  to  revision  of  the  diagnosis; 
but  an  apical  systolic  murmur  is  not  infreciuent  in  cirrhosis,  though  it 
is  seldom  persistent.  In  cases  of  hepatic  asystole  the  history,  the  smooth 
surface  of  the  liver,  the  comparatively  smaller  amount  of  enlargement, 
and  diminution  in  size  following  cardiac  tonics,  together  with  absence  of 
severe  pain  and  of  cachexia,  should  enable  the  observer  to  eliminate 
malignant  disease. 

TREATMENT. 

Treatment  may  be  divided  into  two  heads,  which,  however,  overlap 
to  a  certain  extent.  The  first  and  most  important  is  that  of  the  primary 
heart  disease  or  of  the  combined  lung  and  heart  affections.  Digitalis  is 
the  most  efficacious  drug  and  may  be  given  as  the  tincture  in  x  to  xv 
minim  doses  three  or  four  times  a  day,  or  the  fresh  infusion  in  drachm 
doses.  Digitalin  is  not  so  efficacious  as  the  tincture  or  infusion.  The 
pill  containing  digitalis,  sciuills,  and   mercury  (Addison's   pill  at   Guy's 


96  DISEASES    OF   THE    LIVER. 

Hospital,  Baillie's  pill  at  St.  George's)  is  often  verj^  successful.  Digitalis 
with  citrate  of  caffeine  may  also  be  given.  Strophanthiis,  though  well 
adapted  for  initral  stenosis,  and  convallaria,  are  not  so  powerful  for  good 
in  tricuspid  reflux  as  digitalis.  If  there  be  emphysema  and  bronchitis, 
iodide  of  potassium,  carbonate  of  ammonia,  ipecacuanha,  may  be  given 
in  addition.  Rest  in  bed,  and  if  necessary  paracentesis  of  the  abdomen 
or  tapping  of  the  legs,  are  essential  parts  of  the  treatment. 

In  the  second  place,  the  engorgement  of  the  liver  and  its  results  may 
be  further  treated  by  purgatives,  diuretics,  and  local  applications.  As 
purgatives,  magnesium  sulphate  or  sodium  sulphate  should  be  emploj'^ed 
to  run  off  the  excess  of  fluid  from  the  intestinal  vessels;  mercury  in  the 
form  of  blue  pill  or  calomel  is  a  valuable  remedy.  Aloes  and  I'eau  de  Vie 
allemande  maj^  also  lDe  given  mth  advantage.  As  diuretics  the  cardiac 
tonics  already  mentioned  and  apocynum  may  be  employed. 

The  administration  of  liver  substance  by  the  mouth  is  said*  to  act  as  a  diuretic 
when  the  lesion  is  not  too  advanced  and  to  increase  the  amount  of  urea  and  diminish 
the  abnormal  constituents,  such  as  urobiUn  and  albumin,  present  in  the  urine. 

If  there  be  much  pain  and  perihepatitis  is  present,  jDOultices,  hot 
applications,  leeches  over  the  liver,  or  bleeding  may  be  employed.  The 
diet  should  be  simple,  nutritious,  and  not  mainly  as  liquid,  as  this 
tends  to  aggravate  the  already  w^aterlogged  condition  of  the  patient.  For 
sleeplessness  moiphia  is  the  most  satisfactory  drug;  sulphonal  or  prefera- 
blytrional,  which  acts  more  rapidty,  chloralamide,  or  paraldehyde  may 
also  be  tried,  but  should  not  be  given  constantly;  if  a  sleeping  draught 
is  frequently  needed,  its  composition  should  be  changed.  Spa  treatment 
at  Vichy,  Neuenahr,  Nauheim,  Pougues,  etc.,  may  be  tried  when  the 
patient  is  sufficiently  well  to  bear  the  journey. 

*  Spilhnann  and  Dernange:    Congres  de  Med.  Int.,  Lille,  1899. 


PERICARDITIC  PSEUDO-CIRRHOSIS  OF  THE  LIVER. 

This  condition,  which  for  practical  purposes  nia}'  be  regarded  as  an 
extreme  grade  of  chronic  venous  engorgement  of  the  Hver  in  cardiac 
patients  with  adherent  pericardium,  was  described  by  Pick*  in  1896. 
The  cHnical  features — recurrent  ascites,  an  enlarged  firm  liver,  absent  or 
slight  jaundice,  and  no  oedema  of  the  legs — may  suggest  cirrhosis,  inas- 
much as  during  life  adherent  pericardium  may  be  latent  or  may  be 
overlooked.  The  liver  is  in  an  extreme  stage  of  chronic  venous  engorge- 
ment and  shows  fibrous  hyperplasia.  Any  peritoneal  adhesions  or  thick- 
ening that  may  be  present  were  regarded  by  Pick  as  accidental  or  second- 
ary either  to  chronic  venous  engorgement  of  the  peritoneum  or  to  ascites. 
Cases  of  this  kind  chiefly  occur  in  3'oung  subjects  with  a  history  of  rheu- 
matic endocarditis  and  pericarditis  and  without  any  of  the  usual  ante- 
cedents of  hepatic  cirrhosis. 

This  condition  merges,  on  the  one  hand,  into  chronic  venous  engorge- 
ment of  the  liver,  mth  which  it  is,  to  my  mind,  most  closely  allied;  and, 
on  the  other,  into  cases  of  universal  perihepatitis  associated  with  adherent 
pericardium  (vide  p.  164).  Some  few  adhesions  or  slight  peritoneal 
thickenings  are  comparatively  frequent  in  the  cases  belonging  to  the 
group  described  by  Pick;  when  these  peritoneal  changes  are  advanced,  the 
condition  ceases  to  be  Pick's  pseudo-cirrhosis  of  pericardiac  origin  and 
belongs  to  that  of  chronic  universal  perihepatitis  associated  with  adher- 
ent pericardium  (multiple  serositis).  Kelly  f  groups  together  under  the 
heading  of  multiple  serositis  these  cases  of  Pick's  pseudo-cirrhosis  and 
the  cases  of  "iced  liver,"  or,  as  they  are  usually  called  in  England,'' chronic 
universal  perihepatitis."  To  quote  his  own  words:  "Some  distinction — 
anatomically  at  least — may  be  drawn  between  cases  in  which  the  lesions 
are  confined  to  the  peritoneum  and  cases  in  which  the  lesions  are  more 
widespread.  The  cases  in  which  the  pericardium  is  unaffected  reveal  no 
congestive  alterations  in  the  liver.  Clinically,  however,  the  two  classes 
of  cases  are  very  much  alike,  and  the  '  Zuckergussleber '  may  occur  in 
both."    ^ 

The  following  case,  in  which  there  was  some  chronic  peritonitis, 
otherwise  exactly  resembled  Pick's  pseudo-cirrhosis,  but  from  the  presence 
of  peritoneal  change  it  must  be  regarded  as  occupying  a  position  midway 
between  pseudo-cirrhosis  and  chronic  peritonitis  associatetl  with  adherent 
])ericardium  (multiple  serositis). 

A  girl  aged  four  was  under  my  care  in  St.  George's  Hospital  with  recurrent  ascites, 
chronic  jaundice  of  slight  degree,  a  large  pulsating  liver,  and  pulsating  jugular  veins 
more  marked  on  the  right  side  of  the  neck.  The  heart  was  much  enlarged,  there 
were  systolic  and  diastolic  apical  murmurs,  and  an  accentuated  pulmonary  second 

*Pick:    Zeitschrift  f.  khn.  Med.,  Bd.  xxix,  S.  385. 

t  Kellv,  A.  O.  J.:    American  Journ.  of  Med.  Sciences,  vol.  cxxv,  p.  116. 

7  "  97 


98  DISEASES    OF   THE    LIVER. 

sound.  At  the  autopsy  the  pericardium  was  universally  adherent,  the  left  ven- 
tricle was  dilated,  greatly  hypertrophied,  and  showed  much  chronic  endocarditis 
of  the  musculi  papillares.  The  mitral  valve  segments  were  much  thickened  and 
the  orifice  was  somewhat  dilated.  The  left  auricle  was  also  dilated.  The  right  side 
of  the  heart,  contrary  to  what  was  expected,  was  not  dilated.  The  heart  and  peri- 
cardium weighed  17  ounces.  The  hepatic  veins  were  enormously  dilated  and  were 
each  of  them  as  large  as  the  inferior  vena  cava.  The  liver  was  nutmeggy  and  showed 
scattered  adhesions  to  the  diaphragm.  Microscopically  the  appearances  were  the 
same  as  those  seen  in  figures  14,  15,  viz.,  sporadic  and  subcapsular  fibrosis  and 
extreme  chronic  venous  engorgement.  There  were  a  few  adhesions  and  a  few 
ounces  of  fluid  in  each  of  the  pleurae  8.nd  general  opacity  of  the  peritoneum. 

Eisenmenger,*  who  among  others  disputes  the  existence  of  the  condition  as  a 
distinct  morbid  entity,  believes  that  in  children  the  vessels  of  the  general  systemic 
circulation  have  a  better  tone  and  are  less  disposed  to  allow  transudation  to  occur 
than  in  older  people,  and  that  the  more  marked  hepatic  manifestations  are  thus  ac- 
counted for.  He  further  puts  forward  the  suggestion  that  adhesions  in  connexion 
with  the  adherent  pericardium,  or  a  concomitant  pleural  effusion  may  lead  to  tor- 
sion of  the  inferior  A^ena  cava  close  to  the  diaphragm  and  so  lead  to  ascites;  while 
in  other  instances  local  peritonitis  in  the  portal  fissure  may  be  the  real  cause  of 
ascites. 

MORBID   ANATOMY. 

The  liver  often  shows  some  scattered  adhesions  to  the  diaphragm. 
Its  general  appearance  is  that  of  advanced  chronic  venous  engorgement. 
There  is  no  general  chronic  peritonitis  or  universal  perihepatitis,  but  the 
surface  of  the  liver  is  usually  somewhat  irregular,  as  in  ordinary  chronic 
venous  engorgement,  and  often  opaque.  This  opacity  is  due  to  fibrosis 
under  the  capsule,  due  to  fibrous  replacement,  and  on  superficial  examina- 
tion resembles  chronic  perihepatitis,  for  which  it  has  probably  often  been 
taken.     On  section  the  liver  shows  advanced  chronic  venous  engorgement. 

Microscopic  Appearances. — The  liver  shows  marked  chronic  venous 
engorgement  with  very  irregularly  scattered  islands  of  fibrosis.  Much 
of  this  apparent  increase  in  the  amount  of  fibrous  tissue  is  clue  to  atrophy 
of  the  liver  cells  allowing  the  existing  fibrous  tissue  to  come  into  promi- 
nence. There  is  perhaps  a  little  active  proliferation  or  fibrous  hyper- 
plasia, and,  by  careful  selection,  areas  resembling  multilobular  cirrhosis 
with  the  addition  of  chronic  venous  engorgement  can  be  found  in  micro- 
scopic sections.  Taken  as  a  whole,  however,  the  amount  of  fibrosis  is 
scanty,  and  may  be  absent  in  considerable  areas. 

Under  the  capsule  there  are  extensive  atrophy  of  the  liver  cells  and 
fibrous  replacement.  If  microscopic  examination  was  hmited  to  a  section 
from  this  part  of  the  liyer,  there  would  appear  to  be  extremely  marked 
fibrosis.  But  the  extent  of  the  fibrous  change  is  limited  to  a  small  area 
under  the  capsule.  It  is,  however,  enough  to  produce  very  definite 
opacity,  and,  as  has  already  been  pointed  out,  imitates  universal  chronic 
perihepatitis.  The  two  conditions  are  entirely  different:  in  chronic 
universal  perihepatitis  (''Zuckergussleber,"  "iced  liver")  the  fibrosis  is 
on  the  outer  surface  of  the  capsule.  The  appearances  in  subcapsular 
fibrosis  are  well  shown  in  the  accompanying  draAving  (Fig.  15),  taken  from 
a  case  of  this  kind. 

The  liver  thus  shows  the  changes  of  chronic  venous  engorgement  with 
rather  more  sporadic  fibrosis  than  is  usually  present,  but  tliere  is  no 

*  V.  Ei.senmenger:    Wien.  klin.  Wochen.,  Bd.  xiii,  1900. 


PERICARDITIC    PSEUDO-CIRRHOSIS    OF    THE    LIVER. 


99 


Fig.   14. — Microscopic  Section  from  an  Advanced  Case  of  Nutmeg  Liver  Associated  wiiii 
Adherent  Pericardium.     (Case  on  p.  97.) 
The  blood-capillaries  are  enoimoiisly  dilated,  the  liver  cells  are  compressed  and  distorted,  and  there 
is  sporadic  fibrosis.    This  section  was  specially  chosen  so  as  to  show  "  cardiac  fibrosis."    X  60. 


J^ 


':iM\y. 


/>>■■  /  ■  '■.-■■.■  .•■■.•■•>.  >,''w-"  .•>".'■•  '■ '' 

si..J^«^^   .;.;..  ,      .    ^   •;.,.. ;..fv^ ;■•;,■; ^ 


Fig.  15.— Drawing  from  a  Microscopic  Section  showing  Marked  Sl'bcapsui.ar  Fiuki 
The  real  capsule  is  seen  on  the  free  surface.     (From  the  same  case  as  figure  14. ) 


100  DISEASES    OF    THE    LIVER. 

tendency  to  compression  or  narrowing  of  the  branches  of  the  portal  vein, 
as  in  genuine  portal  cirrhosis.  Although  there  is,  as  a  rule,  no  genuine 
cirrhosis  comparable  to  portal  cirrhosis,  in  cases  of  ordinar}-  adherent 
pericardium  it  appears  from  Diemar's  *  and  Wells'  f  figures  that  when 
calcification  occurs  in  an  adherent  pericardium  well-marked  hepatic 
cirrhosis  is  found  in  the  great  majority  of  cases.  What  relationship,  if 
any,  exists  between  calcified  pericardium  and  hepatic  cirrhosis  is  un- 
known. These  cases  occur  in  adults,  while  the  patients  with  Pick's 
pseudo-cirrhosis  are  usually  children.  I  have  examined  some  of  these 
cases,  expecting  to  find  an  extension  of  fibrosis  from  the  adherent  peri- 
cardium along  the  hepatic  veins  into  the  substance  of  the  Uver,  but 
have  never  found  any  fibrosis,  though  the  inner  walls  of  the  hepatic 
veins  and  inferior  vena  cava  are  opac{ue  and  tliickened,  as  is  commonly 
seen  in  cases  of  backward  pressure.  The  pericardium  is  firmly  adherent 
to  the  heart,  and  usually  to  the  chest  wall  as  well.  These  adhesions  are 
usually  due  to  past  rheumatic  pericarditis,  but  in  some  instances  the 
pericarditis  is  tuberculous,  and  under  these  conditions  the  liver  may  also 
be  tuberculous. 

Mechanism  of  the  Morbid  Processes. — The  pericardial  adhesions 
by  contracting  lead  to  dilatation  of  the  right  auricle,  inferior  vena  cava, 
and  hepatic  veins,  and  by  this  means  the  free  regurgitation  of  blood 
into  the  liver  is  rendered  jDermanent.  It  is  possible  that  at  the  time  of 
the  primary^  pericarditis  inflammation  spreads  to  the  mouths  of  the 
hepatic  veins,  and  by  weakening  their  waUs  leads  to  dilatation  and  so 
to  a  freer  entry  of  blood  into  them.  'W'lien  once  brought  about,  this  dilata- 
tion of  the  hepatic  veins  probably  becomes  permanent.  The  brunt  of 
backward  pressure  thus  falls  on  the  liver,  while  the  other  branches  of 
the  inferior  vena  cava — ^the  renal  and  iliac  veins — suffer  less  than  in 
ordinar}^  cases  of  chronic  engorgement  of  cardiac  origin. 

The  clinical  aspect  of  the  cases  has  already  been  referred  to,  and  the 
absence  of  oedema  of  the  legs,  which  may  tend  to  differentiate  the  con- 
dition from  ordinar}''  backward  pressure  of  heart  disease,  has  been  men- 
tioned. During  life  the  liver  may  be  firm  and  enlarged,  and  so  may 
suggest  cirrhosis,  especially  if  the  presence  of  an  adherent  pericardium 
be  overlooked  and  the  signs  and  symptoms  of  valvular  disease  are  not 
prominent.  In  most  instances  the  associated  cardiac  and  pericardial 
disease  will  be  easily  detected  and  no  doubt  will  arise.  In  these  cases  it 
may  be  necessary  to  tap  the  abdomen  on  a  considerable  munl^er  of  occa- 
sions, but  the  intervals  are  often  prolonged,  thus  differing  from  the 
frequent  paracenteses  necessary  in  chronic  peritonitis.  Jaundice  is  either 
absent  or  slight.  The  following  case  illustrates  the  general  featiu-es  of 
the  condition: 

Girl  aged  eleven  years  was  under  the  care  of  my  colleague,  Dr.  Penrose,  for  three 
years  with  morbis  cordis  and  ascites,  for  which  tapping  had  been  required  ahout 
fifteen  times.  At  the  autopsy  there  was  mitral  and  tricuspid  incompetence  with 
an  adherent  pericardium;  the  liver — 3  pounds  6  oimces — was  enlarged  and  showed 
some  thickening  of  its  capsule  with  a  few  adhesions.     The  liepatic  veins  were  Aery 

*  Diemar:    Zeitsch.  f.  Heilk.,  1899,  Bd.  xx,  S.  2.57. 

t  Wells,  H.  G.:   American  .Tourn.of  Med.  Sciences,  vol.  cxxiii,  p.  2.59,  1902. 


PERICARDITIC    PSEUDO-CIRRHOSIS    OF    THE    LIVER.  101 

prominent  but  there  was  no  fibrosis  around  them.  The  surface  of  the  h\er  was 
irregular  froin  depressed  hues  due  to  atrophy  and  fibrous  increase  around  tlie  sub- 
capsular veins.  On  section  the  liver  was  nutmeggy  and  gave  the  impression  of 
some  fibrous  increase.  Microscopicallj'  there  was  sporadic  fibrosis,  but  no  genuine 
multilobular  cirrhosis,  the  branches  of  the  hepatic  -seins  and  intralobular  venules 
were  greatly  dilated,  and  the  liver  cells  atrophied.  The  appearances  were  those  of 
advanced  chronic  venous  engorgement  with  more  fibrosis  than  usual.  There  was 
no  chronic  peritonitis;  there  were  old  adhesions  in  the  left  pleura  and  recent  ones 
in  the  right  pleura. 

PROGNOSIS  AND  RESULTS. 

When  the  condition  of  hepatic  pseudo-cirrhosis  has  become  estab- 
lished the  prognosis  is  very  bad,  though  hfe  may  be  prolonged  for  a 
considerable  time.  Tuberculous  peritonitis  may  supervene  as  a  secondary 
result;  this  was  proved  to  be  the  sequence  of  events  in  a  case  recorded 
by  Nachocl,*  where  laparotomy  a  year  before  death  proved  the  absence 
of  tubercle  at  that  time.  Secondary  tuberculous  infiltration  of  the  portal 
spaces  may  then  occur.  The  term  cardio-tuberculous  cirrhosis  has  been 
applied  to  advanced  chronic  venous  engorgement  of  the  liver  complicated 
in  this  way  by  tuberculous  infection.f  These  cases,  which  are  chiefly 
met  with  in  children,  are  associated  with  more  advanced  tuberculous 
disease  elsewhere,  especially  in  the  peritoneum  and  pleura. 

These  conditions  of  "hepatic  pseudo-cirrhosis  "  and  cardio-tuberculous 
cirrhosis  are  closely  allied  both  to  nutmeg  liver  and  to  the  cases  of  general 
perihepatitis  secondary  to  adherent  pericardium.  Clinically  the  chief  dif- 
ference from  nutmeg  liver  is  the  absence  of  any  signs  of  cardiac  valvular 
disease.  The  proper  treatment,  however,  is  that  of  chronic  venous 
engorgement  of  the  liver,  viz.,  cardiac  tonics  and  diuretics.  The  treat- 
ment suitable  for  cirrhosis  is  of  no  use  in  these  conditions. 

*Nachod:    Prag.  med.  Wochenschrift,  1898,  S.  330. 

"f  Vide  Moizard  and  Phulpin:  Archiv.  de  Medicine  des  Infants,  Aug.:  1899. 
Cousin:  Gaz.  hebd.  de  Med.  et  de  Chirurg.,  Jan.  14,  1900.  Wells,  H.  G.:  American 
Jour.  Med.  Sciences,  vol.  cxxiii,  p.  299. 


INFARCTS  IN  THE  LIVER. 

Infarcts  are  usually  considered  to  be  rare  in  the  liver.  Contrary  to 
what  might  be  supposed  from  the  fact  that  the  liver  has  a  double  blood- 
supply,  from  the  heiDatic  artery  and  portal  vein,  appearances  resembling 
infarcts  in  other  organs  do  occur  in  the  liver  and  are  not  so  rare  as  is 
usually  beUeved. 

Infarcts  in  the  liver  usually  show  some  differences  frpm  those  in  the 
spleen  and  kidney  wliich  have  true  end-arteries. 

(1)  They  are  generalty  hsemorrhagic,  whereas  bland  infarcts  in  the 
kidney  and  spleen  are  usually  ansemic.  The  hsemorrhagic  state  of  the 
hepatic  infarcts  is  doubtless  clue  to  the  double  blood-suj^ph^,  and  in  this 
way  infarcts  of  the  hver  and  lung,  both  of  them  organs  with  a  double 
blood-supply,  resemble  each  other. 

(2)  Necrosis  and  coagulation  necrosis  seldom  occur,  inasmuch  as  the 
nutrition  of  the  liver  cells  is  maintained  by  the  collateral  circulation. 

(3)  As  there  is  usually  no  necrosis,  fibrous  substitution  seldom  occurs 
to  more  than  a  slight  extent,  and  it  is  doubtful  whether  a  depressed  scar 
on  the  site  of  the  uifarct  is  ever  produced. 

It  might  perhaps  be  thought  convenient  to  make  some  distinction 
between  the  infarcts  in  the  liver  and  those  in  the  spleen  and  kidney. 
The  term  pseudo-infarcts  is  open  to  objection  as  being  a  contradiction 
in  terms.  Professor  Adami  has  suggested  in  a  letter  to  me  that  the 
term  subinfarct  might  be  employed  to  indicate  a  condition  approaching 
but  not  exactly  the  same  as  an  infarct  in  the  spleen  and  kidneys.  This 
term  would  also  be  of  use  in  distinguishing  between  true  ansemic  infarcts  of 
the  liver  (as  Baldwin's  case  *)  with  necrosis  and  the  hsemorrhagic  sub- 
infarcts  in  which  necrosis  of  the  liver  cells  does  not  occur. 

Infarcts  in  the  liver  may  be  either  hsemorrhagic  or  anaemic.  The 
hsemorrhagic  variety  is  more  frecjuent. 

In  32  cases  collected  by  Lazarus-Barlow, f  including  Chiari'sJ  17  cases,  2S  were 
haemorrhagic  and  four  anaemic.  In  40  cases,  including  most  of  Lazarus-Barlow's, 
29  were  hsemorrhagic,  10  were  anfemic,  and  in  one  case  of  Pitt's  §  both  htemor- 
rhagic  and  antemic  infarcts  were  present. 

MORBID  ANATOMY. 

Hsemorrhagic  infarcts  in  the  liver  are  weU-defined  areas,  sometimes 
square  or  p^'-ramidal.  In  their  general  appearance  they  resemble  hepatic 
nsevi,  but  the}'  are,  as  a  rule,  much  larger.  They  are  not  raised  above  the 
surrounding  surface  of  the  liver;    in  fact,  Zahn  has  sjioken  of  them  as 

*  Baldwin,  F.  A.:   Journ.  Medical  Research,  vol.  viii,  p.  431. 
t  Lazarus-Barlow,  W.  S.:    Brit.  Med.  Jour.,  1S99,  vol.  ii,  p.  1342. 
~  JChiari:    Zeitschrift  f.  Heilkunde,  Bd.  xix,  S.  475. 
§  Pitt,  G.  X.:    Trans.  Path.  Soc,  vol.  xlvi,  p.  75. 

102 


IXFARCTS    IX    THE    LIVER. 


lOJ 


atrophic  h^emorrhagic  infarcts.  Histologicallj'the  liver  cells  are  atrophied, 
granular,  and  may  contain  fat  glol)iiles,  while  the  nuclei  do  not  stain  well. 
There  is,  however,  no  coagulation  necrosis.  The  capillaries  are  engorged 
with  blood.  There  may  be  a  considerable  numl^er  of  leucocj'tes  infiltra- 
ting the  affected  area. 

In  Anaemic  Infarcts. — The  affected  area  of  the  liver  is  of  a  whitish- 
yellow  colour  and  is  sharph'  marked  off  from  the  surrounding  health}' 
liver  substance.  There  may  be,  but  is  not  necessarih',  a  zone  of  conges- 
tion immediately  at  the  junction  of  the  infarct  and  the  healthy  liver  tissue. 


Fig.  16.— Anemic  Infarct  in  thk  Livicr  from  a  case  wiikhf.  tiii;rk  was  Thrombosis  of  tiif. 
Intraiif.patic  Branchus  of  thic  Poktai,  Vi-.in  and  an  Rmi'Yic.ma.  (Drawn  bv  L.  Jones,  M.B., 
F.K.C.S.) 


The  infarct  has  much  the  same  appearance,  only  it  is  larger  and  more 
prominent,  as  the  white  patches  seen  on  the  surface  of  the  liver  in  many 
infectious  diseases  which  on  microscopic  examination  show  local  fatty 
change.  Microscopically  in  an  anaemic  infarct  the  capillaries  are  empty 
instead  of  being  engorged  as  in  a  haemorrhagic  infarct.  The  liver  cells 
are  atrophied  and  degenerated.  Baldwin  *  described  necrosis  of  the  cells 
and  laid  stress  on  this  ()bser\-ation  as  showing  that  the  condition  was 
the  same  as  anaemic  infarcts  in  other  organs.     At  the  mariiin  of  the 


*  Baldwin:  Jourii.  Med.  Research,  vol.  viii,  431. 


104  I)ISEAST']S    OF   THE    LIVER. 

infarct   there   are   a   number  of  leucocytes,    red   blood-corpuscles,   and 
altered  blood-pigment. 

x4ls  a  result  of  infarction  a  slight  amount  of  localized  replacement 
fibrosis  may  result,  but  probably  not  enough  to  give  rise  to  a  cicatrix. 
Frerichs  *  described  depressed  areas  of  atrophy  on  the  surface  of  the 


V. 

V. 


Fig.  17. — Photomicrograph  of  Infarct  in  the  Liver. 
In  part  of  the  section  the  liver  cells  have  lost  their  outline  and  their  nuclei  only  remain.     (S.  G.  Penny, 

Esq.) 

liver,  producing  lobulation,  as  due  to  thrombosis  of  branches  of  the  portal 
vein;  it  is  conceivable  that  in  their  earliest  stages  these  areas  were 
infarcts.  Infarct  of  the  li^'er  cannot  be  recognized  clinicalh'  and  is 
only  of  pathological  interest. 

ETIOLOGY. 

The  conditions  which  have  been  thought  to  pla}'-  a  part  in  producing 
infarction  of  the  liver  are : 

1.  Obstruction  of  the  branches  of  the  portal  vein,  either  b}'  embolism 
or  thrombosis. 

2.  Obstruction  of  the  branches  of  the  portal  or  hepatic  veins  In' 
neAV-growth. 

3.  Obstruction  of  both  the  portal  and  hepatic  veins  at  the  same  time. 

4.  Embolism  of  the  hepatic  artery. 

5.  Endarteritis  of  the  hepatic  artery. 

6.  Retrograde  embolism  of  the  hepatic  veins. 

7.  Severe  traumatism. 

*  Frerichs:  Diseases  of  the  I^iver,  vol.  ii,  p.  890.     Translated  by  Xew  Sydenham 
Soc. 


INFARCTS    IX    THE    LIVER.  105 

(1)  Embolism  and  Thrombosis  of  the  Branches  of  the  Portal 
Vein. — The  most  frequent  vascular  lesion  found  in  cases  of  infarcts  in 
the  liver  is  the  presence  of  antemortem  blood-clot  in  the  intra-hepatic 
branches  of  the  portal  vein,  either  embohc  and  conveyed  from  thrombosis 
in  its  tributaries,  or  formed  in  situ. 

Embolism. — Chiari  records  15  cases  of  hemorrhagic  infarcts  in  the 
liver  due  to  embolism.  This  number  is  comparatively  large  and  rather 
contrasts  with  the  isolated  observations  of  others,  Avhich,  though  less 
numerous,  point  to  thrombosis  of  the  vein  as  a  more  frequent  antecedent. 
Chiari's  cases,  however,  include  embolism  with  fragments  of  new-growth 
as  well  as  with  detached  blood-clot. 

Thrombosis. — Thrombosis  of  branches  of  the  portal  vein,  without  any 
other  vascular  obstruction,  such  as  embolism  of  the  hepatic  arter}'^  or 
thrombosis  of  the  hepatic  veins,  has  been  found  in  cases  of  hepatic 
infarction  by  Osier,*  Pitt,t  Chiari, J  and  others.  I  ha^•e  certainly  seen 
this  association  on  three  occasions.  As  examples  of  hepatic  infarcts  due 
to,  or  at  least  associated  with,  thrombosis  in  the  intra-hepatic  branches 
of  the  portal  vein  the  folloAving  cases  may  be  quoted : 

A  man  aged  forty-six,  under  the  care  of  Dr.  Penrose,  died  on  May  3,  1902,  in 
St.  George's  Hospital  with  a  right-sided  empyema  and  a  dilated  heart;  there  had 
been  no  abdominal  symptoms  and  no  ascites.  The  main  trunk  of  the  portal  vein 
had  an  adherent  parietal  thrombus,  and  some  of  the  branches  of  the  portal  A-ein 
in  the  right  lobe  of  the  liver  were  occluded  with  firm  clots.  There  were  two  ansemic 
infarcts,  one  as  large  as  one's  hand,  the  other  a  quarter  of  that  size.  The  veins 
going  to  these  areas  were  thrombosed.  The  hepatic  artery  was  opened  up  and  was 
found  to  be  free  from  embolism,  thrombosis,  or  arteriosclerosis.  The  infarcted 
areas  were  distinctly  raised  aboA'e  the  level  of  the  surrounding  liver  substance. 
Although  the  macroscopic  appearances  were  those  of  an  anaemic  infarct,  the  micro- 
scopic were  those  of  a  hsemorrhagic  infarct,  the  capillaries  being  full  of  blood.  It 
is  possible  that  in  this  case  backward  pressure  from  the  dilated  heart  and  sepsis 
played  some  part  in  addition  to  portal  thrombosis  in  inducing  the  infarctions. 

A  man  aged  forty-eight  under  the  care  of  Sir.  W.  Bennett  and  myself 
was  operated  upon  for  a  locahzed  subphrenic  abscess  due  to  a  perforated  gastric 
ulcer.  Thrombosis  of  the  right  popliteal  vein  developed  before  death,  and  at  the 
autopsy  thrombosis  of  a  branch  of  the  right  division  of  the  portal  vein  with  a  sharply 
marked  hsemorrhagic  area  was  found  in  the  corresponding  part  of  the  liver. 

(2)  Obstruction  of  Branches  of  the  Portal  and  Hepatic  Veins  in 
the  Substance  of  the  Liver  by  New-growth. — Both  these  conditions 
may  be  associated  with  infarction  of  the  liver.  AVhen  the  intra-hepatic 
branches  of  the  portal  vein  are  obstructed  by  growth  the  process  is  usually 
embohc  and  due  to  small  emboli  of  infective  cells  derived  from  a  carcinoma 
in  the  stomach,  colon,  or  other  organs  within  the  territory  of  its 
tributaries.  When  the  hepatic  veins  are  occluded,  the  groMi;h  may  in- 
volve them  from  without,  spread  through  the  ca])illaries  from  embolic 
growths  in  the  portal  vein,  or  in  rare  cases  be  due  to  retrograde  eml)()lisin. 
(Vide  p.  51.) 

In  a  Avoman  aged  forty  who  died  in  St.  George's  Hospital  with  u  sijindlc-celled 
sarcoma  surrounding  the  pancreas  there  were  secondary  growths  in  the  liver  Avhich 
blocked  up  some  branches  of  the  hepatic  veins  and  gave  rise  to  hirmorrhagic  infarcts 

*  Osier:   Trans.  Assoc.  American  Physicians,  vol.  ii,  p.  13G,  1SS7. 

tPitt:    Trans.  Path.  Soc,  vol.  xlvi,  p.  75. 

J  Chiari:    Zeitschrift  f.  Heilkundc,  M.  xix,  S.  475. 


106  DISEASES   OF  THE   LIVER. 

in  the  corresponding  areas.  There  were  anaemic  infarcts  in  the  spleen  due  to  block- 
ing of  the  splenic  vein.  There  was  no  evidence  of  arterial  embolism.  Longcope* 
describes  an  aneemic  infarct  associated  with  thrombosis  of  the  hepatic  vein,  and  a 
hsemorrhagic  infarct  associated  with  thrombosis  of  the  portal  vein;  in  both  Long- 
cope's  cases  the  thromboses  were  secondary  to  gastric  carcinoma. 

(3)  Combined  Portal  and  Hepatic  Vein  Thrombosis. — Thrombosis 
of  the  portal  vein  may,  when  combined  with  thrombosis  of  the  hepatic 
veins,  give  rise  to  infarction  of  the  Hver.  Thus,  Pitt  f  records  a  case  of 
very  widespread  thrombosis  in  the  abdominal  aorta,  splenic,  left  renal,  and 
right  middle  cerebral  arteries,  in  the  right  hepatic  and  the  branches  of 
the  portal  veins.  There  were  both  anaemic  and  hsemorrhagic  infarcts  in 
the  liver.  But  in  a  case  of  combined  hepatic  and  portal  vein  thrombosis 
that  I  examined  there  was  no  appearance  of  infarction  in  the  liver. J 

(4)  Embolism  of  the  hepatic  artery  is  very  rare.  It  has  been  found 
both  in  man  and  experimentally  to  lead  to  necrosis  of  the  liver.  {Vide 
p.  45.)     Embolism  of  its  branches  may  give  rise  to  anaemic  infarcts. 

In  a  case  of  embolism  of  the  bifurcation  of  the  hepatic  artery  by  a  vegetation 
derived  from  the  aortic  valves  C.  Ogle  §  found  anaemic  infarcts  in  the  liver. 

In  a  case  of  aortic  and  mitral  disease  Baldwin  ||  found  between  20  and  30  anaemic 
infarcts  in  the  liver  which  were  genuinely  necrotic.  The  corresponding  branches 
of  the  hepatic  artery  contained  old  thrombi.  There  were  infarcts  in  the  spleen, 
kidneys,  brain;    so  there  is  little  doubt  that  the  infarcts  in  the  liver  were  einbolic. 

It  is  highly  probable  than  in  some  cases  there  is  embolism  of  the 
intra-hepatic  branch  of  the  hepatic  artery  going  to  the  infarcted  area 
in  the  liver,  but  that  it  is  not  found ;  in  the  following  case  this  hypothesis 
is  quite  conceivable. 

In  a  man  aged  fifty-three  years  who  died  in  St.  George's  Hospital  in  November, 
1902,  with  an  abscess  and  pneumonia  of  the  right  lung,  there  was  a  hsemorrhagic 
infarct  in  the  liver;   the  portal  vein  and  hepatic  artery  appeared  normal. 

(5)  Endarteritis  obliterans  of  the  branches  of  the  hepatic  artery 
has  been  described  by  Bonome  **  as  the  cause  of  haemorrhagic  and  of 
necrotic  infarcts  in  the  liver  in  cases  of  cirrhosis. 

(6)  Retrograde  Embolism. — Embolism  of  one  of  the  hepatic  veins 
by  a  clot  derived  from  the  heart  which  had  worked  its  way  against  the 
flow  of  blood — or  retrograde  embolism — has  been  observed  to  be  associated 
with  an  hepatic  infarct.     (Arnold. ft) 

(7)  Traumatism  may  lead  to  the  production  of  appearances  resem- 
bling infarcts  in  the  liver. .  But  these  appearances  are  in  reality  different 
both  in  their  minute  structure  and  causation  from  the  infarcts  already 
described. 

Appearances  Resembling  a  Hcemorrhagic  Infarct. — In  rare  instances 
traumatism  may  lead  to  the  passage  of  part  of  the  liver  through  a  hole 

*  Longcope,  W.  T. :  University  of  Pennsylvania  Med.  Bull.,  Aug.,  1901,  p.  223. 
t  Pitt:    Trans.  Path.  Soc,  vol.  xlvi,  p.  75. 
X  RoUeston:   Trans.  Path.  Soc,  vol.  1,  p.  148. 
§  Ogle,  C:   Trans.  Path.  Soc,  vol.  xlvi,  p.  73. 
II  Baldwin,  F.  A.:   Journ.  of  Medical  Research,  vol.  viii,  p.  431. 
**  Bonome:    Lo  Sperimentale,  anno  53,  fasc.  4,  p.  319.     Rev.  general  de  Path. 
Intern.     1900,  p.  70. 

ft  Arnold:    Virchow's  Archiv,  Bd.  cxxiv,  S.  3SS. 


INFARCTS    IX    THE    LIVER.  107 

or  rupture  in  the  diaphragm.  If  the  piece  of  hver  becomes  strangulated, 
haemorrhage  takes  place  into  the  liver  and  the  appearance  resembles  that 
of  a  hsemorrhagic  infarct. 

In  a  remarkable  case  recorded  by  C.  Ogle,*  part  of  the  left  lobe  of  the  liver, 
measuring  5  by  4  inches,  was  herniated  through  the  diaphragm,  and  to  the  naked 
eye  resembled  a  section  of  a  cardiac  spleen.  Microscopically  the  liver  tissue  was 
disorganized  and  showed  much  blood  pigment,  red  blood-corpuscles,  and  the  re- 
mains of  liver  cells,  but  differed  considerably  from  the  appearances  in  an  ordinary 
hsemorrhagic  infarct  of  the  organ.  I  had  an  opportunity  of  cutting  sections  of  the 
specimen. 

Ancemic  Infarcts. — Severe  traumatism  may,  by  producing  rupture  of 
the  liver,  cut  off  the  vascular  supply  to  a  part  or  parts  of  the  liver.  If 
life  is  prolonged  for  some  days,  the  areas  of  the  liver  thus  deprived  of 
their  blood-supply  present  to  the  naked  eye  an  appearance  resembling  an 
anaemic  infarct.  The  areas  are  firm  and  white  in  colour  and  have  been 
regarded  as  infarcts  by  Klebs,t  Lubarsch,}  Lazarus-Barlow,  §  Heile.  || 
Microscopic  examination  shows  that  there  is  undoubted  necrosis  in  these 
areas  and  that  they  correspond  to  true  infarcts  in  the  kidney  and  spleen. 
There  is  therefore  a  distinct  difference  between  them  and  the  so-called  in- 
farcts of  the  liver  previously  described,  with  the  exception  of  Baldwin's. 

(8)  There  may  be  no  manifest  vascular  obstruction  to  be  found.  In 
such  cases  a  septicsemic  or  toxsemic  condition  is  possibly  responsible  for 
the  lesion.  I  have  seen  an  infarct  in  the  liver  without  any  evidence  of 
portal  thrombosis  or  embolism  of  the  hepatic  artery.  The  patient  was 
a  man  aged  twenty-five  who  died  with  a  localized  peritonitis  in  the  lesser 
sac  due  to  acute  pancreatitis. 

PATHOLOGY. 

Experimentally  Cohnheim  and  Litten**  injected  coarsely  powdered 
chromate  of  lead  and  wax  into  the  portal  vein  and  produced  portal 
thrombosis  but  no  infarcts.  Zahn,'j""|'  however,  is  quoted  by  Welch  to  the 
effect  that  sterilized  mercury  injected  into  the  mesenteric  veins  was  fol- 
lowed after  an  interval  of  eight  days  by  hsemorrhagic  infarcts.  But  in 
actual  practice  thrombosis  of  the  portal  vein  or  its  branches  is  so  fre- 
quently seen  without  any  accompanying  infarction  that  it  would  appear 
that  some  other  factor  is  necessary.  Rattone  suggested  that  the  addi- 
tional_  factor  is  blocking  of  the  hepatic  artery,  but  this  is  hardly  ever 
found  to  be  the  case;  Chiari  argued  in  favor  of  a  feeble  circulation  and 
low  blood-pressure  in  the  hepatic  artery  associated  with  venous  con- 
gestion. KohlerJJ  thought  that  backward  pressure  in  the  hepatic  veins 
was  a  necessary  adjunct,  but  this,  again,  is  not  borne  out  by  the  facts 

*  Ogle,  C:    Trans.  Path.  Soc.  vol.  xlviii,  p.  114. 

tKlebs:    Virchow's  Festschrift,  1S91,  S.  8. 

X  Lubarsch:    Fortschritte  d.  Med.,  1893. 

§  Lazarus-Barlow:    Brit.  Med.  Journ.,  1900,  vol.  ii,  p.  1362. 

il  Heile:    Ziegler's  Beitnlge,  Bd.  xxviii,  S.  443,  1900. 
**  Cohnheim  and  Litlen:    Virchow's  Archiv,  Bd.  Ixvii,  S.  153. 
tt  Zahn:   Ceutralblatt  f.  allg.  Patli.,  viii,  S.  860,  1897. 
XX  Kohler:  Quoted  by  Welch,  Allbutt's  System,  vol.   vi,  p.  280. 


108  DISEASES    OF   THE   LIVER. 

of  morbid  anatomy.     It  is  probable,  therefore,  that  infarction  of   the 
liver  is  not  solely  a  mechanical  process. 

By  the  injection  of  tissue  fibrinogen  Wooldridge  *  produced  portal 
thrombosis  with  haemorrhages  and  necrotic  areas  'in  the  liver.  The 
necrosis  is  a  more  advanced  change  than  that  seen  in  the  ordinary  so- 
called  infarcts  in  the  liver.  Wooldridge's  results  suggest  that,  in  addi- 
tion to  vascular  disturbances,  such  as  thrombosis  or  embolism  of  the 
blood-vessels  of  the  liver,  a  toxsemic  or  septicsemic  condition  is  necessary 
or  at  least  very  favourable  to  the  production  of  infarction  in  the  liver. 
Possibly  a  low  arterial  blood-pressure,  which  is  favoured  by  septicsemia, 
may,  when  combined  with  a  septic  or  toxic  blood  state,  be  sufficient  to 
produce  hepatic  infarction.  The  importance  of  a  septic  condition  is  sup- 
ported by  the  fact  that  Apert  f  produced  multiple  anaemic  infarcts, 
resembhng  the  early  stage  of  abscess  formation,  in  the  liver,  heart,  and 
kidneys  of  a  rabbit  by  injecting  pus  containing  colon  and  numerous 
anaerobic  micro-organisms  into  the  vein  of  the  ear. 

*  Wooldridge,  L.  C:    Trans.  Path.  Soc,  vol.  xxxix,  p.  421. 
t  Apert:   Bull.  Soc.  Anat.  Paris,  1900,  tome  ii,  p.  204. 


ACUTE  CONGESTION  OF  THE  LIVER. 

Active  acute  congestion  of  the  liver  is,  of  course,  the  first  stage  of 
acute  hepatitis,  which  may,  like  similar  processes  elsewhere,  abort  and 
be  followed  by  a  rapid  return  to  the  normal  condition.  It  is  therefore 
impossible  to  draw  a  hard  and  fast  line  between  the  clinical  manifestations 
of  active  congestion  and  of  acute  hepatitis  in  an  early  stage.  Acute  con- 
gestion of  the  liver  is  both  more  frequent  and  of  more  importance  in 
warm  countries,  where  malaria  and  dysenter}'  are  rife,  than  in  temperate 
countries. 

From  a  systematic  standpoint  the  causes  of  active  congestion  of  the 
liver  may  be  first  divided  into : 

(I)  Active  vaso-dilatation  of  the  capillaries  of  the  hepatic  arter}^; 
this  may  be  reflex  and  due  to  the  effects  of  cold  applied  to  the  surface 
of  the  body.  This  is  the  mechanism  by  which  chills  produce  active  con- 
gestion of  the  liver.  In  England  cold  does  not  act  in  this  way  to  any- 
thing Hke  the  same  extent  that  it  does  in  tropical  climates,  where  the 
resistance  of  the  liver  is  often  much  diminished  from  past  attacks  of 
congestion  or  inflammation  in  connexion  with  malaria  and  dysenter}'. 
In  persons  who  have  had  dysentery  or  repeated  attacks  of  malaria 
exposure  to  cold  readily  produces  active  congestion  of  the  liver;  this  is 
sometimes  spoken  of  as  "a  chill  on  the  liver."  But  all  cases  described 
in  these  words  are  not  thus  explained;  the  efl"ects  of  excessive  eating  and 
drinking,  dyspepsia,  gastro-intestinal  catarrh,  and  constipation  are  some- 
times described  in  these  euphemistic  terms.  Exposure  to  high  tempera- 
ture in  the  tropics  is,  especialty  if  followed  b}'  an  accidental  chill,  a 
cause  of  acute  congestion  of  the  liver.  Direct  nerv'ous  stimulation  has 
been  suggested  to  explain  active  congestion  of  the  liver  in  diabetes,  but. 
as  Hunter  *  points  out,  the  voracious  appetite  of  diabetic  patients  prob- 
ably accounts  for  any  active  hepatic  congestion.  Experimentally,  how- 
e^-er,  irritation  of  the  diabetic  centre,  as  b}-  Bernard's  puncture  experi- 
ment, gives  rise  to  intense  hyperaemia  of  the  liver. 

(II)  The  more  reasonable  and  by  far  the  commonest  cause  of  active 
hepatic  congestion  is  to  be  found  in  toxic  bodies  reaching  the  organ 
through  the  blood-stream.  This  may  occur  (a)  through  the  hepatic 
artery,  as  in  fevers,  especially  malaria,  and  various  septic  conditions, 
though  in  the  latter  the  process  may  pass  on  into  inflammation  or  sup- 
puration. It  probably  occurs  in  the  early  stages  of  icterus  gravis,  and  no 
doubt  is  partly  responsible  for  the  enlargement  of  the  liA'er  seen  in  that 
disease  and  in  the  early  stage  of  acute  yellow  atrophy. 

Experimentally  it  has  been  shown  that  subcutaneous  or  intravenous  injection 
of  the  extract  obtained  from  muscular  tissue  gave  rise  to  intense  congestion  of 
the  Hver  in  animals.     (Richet.t) 

*  Hunter:    Allbutt's  System,  vol.  iv,  p.  46. 

t  C.  Richet:  Acad.  desSciences,  Dec.  31,  1900.     Le  progres  Medical,  1901 ,  p.  23. 

109 


110  DISEASES   OF  THE   LIVER. 

(5)  But  generally  the  poison  is  derived  from  the  gastro-intestinal 
tract  and  reaches  the  liver  by  the  portal  vein.  It  therefore  fohows  over- 
eating, and  especially  alcohohc  excess,  gout,  gastritis,  indigestion,  dysen- 
tery. Physiologically  active  congestion  of  the  liver  occurs  in  digestion 
and  is  heightened  by  spices,  pepper,  mustard,  and  curries ;  in  great  excess 
such  condiments  may  no  doubt  in  a  suitable  subject  set  up  acute  and 
active  hepatic  congestion.  Alcohol  is  an  important  factor,  especially  in 
hot  cHmates,  in  producing  acute  congestion.  Other  toxines  may  be  carried 
by  the  portal  vein,  as  in  constipation,  or,  to  take  a  more  extreme  case, 
in  phosphorus  poisoning.  The  suppression  of  menstruation  or  of  habitual 
haemorrhages  from  piles,  and  the  chmacteric  have  been  thought  to  give 
rise  to  active  hypersemia  of  the  liver,  but  the  evidence  is  somewhat 
slender. 

MORBID  ANATOMY. 

The  hver  is  enlarged,  dark  in  colour,  the  uniform  congestion  contrasting 
with  the  partial  engorgement  seen  in  the  chronic  venous  stagnation  of 
mitral  disease.  The  liver  cells  show  cloudy  swelling,  and  may  be  fatty 
and  pigmented,  while  the  capillaries  are  dilated  and  full  of  red  blood- 
coipuscles.  The  small  bile-ducts  may  show  proliferation  of  their  living 
epithelium  (cholangitis),  which  accounts  for  jaundice  when  present. 

CLINICAL  PICTURE. 

The  symptoms  vary.  Sometimes  the  patient  is  so  ill  that  he  must 
remain  in  bed;  in  other  cases  exercise  can  quite  well  be  taken.  There 
is  malaise,  with  headache,  giddiness,  mental  depression,  irritability, 
insomnia,  and  gastro-intestinal  symptoms,  such  as  loss  of  appetite, 
a  foul  tongue,  a  bad  taste  in  the  mouth,  sometimes  nausea,  flatulence, 
and  constipation.  There  is  a  feehng  of  discomfort  and  weight  in  the 
hepatic  region,  while  there  is  pain  in  the  right  shoulder.  The  conjunc- 
tivae become  muddy  and  shghtly  icteric,  the  face  is  often  congested,  and 
the  skin  shares  in  these  changes  and  may  be  irritable.  The  bowels  are 
irregular;  there  may  be  bilious  diarrhoea  or  constipation.  Epistaxis 
sometimes  occurs. 

The  symptoms  of  acute  congestion  of  the  liver  are  much  the  same  as 
some  of  those  described  by  Murchison  as  lithsemia  and  regarded  by  him 
as  due  to  functional  inadequacy  of  the  liver.  The  liver  is  usually  en- 
larged and  may  project  two  or  three  fingers'  breadths  below  the  costal 
arch  in  the  nipple  line.  It  is  decidedly  tender  on  palpation.  As  a  result 
of  repeated  attacks  of  hepatic  congestion  piles  may  be  produced.  Some 
writers  describe  oedema  of  the  feet  in  acute  hepatic  congestion. 

The  urine  is  high  coloured,  lithatic,  concentrated,  and  of  high  specific 
gravity.  The  amount  of  urobihn  is  increased.  The  amount  of  ammonia 
in  the  urine  is  little,  if  at  all,  above  the  normal,  and  thus  contrasts  with 
the  increase  of  ammonia  found  in  the  urine  of  patients  with  cirrhosis 
(Bain*).     If  there  is  jaundice,  bile-pigment  will  be  found  in  the  urine. 

*  Brit.  Med,  Journ.,  1898,  vol.  ii,  p.  941. 


ACUTE    CONGESTION    OF   THE    LIVER.  Ill 

Albuminuria  only  occasionally  occurs;  it  is  transitory  and  can  be  ex- 
plained as  the  result  of  poisons  passing  from  the  bowel  and  failing  to  be 
stopped  by  the  liver;  the  kidneys  are  thus  affected,  and  toxic  albuminuria 
results. 

The  term  tro-pical  liver  describes  the  condition  found  in  persons  who 
have  had  many  attacks  of  acute  congestion  in  hot  climates.  According 
to  Cantlie,  there  is  usually  a  history  of  malaria,  diarrhoea,  dysentery, 
or  long-standing  indigestion.  Ansemia,  weakness,  nervous  irritability, 
and  irregularity  of  the  bowels  are  essential  features.  The  spleen  is 
generally  enlarged  in  addition  to  the  liver.  Probably  some  of  these 
cases  are  in  the  early  or  pre-ascitic  stage  of  cirrhosis. 

Duration. — ^Acute  congestion  when  treated  usually  lasts  about  a 
week,  but  may,  if  neglected,  become  chronic,  and  may  then  be  a  pre- 
liminary stage  to  cirrhosis. 

TREATMENT. 

In  marked  cases  the  patient  should  be  confined  to  bed  and  kept  on 
a  milk  diet.  If,  as  sometimes  happens,  ordinary  milk  cannot  be  borne, 
skimmed  milk,  junket,  milk  jelly,  or  whey  should  be  tried,  and  if  necessary 
chicken  broth  or  raw  meat-juice  should  be  given.  Plenty  of  water  should 
be  allowed,  but  alcohol  must  be  strictly  prohibited.  Intestinal  antisep- 
tics, such  as  fractional  doses  of  calomel,  perchloride  of  mercury,  or  salol, 
should  be  given  and  the  bowels  kept  freely  open  by  calomel  and  salines, 
such  as  Carlsbad  or  Epsom  salts  and  mineral  waters.  By  free  purgation 
the  congestion  is  greatly  relieved,  as  shown  by  diminution  in  the  size 
and  disappearance  of  tenderness  of  the  liver.  Medicinally  chloride  of 
ammonium  in  xx-grain  doses  has  been  credited  with  the  power  of  re- 
ducing the  congestion  and  preventing  inflammation  and  suppuration.  At 
the  outset,  if  there  are  symptoms  of  gastritis  a  soothing  ixdxture  con- 
taining bismuth  and  bicarbonate  of  soda  should  be  given. 

Local  Application. — For  the  pain  in  the  hepatic  region  a  large 
linseed  poultice  may  be  applied,  and  if  it  gives  relief,  be  changed  every 
three  hours.  Cold  compresses  or  dry  cupping  may  be  employed  if 
poultices  fail.  If  there  is  pain  on  respiration,  resembling  that  of  pleurisy 
and  due  to  perihepatitis,  the  side  should  be  strapped  as  for  fractured 
ribs.  Leeches  apphed  over  the  hepatic  region  or  at  the  margin  of  the 
anus  have  been  employed  to  deplete  the  congested  liver.  Pain  is  im- 
doubtedly  relieved  by  leeching  the  skin  over  the  liver,  although  it  is 
hardly  probable  that  much  blood  is  withdraAvn  from  the  liver  through 
dilated  venous  anastomoses  between  the  A^eins  of  the  abdominal  wall  and 
the  parumbilical  veins  in  the  falciform  ligament.  Neither  is  it  likely 
that  leeches  apphed  to  the  anus  draw  off  much  blood  from  the  portal 
vein.  Venesection  from  the  veins  of  the  elbow  was  formerly  much  in 
vogue  in  hepatic  congestion,  but  has  almost  completely  gone  out  for 
many  years.  Direct  aspiration  of  the  liver  and  abstraction  of  blood  is 
highly  spoken  of  by  man}'.  In  performing  this  risky  operation  the 
piuicture  of  the  liver  may  have  to  be  performed  several  times  before  a 
vessel  of  sufficient  size  to  bleed  freely  is  struck. 


112  DISEASES    OF   THE    LIVER. 

This  withdrawal  of  blood  from  the  liver  is  by  no  means  a  harmless 
proceeding.  If  a  large  branch  of  the  portal  vein  or  the  inferior  vena 
cava  is  wounded,  fatal  haemorrhage  may  take  place  into  the  peritoneal 
cavity.  Indian  surgeons,  such  as  Hatch*  and  Maitland,t  who  have  had 
fatal  experience  of  aspirating  the  liver,  naturally  condemn  the  procedure. 
Cantlie,$  by  limiting  the  length  of  the  aspirating  needle  to  3 J  inches  or 
so,  considers  that  the  danger  of  wounding  the  inferior  vena  cava  is 
obviated. 

When  the  more  acute  symptoms  have  passed  off,  the  patient's  diet 
should  be  improved,  and  tonics,  such  as  strychnine  in  an  acid  mixture, 
should  be  given.  When  convalescent,  the  patient  will  be  benefitted  by 
change  of  air.  A  cool,  somewhat  high,  inland  resort  is  usually  most 
suitable.  The  seaside,  especially  when  the  patient  lives  near  the  shore, 
is  often  harmful  and  gives  rise  to  constipation  and  so  to  a  return  of 
hepatic  congestion. 

In  the  slighter  forms  of  active  congestion  of  the  liver  due  to  over- 
eating, drinking,  and  aggravated  by  constipation  and  a  sedentary  life, 
free  purgation  with  blue  pill  and  haustus  sennse,  followed  by  a  simple 
diet  and  exercise,  should  be  enjoined.  Exercise  on  horseback  or  on  a 
bicycle  will  in  many  cases  act  like  a  charm. 

Treatment  at  a  spa,  such  as  Vichy,  Ems,  Neuenahr,  Carlsbad, 
Marienbad,  Harrogate,  Leamington,  Llandrindod,  has  a  beneficial  effect 
both  by  reducing  congestion  of  the  liver  through  purgation  and  by 
preventing  indiscretions  in  diet,  while  the  freedom  from  business  worries 
has  a  good  influence  on  the  mental  condition. 

PROPHYLAXIS. 

In  gouty  patients  care  as  to  diet  should  be  taken  to  prevent  undue 
hepatic  congestion;  but  it  is  chiefly  in  persons  who  are,  or  have  lived, 
in  the  tropics  and  have  suffered  from  malaria  that  active  congestion  of 
the  liver  is  likely  to  occur,  and  in  whom,  therefore,  special  care  should 
be  taken  to  avoid  causes,  such  as  chills,  and  alcoholic  or  dietetic  excess, 
etc.,  which  bring  on  this  condition. 

Exposure  to  east  wind,  cold  draughts,  and  the  risk  of  chills  should 
be  avoided  by  a  malarial  patient.  The  parts  of  the  body  exposure  of 
which  to  cold  is  most  liable  to  give  rise  to  hepatic  congestion  are  the 
abdomen,  the  back  of  the  neck,  and  the  legs  and  feet  (Brunton).  These 
parts  should  be  suitably  protected;  a  good  plan  is  to  wear  a  knitted 
cholera  belt  over  the  abdomen,  which  should  always  be  changed  after 
free  action  of  the  skin.  Alcohol  is  best  avoided,  and  if  taken  at  all 
should  be  in  small  quantities  well  diluted  at  meal  times.  Made  dishes, 
much  meat,  pastry,  and  sauces  should  be  avoided. 

Constipation  should  be  guarded  against  by  diet,  viz.,  fruit  and  vegeta- 
l)les,  porridge,  and  a  sufficiency  of  water.     If  necessary,  small  doses  of 

*  Hatch,  W.  K.:   Indian  Med.  Gaz.,  April,  1S9S. 
t  Maitland:    Brit.  Med.  Journ.,  1902,  vol.  i,  p.  45S. 
t  Cantlie,  J.:    Brit.  Med.  Journ.,  1903,  vol.  ii,  p.  656. 


ACUTE    CONGESTION   OF  THE   LIVER. 


113 


calomel  or  blue  pill  followed  by  a  saline  should  be  given.  Active  exercise, 
not  merely  walking,  but  riding,  climbing,  and  other  forms  of  exertion, 
such  as  rowing,  skipping,  which  lead  to  compression  of  the  liver  between 
the  diaphragm  and  the  abdoixdnal  wall,  a  kind  of  natural  massage, 
should  be  taken  by  persons  whose  strength  and  physique  are  suitable. 


ACUTE  HEPATITIS, 

There  are  a  large  number  of  different  conditions  in  whicli  the  liver 
is  acutely  inflamed.  At  the  outset  a  division  into  suppurative  and  non- 
suppurative hepatitis  may  conveniently  be  made.  The  suppurative 
forms  of  hepatitis  are  described  elsewhere  under  other  headings,  such  as 
abscess,  pylephlebitis,  cholangitis.  Acute  non-suppurative  hepatitis  may 
chiefly  attack  the  liver  cells,  as  in  icterus  gravis  and  in  acute  yellow 
atroph}^,  or  the  brunt  of  the  change  may  faU  on  the  connective-tissue 
framework,  as  in  the  hepatitis  seen  after  scarlet  fever  (Klein*).  {Vide 
also  p.  192.)  In  malaria  the  liver  cells  are  affected,  but  not  in  the  same 
degree  as  in  icterus  gravis.  The  focal  necroses  seen  in  t^-phoid  fever, 
puerperal  eclampsia,  and  in  some  other  infections  and  intoxications  are 
allied  to  acute  parenchymatous  hepatitis,  and  represent  a  patchy  or 
locaHzed  distribution  of  the  process,  which  when  diffuse  gives  rise  to 
acute  yeUow  atrophy. 

Acute  active  congestion  of  the  liver  and  non-suppurative  hepatitis  are 
often  two  stages  of  the  same  process,  and  any  attempt  to  clistinguish 
sharply  between  them  clinically  is  difficult  or  impossible. 

MORBID  ANATOMY. 
So  many  different  forms  of  pathological  change  are  included  under 
the  title  of  "acute  hepatitis"  that  no  one  description  can  possibly  be 
inclusive.  The  appearance  of  the  liver  vail  xsiry  according  to  the  nature 
and  intensity  of  the  inflammation.  In  the  more  acute  changes  affecting 
the  cells  of  the  Uver  the  condition  \n]l  resemble  that  seen  in  icterus 
gravis  or  in  acute  yeUow  atrophy,  while  in  less  severe  types  of  inflamma- 
tion the  aspect  of  the  hver  wiU  resemble  that  in  active  congestion. 
(Vide  p.  110.)  In  acute  hepatitis  as  seen  in  pysemia  the  lobules  of  the 
liver  may  be  very  sharply  marked  out  as  bile-stained  areas  surrounded 
by  greyish  white  rings. 

In  a  case  of  hepatitis  in  a  patient  who  had  had  a  prolonged  attack  of  dysentery 
the  Uver  was  deeply  congested,  cedematous,  and  almost  ftuctuating  when  it  was 
seen  during  an  operation  undertaken  by  Berard  t  under  the  idea  that  there  was  an 
abscess.  The  Uver  was  explored  in  four  places;  blood  alone  came  out  and  the 
patient  rapidly  recovered. 

The  Uver  of  severe  malarial  infection,  which  is  a  definite  form  of  acute 
inflammation,  is  usually  swollen,  enlarged,  and  more  or  less  pigmented, 
from  a  brownish  to  a  slaty  black  tint.  The  outhne  of  the  lobules  is 
indistinct.  In  more  chronic  malarial  infection  two  forms  of  hepatitis, 
described  by  Kelsch  and  Kiener,t  should  be  mentioned  here:  (I)  Hyper- 

*  Klein:    Trans.  Path.  Soc,  vol.  xxviii,  p.  439. 
t  Berard:    Lyon  Medical,  May  18,  1902. 

t  Kelsch  and  Kiener:  Archiv.  de  Phvsiol.  norm,  et  path.,  1878,  p.  571;  1879, 
p.  354. 

114 


ACUTE    HEPATITIS. 


115 


emie  plilegmasique,  in  which  the  enlarged  and  soft  Hver  shoAvs  peri- 
hepatitis, cloudy  swelling,  and  karyokinesis  of  the  liver  cells  with  small- 
cell  infiltration  of  the  portal  spaces.  (II)  Nodular  parenchymatous  hepa- 
titis, in  which  there  is  hj-perplasia  of  the  liver  cells  forming  smaU  nodules 
on  the  surface  of  the  organ,  which  may  resemble  multiple  adenomata 
or  even  masses  of  secondary  new-groTvih,  though  they  are  not  umbilicated. 
Attention  may  also  be  drawn  to  a  rare  form  of  acute  parenchymatous 
hepatitis  which  is  practical^  a  subacute  form  of  acute  yellow  atrophy, 
and  shows  in  a  marked  degree  compensatory  hyperplasia  of  the  liver 
cells.  The  condition  is  very  closely  allied  to  the  nodular  parenchymatous 
hepatitis  just  described,  Init  is  not  confined  to  malarial  infection,  and 


■■  ■  ■■.%*■■■•••".-••.■■■;•,••• 
■■■■,,W'«;m«?'rvV-;   ..•■•• 


Fig.   18. — Drawing  from  a  Microscopic  Section  from  a  Case  of  Pyemia  duf,    to   Acute 

Necrosis  of  both  Fibdl.e. 

Shows  cloudy  swelling  of  the  liver  cells  in  the   intermediate  zone  of  the  liver,  and  small-cell 

infiltration  at  the  margin  of  the  lobule. 


is,  as  has  already  been  hinted,  much  the  same  as  those  cases  of  acute 
yeUow  atrophy  in  which  recovery,  or  rather  partial  recovery,  with  much 
hyperplasia  of  the  liver  cells,  occurs. 

I  described  a  case  of  this  kind  in  1S91,*  but  the  morbid  growths  committee  of 
the  Pathological  Society  did  not  take  my  view,  and  regarded  the  condition  as  allied 
to  cirrhosis.  Professor  S.  Delepine  has  most  kindlj^  communicated  to  me  full  details 
of  a  case  showing  acute  interstitial  and  parenchymatous  inflammation  with  imperfect 
regeneration  of  the  liver  cells,  forming  tubules  containing  plugs  of  bile,  and  giving 
rise  to  hyperplastic  nodules.  The  patient,  aged  eleven  years,  was  imder  Sir  T. 
Lauder  Brunton's  care  in  ISS7  for  jaundice  after  one  of  the  acute  .specific  fevers; 
from  this  recovery  occurred,  but  six  months  later  the  jaundice  recurred  and  proved 
fatal.  The  liver  weiglied  44  ounces  and  showed  yellow  areas  of  nodular  liyperplasia 
in  whicli  the  cells  had  undergone  fatty  degeneration  and  so  led  to  the  fatal  result. 

*  Trans.  Path.  See,  vol.  xliii,  p.  81. 


116 


DISEASES    OF   THE    LIVER, 


The  histological  appearances  in  acute  hepatitis  are  those  already  de- 
scribed in  acute  congestion  of  the  liver,  viz.,  dilatation  of  the  capillaries, 


Fig.  19.— Photomicrograph  op  Acute  Hepatitis. 
The   liver  cells  are  separated  from  each  other  by  small  round-celled  infiltration.      From  a 
section  prepared  by  Dr.  Bolam.      (Photomicrograph  by  Dr.  H.  Spitta.) 


cloudy  sAvelling,  fatty  degeneration  and  pigmentation  of  the  li^•er  cells, 
and  catarrhal  inflammation  of  the  small  bile-ducts.     In  addition  tlio  liver 


ACUTE    HEPATITIS.  117 

cells  may  show  focal  necroses,  with  thrombosis  of  small  vessels,  and  m 
some  instances  a  \-an'ing  degree  of  small-ceU  infiltration.  The  smaU  cells 
are  partly  polymorjDhoniiclear  and  other  leucocytes,  and  partly  yoimg 
connective-tissue  cells,  and  are  foimd  in  the  areas  of  focal  necrosis  and 
at  the  peripher}^  of  the  lobules. 

In  some  cases  there  is  a  diffuse  small-cell  infiltration,  which  is, 
like  the  hepatitis  of  congenital  syphilis,  pericellular.  A  photomicro- 
graph of  a  case  of  acute  hepatitis  accompanied  by  fever  and  jaimdice 
and  without  any  suppuration  of  the  liver  illustrates  this  condition. 
I  am  indebted  to  Dr.  R.  A.  Bolam,  of  Newcastle-upon-Tyne,  for  this 
section. 

In  the  liver  of  severe  malaria  there  are,  in  addition,  many  large 
phagocytes  containing  the  parasites  and  pigment.  As  weU  as  leucocj^tes, 
the  endothelial  cells  of  the  \-essels  and  Kupffer's  star-like  cells  act  as 
phagocytes.*  The  liver  cells  undergo  degeneration  and  contain  pigment, 
granules  of  bile  and  of  h^emosiderin.  There  is  but  little  fatty  change  in 
the  cells.  Dilatation  of  capillaries  may  lead  to  the  production  of  areas 
resembling  cavernous  tissue  (E^^angf). 

SYHPTOHATOLOGY. 

Acute  non-suppurative  hepatitis  due  to  a  general  hsemic  infection 
may  show  itself  by  jaundice.  If  the  constitutional  symptoms  accompany- 
ing the  jaundice  are  severe,  the  condition  is  that  described  under  ictenjs 
gravis.  But  if  there  is  a  milder  grade  of  clinical  manifestations,  the 
jaundice  is  spoken  of  as  infectious  or  toxsemic  jaundice,  or  may 
conform  to  the  type  of  Weil's  disease.  Wlien  hepatitis  due  to  a 
general  hsemic  infection  is  not  accompanied  b}^  jaundice,  there  may  he 
little  to  attract  attention  to  the  liver,  though  on  examination  it  may 
he  found  to  be  somewhat  enlarged  and  tender.  The  condition,  which  is, 
perhaps  rather  vaguely,  usually  spoken  of  as  acute  hepatitis,  occurs  in 
patients  who  have  suffered  from  frequent  attacks  of  malaria,  from  dysen- 
tery, or  from  both  diseases.  As  the  result  of  exposure  to  cold  or  of 
excess  in  eating  or  drinking  they  suffer  from  the  train  of  symptoms 
described  later  on. 

Clinically  acute  hepatitis  is  seldom  seen  in  England  except  in  persons 
who  have  returned  from  the  tropics.  It  is  an  acute  form  of  the  reaction 
to  irritants  which  in  temperate  climates  is  chronic  and  eventually  gives 
rise  to  cirrhosis.  The  irritant  causing  hepatitis  is  in  manj-  instances 
derived  from  the  gastro-intestinal  tract.  The  symptoms  are  the  same 
as  those  of  active  congestion  of  the  liver,  to  which  reference  should  be 
made,  but  are  more  marked.  The  temperature  in  hepatitis  is  raised,  and 
on  the  degree  of  fever  a  clinical  distinction  has  l^een  drawTi  between 
active  congestion  and  hepatitis;  when  the  temperature  is  above  100° 
the  condition  is  regarded  as  inflammatory,  and  when  below  this  point, 

*  See  valuable  papers  bv  Barker:  Johns  Hopkins  Hospital  Reports,  vol.  v, 
p.  221. 

t  Ewing:    Journal  of  Experimental  Med.,  1902,  p.  154. 


118  DISEASES    OF   THE    LIVER. 

active  congestion  is  considered  to  be  present.*  The  gastro-intestinal 
symptoms  described  in  acute  congestion  are  accentuated  and  vomiting 
is  more  frequent.  The  bowels  may  be  constipated,  or  there  may  be 
diarrhoea;  in  both  cases  the  motions  are  very  offensive.  The  pain  in 
the  shoulder  is  more  marked  than  in  simple  congestion,  and  from  exten- 
sion of  hepatitis  to  the  capsule  of  the  liver  the  case  may  become  com- 
pUcated  by  perihepatitis.  This  makes  the  descent  of  the  diaphragm 
painful  and  leads  to  shallow  respirations.  The  patient  is  irritable,  low- 
spirited,  and  sits  up  in  bed.  The  abdomen  is  rigid  and  the  hver  is  uni- 
formly enlarged  and  tender.  "VATien  there  is  concomitant  malaria,  the 
spleen  is  also  enlarged.  Toxic  albuminuria,  which  has  been  spoken  of 
as  hepatogenic  (Teissierf),  is  occasionally  seen. 

DIAGNOSIS. 

When  there  is  distinct  jaundice,  a  diagnosis  must  be  made  in  the 
most  severe  cases  from  acute  yeUow  atrophy  and  from  phosphorus 
poisoning.  In  acute  yeUow  atrophy  the'  rapid  course,  the  presence  of 
nen^ous  sjmiptoms,  and  the  fact  that  the  liver,  if  at  first  increased  in 
size,  soon  diminishes,  are  characteristic  points.  In  phosphorus  poisoning 
the  hsemorrhagic  condition  of  the  vomit  and  stools  and  the  history  are 
points  of  importance.  But  in  both  these  conditions  the  constitutional 
symptoms  are  far  more  severe  than  in  acute  hepatitis.  When  the  jaun- 
dice is  slight,  infectious  jaundice  should  be  thought  of. 

In  some  cases  where  the  liver  is  very  considerably  enlarged  and  the 
other  symptoms  severe  it  may  be  verv^  difficult  or  impossible  to  be  sure 
that  there  is  not  suppuration  in  the  hver,  especially  as  acute  hepatitis 
may  be  the  first  stage  of  a  tropical  abscess.  This  difficulty  not  uncom- 
monly occurs  in  malarial  patients. 

Berard's  case,  already  referred  to,  is  an  example  of  the  difficulty  in  making 
a  diagnosis  between  acute  hepatitis  and  hepatic  abscess.  Remhngerl^j:  Bozzolo,§ 
and  others  have  described  a  form  of  acute  hepatitis  under  the  name  of  the  infective 
liver  which  clinically  imitates  hepatic  abscess. 

The  same  difficulty  may  arise  in  differentiating  the  condition  from 
more  diffuse  forms  of  hepatic  suppuration,  such  as  suppurative  pjde- 
phlebitis  and  cholangitis.  In  these  cases  some  time  may  be  required 
before  an  accurate  differential  diagnosis  can  be  made. 


TREATMENT. 

The  treatment  is  on  the  same  general  fines  as  in  simple  congestion, 
but  is  rather  more  active.  The  patient  should  be  kept  in  bed  on  a  low 
diet,  and  the  local  pain  and  tenderness  over  the  fi-^-er  refie\-ed  by  cold 
applications,  poultices,  scarifying  the  skin,  leeching,  dry  cupping,  or  by 
strapping  the  hepatic    region  with  narrow  strips   of    plaster  as  if  for 

*  Cantlie:  Encycl.  Med.,  vol.  vii. 

t  J.  Teissier:   Les  Albuminuries  Curables,  p.  34. 

t  Remhnger:   La  Presse  Medicale,  1903,  p.  86. 

J  Bozzolo:    Rev.  crit.  di  Clinica  Med.    March  1.5,  1902 


ACUTE    HEPATITIS.  119 

fractured  ribs.  ]\lilk  or  the  modifications  of  it  mentioned  on  page  111 
(congestion)  is  the  staple  diet,  but  if  it  disagrees,  raw  meat -juice,  chicken 
broth,  jelly,  or  other  similar  preparations  should  be  substituted.  Plenty 
of  water  should  be  given  or  its  equivalent,  such  as  soda  water,  lemon- 
ade.    But  alcoholic  drinks  of  all  kinds  should  be  strictly  tabooed. 

The  bowels  should  be  kept  freely  open  by  sahnes,  such  as  sulphate 
of  soda  or  of  magnesia,  or  calomel  may  be  given  with  advantage.  Vomit- 
ing and  signs  of  gastritis  should  be  allayed  by  bismuth,  hydrocyanic  acid, 
bicarbonate  of  soda,  etc.  Chloride  of  ammonium  in  twenty-grain  doses 
should  be  given  three  times  a  day  during  the  acute  stage,  and  may  be 
combined  with  dilute  hydrochloric  acid  and  a  few  ininims  of  liquor 
strychninse.  If  there  is  a  historj^  or  evidence  of  malaria,  quinine  should 
be  given  as  soon  as  the  gastro-intestinal  symptoms  have  subsided. 

The  abstraction  of  10  to  15  ounces  of  blood  from  the  substance  of 
the  liver  by  means  of  an  aspirator  is  much  advocated  and  has  been 
thought  to  prevent  the  further  development  of  suppuration.  It  is,  how- 
ever, not  entirely  without  risk,  as  fatal  hsemorrhage  into  the  peritoneal 
cavity  has  been  known  to  follow.*  (Vide  remarks  on  treatment  of  acute 
congestion.)  Wlien  convalescent,  the  patient  should  go  to  a  cool,  fairly 
bracing  climate,  and  will  get  benefit  from  spa  treatment,  such  as  Harro- 
gate, Carlsbad,  Marienbad,  Neuenahr,  Ems,  Vichy.  The  prophylactic 
treatment  is  that  of  acute  congestion.     (Vide  p.  112.) 

*  Hatch:  Indian  Med.  Gaz.,  April,  1898.  Maitland:  Brit.  Med.  Joum.,  1902, 
vol.  i,  p.  458. 


HEPATIC  ABSCESS. 

Intra-hepatic  suppuration  may  be  conveniently  divided  into  two  main 
groups:  (I)  Where  the  abscess  is  large  and  single,  the  "tropical"  abscess, 
and  (II)  multiple  abscesses.  Strictly  speaking,  this  classification  is  not 
entirely  satisfactory;  for  occasionally  there  may  be  two  large  abscesses 
in  the  liver,  and  a  single  abscess  may  infect  the  remainder  of  the  liver 
and  give  rise  to  several  secondary  abscesses ;  while,  on  the  other  hand, 
multiple  abscesses  may  unite  and  eventually  form  a  large  areolar  abscess. 
It  has,  however,  a  practical  advantage,  for  cases  of  large  single,  solitary 
or  tropical  abscess  are  accompanied  by  more  characteristic  signs  and  are 
in  general  curable  by  operation,  while  multiple  abscesses  are  less  easy 
to  diagnose  and  cannot  be  benefitted  by  surgical  treatment. 


SINGLE  OR  TROPICAL  ABSCESS. 

ETIOLOGY. 
Dysentery. — There  can  be  no  question  that  the  causation  of  tropical 
abscess  is  more  closely  related  to  dysentery  than  to  any  other  condition. 
Some  statistics  show  a  close  association  between  the  diseases  termed 
dysentery  and  the  subsequent  development  of  hepatic  abscess.  Azevedo 
Sodre,*  adding  together  the  statistics  of  Moore,  Macpherson,  Marshall, 
Morehead,  and  Dutrouleau,  found  that  in  1997  autopsies  on  dysentery 
there  were  407  hepatic  abscesses,  or  20  per  cent.  In  314  selected  cases 
of  hepatic  abscess  taken  by  Kelsch  and  Kiener,t  268,  or  75  per  cent., 
had  had  dysentery.  In  a  later  analysis  by  Kelsch  |  of  500  cases  of 
hepatic  abscess  dysentery  was  present  in  85  per  cent.  On  the  other 
hand,  E.  J.  Waring's  §  statistics  from  India  do  not  show  such  a  close 
relationship;  thus,  in  2758  cases  of  dysentery  treated  in  the  Madras 
Presidency  between  the  years  1826  and  1843  there  were  68  cases  of 
abscess,  or  2.5  per  cent.;  while  in  his  300  fatal  cases  of  abscess,  only 
82,  or  27  per  cent.,  were  admitted  for  dysentery.  Buchanan's  ||  figures 
also  show  that  there  is  a  want  of  parallelism  between  the  curves  of  the 
incidence  of  dysentery  and  hepatic  abscess  in  India.  Thus,  the  natives 
suffer  more  severely  from  dysentery  and  less  from  hepatic  abscess,  while 
the  converse  holds  good  among  European  soldiers. 

In  79,723  cases  of  dysentery  among  the  natives  there  were  127  cases  of  hepatic 
abscess,  or  1  in  628 ;  while  in  the  European  army  during  four  years  (1893-96)  there 
were  7972  cases  of  dysentery  and  441  cases  of  abscess,  or  1  in  iS. 

*  Azevedo  Sodr^:  XXth  Century  Practice  of  Medicine,  vol.  xvi,  p.  253. 
t  Kelsch  and  Kiener:  Traite  des  Maladies  des  Pays  Chauds,  Paris,  1889. 
t  Kelsch:    La  Sem.  Med.,  1900,  March  7,  p.  80. 

§  E.  J.  Waring:    Abscess  in  the  Liver  in  the  East  Indies,  1854,  p.  123. 
IIBuchanan,  W.  J.:    Journ.  Trop.  Med.,  vol.  i,  p.  173,  1899. 

120 


SINGLE    OR   TROPICAL    ABSCESS.  121 

The  following  arguments  have  also  been  urged  against  the  too  ex- 
clusive view  of  the  dysenteric  origin  of  hepatic  abscess : 

(I)  That  hepatic  abscess  is  much  commoner  among  English  soldiers 
in  India  than  in  other  tropical  countries,  such  as  Jamaica,  where  dysentery 
is  as  frequent  as  it  is  in  India. 

(II)  That  an  increase  in  the  curve  of  dysentery — for  example,  in  war- 
time— is  not  accompanied  or  followed  by  any  increase  in  the  hver  abscess 
curve.* 

In  the  bacillary  dysentery  of  Japan  Shiga  has  never  seen  hepatic  abscess  as  a 
complication,  and  in  the  dysentery  seen  in  the  South  African  War,  1899-1902,  which 
was  not  amoebic,  hepatic  abscess  was  very  rare. 

In  250  cases  observed  by  Washbourn  and  Richards  f  at  the  Imperial  Yeomanry 
Hospital,  Deelfontein,  there  was  only  one  hepatic  abscess;  out  of  466  cases  of 
dysentery  treated  at  the  Imperial  Yeomanry  Hospital,  Pretoria,  there  were  two 
fatal  cases  of  pylephlebitis,  and  another  case,  in  which  after  an  operation  for  piles 
performed  some  six  months  after  an  attack  of  dysentery,  a  single  hepatic  abscess 
developed  and  was  successfully  operated  upon.  While  in  South  Africa  (1901)  I 
made  enquiry  from  medical  officers,  who  all  agreed  that  single  hepatic  abscess  as  a 
sequela  of  South  African  dysentery  was  extremely  rare. 

Dysentery  in  temperate  climates  occurs  sporadically  as  "ulcerative 
colitis"  and  in  epidemics  in  asylums.  Asylum  dysentery  has  been 
specially  studied  in  this  country  by  Mott  and  Durham,  J  and  in  America 
by  Vedder  and  Duval.  §  The  latter  observers  have  shown  that  asylum 
or  institution  dysentery,  which  was  formerly  called  ulcerative  cohtis,  is 
due  to  a  bacillus  identical  with  that  described  by  Shiga  and  Flexner  as 
the  cause  of  acute  epidemic  dysentery.  Liver  abscess  is  very  rare  after 
asylum  dysenteiy.  In  Gemmel's  |1  80  cases  examined  after  death  at  the 
Lancaster  Asylum  there  were  two  cases;  while  in  the  epidemics  of  dysen- 
tery at  Milbank,  1840-47,  W.  Baly  **  did  not  find  any  case  of  abscess. 
The  rarity  of  hepatic  abscess  in  asylum  dysentery  is  quite  in  accord 
with  the  fact  that  abscess  hardly  ever  occurs  in  bacillary  dysentery  in 
the  tropics. 

(III)  That  in  some  cases  of  hepatic  abscess  there  is  no  history  of 
dysentery,  and  that  after  death  the  colon  may  appear  quite  healthy. 

In  456  cases  of  fatal  hepatic  abscess  recorded  in  the  annual  reports  of  the  sanitary 
commissioner  of  India  during  the  five  years  1896  to  1900  the  intestines  were  free 
from  ulceration  in  47  per  cent. 

Even  amoebic  abscess  of  the  liver,  which  according  to  Lafleur  ff  must 
for  the  present  be  considered  as  invariably  secondary  to  active  or  latent 
amoebic  dysentery,  has  been  found  to  occur  in  cases  where  the  colon  was 
normal  at  the  autopsy.  J  J    It  is  possible  that  in  such  cases  the  amoebae 

*  Editorial,  Indian  Med.  Gaz.,  May,  1902,  p.  193. 
t  Washbourn  and  Richards:    Brit.  Med.  Journal,  1900,  vol.  ii,  p.  668. 
JMott:    Trans.  Epidemiolog.  Soc,  1902. 

§  Vedder  and  Duval:  The  Journ.  of  Experimental  Medicine,  vol.  vi,  p.  181. 
II  Gemmel:  Idiopathic  Ulcerative  Colitis,  p.  29,  1898. 
**  Baly,  W.:   Med.  Gaz.,  vol.  iv,  p.  885. 
tt  Lafleur:    Allbutt's  Svstem  of  Medicine,  vol.  iv,  p.  155. 

it  Burton,  J.  T.:  Proc.  Philadelphia  Path.  Soc,  Jan.,  1899.  Flexner,  S.:  Ameri- 
can Journal  of  Medical  Sciences,  May,  1897.  Thompson:  Manchester  Medical 
Students'  Gaz.,  1903,  p.  146.  Futcher:  Jour.  American  Med.  Assoc,  vol.  xli,  p. 
480,  Aug.  22,  1903. 


122  DISEASES    OF   THE    LIVER. 

have  gained  entrance  to  the  portal  system  by  some  minute  lesion  which 
subsequently  healed  over. 

The  fact  that  there  may  be  no  history  of  dysentery  in  cases  of  hepatic 
abscess  may  in  some  cases  be  explained  by  its  having  remained  latent. 
In  cases  where  evidence  of  past  dysentery  is  found  at  the  autopsy,  and 
where  no  history  has  been  forthcoming,  the  original  attack  may  have 
been  forgotten,  since  an  abscess  may  occur  years,  even  ten,*  after  dysen- 
tery, or  may  be  remembered  and  spoken  of  as  diarrhoea. 

In  five  out  of  twenty-seven  cases  of  amoebic  abscess,  intestinal  symptoms  of 
dysentery  were  not  noticed  by  the  patients.      (Futcher.f) 

(IV)  It  has  been  thought  that  the  dysenteric  ulceration  of  the  colon 
is  secondary  to  the  abscess.  The  older  observers  believed  that  pus  passed 
down  the  bile-ducts  into  the  intestine  and  set  up  diarrhoea  and  ulceration. 
This  explanation  is  no  longer  accepted.  But  that  septic  absorption  from 
the  abscess  may  set  up  diarrhoea  and  intestinal  ulceration  is  shown  by 
some  cases  of  fatal  hepatic  abscess  where  a  recurrence  of  dysentery  or 
recent  ulceration  is  seen  in  a  colon  showing  evidences  of  old  dysentery. 
Flexner,t  indeed,  considers  that  even  in  amoebic  dysentery  the  intestinal 
lesions  may  be  secondary  to  the  amoebic  hepatic  abscess. 

(V)  Another  view  which  has  been  put  forward  is  that  the  two  diseases 
are  both  independent  results  of  the  same  infection.  Some  evidence  in 
favour  of  this  has  been  brought  forward.  Thus,  it  has  been  urged  that 
when  dysentery  breaks  out  patients  may  develop  hepatic  abscess  who 
have  not  shown  any  signs  of  dysentery,  while  those  who  contract  dysen- 
tery do  not  necessarily  become  the  subjects  of  hepatic  abscess. 

The,  at  first  sight,  puzzling  difference  which  is  shown  in  various 
parts  of  the  world  between  the  relation  of  the  disease  called  dysentery 
and  the  subsequent  development  of  a  single  hepatic  abscess,  may  be 
explained  in  the  following  way :  Under  the  heading  dysentery  at  least 
two  distinct  forms  of  colitis  have  been  included  in  the  past;  (a)  amoebic 
dysentery  of  a  chronic  type,  which  is  followed  by  the  single  or  tropical 
hepatic  abscess,  and  (b)  acute  bacillary  dysentery,  which  is  not  followed 
by  single  hepatic  abscess.  BaciUary  dysentery  was  described  in  Japan 
by  Shiga,  §  where  it  was  extremely  severe,  by  Flexner||  in  Manila,  and, 
as  already  mentioned,  by  Duval  and  Vedder**  in  America,  and  by 
Kruse  |f  in  Germany.  Amoebic  and  bacillary  dysentery  may  occur  side 
by  side.  The  two  diseases  were  studied  and  could  be  distinguished 
from  each  other  in  Manila  during  the  Spanish- American  war. 

Tropical  dysentery  is  more  often  followed  by  abscess  than  the  dysen- 

*  Josserand:    Journ.  de  Med.,  July  25,  1898. 

t  Futcher,  T.  B.:   Jour.  American  Med.  Assoc,  vol.  xli,  p.  480,  Aug.  22,  1903. 
j  Flexner:    American  Journal  of  Medical  Sciences,  vol.  cxiii,  p.  553,  May,  1897. 
§  Shiga:  Centralblatt  f.  Bakteriol.  u.  Parasit.,  Bd.  xxiii,  S.  549;  Bd.  xxiv,  S.  817, 
870,  913. 

II  Flexner:  Johns  Hopkins  Hospital  Bull.,  Feb.,  1900.  Brit.  Med.  Journ.,  1900, 
vol.  ii,  p.  20.     Univ.  Pennsylv.  Med.  Bull.,  Aug.,  1901. 

**  Vedder  and  Duval:   Journ.  Experimental  Medicine,  vol.  vi,  p.  181. 
tt  Kruse:    Deutsche  med.  AVochen.,  1900,  S.  637. 


SINGLE   OR   TROPICAL    ABSCESS.  123 

ter}^  seen  in  temperate  countries;  this  was  correlated  by  Councilman  and 
Lafleur  with  the  amoebic  nature  of  the  tropical  form. 

In  2590  cases  of  tropical  dysentery  hepatic  abscess  occurred  in  507.  (Council- 
man and  Lafleur.*) 

According  to  Lafieur,  amoebic  abscess  of  the  liver  is  secondary  to 
and  a  complication  of  amoebic  dysentery,  while  non-amoebic  hepatic 
abscesses  are  usually  independent  of  any  intestinal  affection. 

Very  few  statistics  are  available  to  show  the  incidence  of  hepatic  abscess  in 
amoebic  dysentery.  In  119  cases  of  amoebic  dysentery  treated  in  the  Johns  Hop- 
kins Hospital  27,  or  22.6  per  cent.,  had  hepatic  abscess  (Futchert) ;  while  in  Strong's 
79  autopsies  on  cases  of  amoebic  dysentery  14  had  liver  abscess. 

Other  Causes  of  Single  or  Tropical  Abscess. — ^Apart  from  dysentery 
the  factors  which  can  be  regarded  as  having  a  causal  relationship  to 
hepatic  abscess  are  comparatively  insignificant. 

Traumatism  may  give  rise  to  hepatic  abscess  either  (I)  directly, — 
for  example,  when  a  penetrating  wound  introduces  micro-organisms  into 
the  liver  substance, — or  (II),  indirectly,  by  so  reducing  the  resistance  of 
the  liver  that  any  pus-producing  micro-organisms  which  happen  to  reach 
the  liver  either  from  the  general  circulation  by  means  of  the  hepatic 
artery,  or  from  the  alimentary  canal  are  then  enabled  to  grow  and  multi- 
ply. Thus  a  blow  on  the  liver  may  produce  a  small  rupture  inside  the 
liver  without  damaging  the  capsule;  recovery  should  then  occur,  but  if 
micro-organisms  have  previously  gained  access  to  the  damaged  part  of 
the  liver,  an  abscess  may  follow. 

(I)  Penetrating  wounds  with  a  dagger,  knife,  or  bullet  ma}^  carry 
with  them  infecting  micro-organisms,  or  infection  may  occur  later.  A 
bullet  may  carry  some  of  the  patient's  clothing  into  the  wound  with  it, 
and  thus  micro-organisms  may  be  introduced  at  the  time  of  the  wound. 
Infection  may  also  supervene  either  from  the  wound  or  possibly  from 
the  blood-stream. 

It  appears  probable  that  a  foreign  body  may  remain  encysted  in  the 
liver  for  a  consideraVjle  time  and  that  suppuration  may  eventually  super- 
vene around  it.  In  such  cases  it  is  probable  that  this  part  of  the  liver 
having  its  resistance  diminished,  thus  becomes  infected  more  easily  by 
the  blood-stream.  It  is  hardly  likely  that  micro-organisms  introduced 
at  the  same  time  as  the  foreign  body- — a  bullet,  for  example — have  re- 
mained latent.  In  rare  instances,  a  pin,  needle,  or  fish-bone  may  pene- 
trate the  alimentary  canal  and  enter  the  liver  substance,  thus  giving  rise 
to  hepatic  abscess. 

(II)  Traumatism  without  any  penetrating  wound  may  be  followed 
by  hepatic  abscess.  This  is  not  a  common  event.  F.  C.  Turner  J  in  1882 
was  only  able  to  refer  to  12  cases,  but  this  estimate  must  not  be  taken 
as  actually  representing  its  incidence.     On  the  other  hand,  the  relation 

*  Councilman  and  Lafleur:  Amoctiic  Dysentery,  Johns  Hopkins  Hospital 
Reports,  1890-91. 

t  Futcher:    Jour.  American  Med.  Assoc,  vol.  xli,  p.  480. 
i  Turner,  F.  C:   Trans.  Path.  Soc,  vol.  xxxiii,  p.  177. 


124  DISEASES    OF   THE    LIVER. 

between  traumatism  and  abscess  may  be  merely  that  after  traumatism 
a  latent  abscess  increases  in  size  or  by  leakage  sets  up  a  perihepatic 
or  subphrenic  abscess. 

Extension  of  Inflammation  from  Adjacent  Parts. — This  method  of 
formation  of  a  single  hepatic  abscess  is  very  rare,  and  not  of  much  impor- 
tance. In  a  few  instances  calculi  in  the  gall-bladder  may,  by  giA'ing 
rise  to  ulcerative  cholecystitis  and  perforation,  set  up  suppuration  in 
the  adherent  liver  substance. 

Weir  *  records  a  case  of  suppurative  cholecystitis  in  a  woman  aged  thirty-five 
with  perforation  of  the  wall  of  the  gall-bladder  leading  into  a  smaU  abscess  cavity 
containing  rather  more  than  an  ounce  of  pus. 

Perforation  of  a  simple  or  of  a  malignant  gastric  ulcer  into  the  hver 
may  set  up  suppuration  in  a  comparatively  limited  area.  In  these 
cases  the  abscess  cavity  may  show  necrotic  changes  which,  according  to 
Gilbert  and  Lippmann,j  depend  chiefly  on  anaerobic  micro-organisms. 

I  have  twice  seen  mahgnant  disease  of  the  cardiac  end  of  the  stomach  grow 
directly  into  the  substance  of  the  left  lobe  of  the  liver  and  give  rise  to  a  suppurating 
cavity  in  its  substance.  In  one  of  these  cases  death  was  caused  by  peritonitis  due 
to  leaking  from  the  abscess. 

An  empyema  or  an  abscess  in  the  base  of  the  right  lung,  suppuration  in 
or  around  the  right  kidne}",  or  a  localized  subphrenic  abscess  have  also 
been  described  as  extending  into  and  giving  rise  to  suppuration  inside 
the  liver.  But  in  these  cases  it  is  not  always  certain  whether  the  sup- 
puration began  in  the  organ  named  and  extended  into  the  liA^er,  or 
whether  it  originated  in  the  liver. 

Typhoid  Fever. — Hepatic  suppuration  is  rare  in  t}"phoid  fever.  The 
gaU-bladder  is  more  often  affected  than  the  hver  itself.  In  very  rare 
instances  a  sohtary  hepatic  abscess  foUows  typhoid  fever.  It  is  said  to 
be  less  rare  in  the  tropics  than  in  temperate  countries  (Bertrand  and 
Fontan  §),  and  possibly  this  is  due  to  the  influence  of  dysentery  or  to  the 
diminished  resistance  of  the  liver  induced  by  dysentery,  malaria,  alcohol- 
ism, etc.  When  a  sohtary  abscess  foUows  tj^phoid  fever,  it  may  be  due 
to  infection  from  some  secondary  abscess,  such  as  suppuration  of  the 
parotid,  and  is  rarely  a  direct  result  of  typhoid  fever. 

In  2000  fatal  cases  of  typhoid  fever  examined  at  Munich  Holscher  §  found 
twelve  cases  of  sohtary  hepatic  abscess:  his  figures  probably  include  Dopfer'sJI  927 
autopsies  on  typhoid  fever  with  ten  solitary  abscesses  of  the  liver  (Osier**).  W.  W. 
Keenft  has  collected  sixteen  additional  cases,  in  some  of  which  there  were  secondary 
abscesses  elsewhere  in  the  body;  in  Louis'  case — one  of  the  earliest  on  record — and 
in  Osler'slJ  there  was  parotitis,  and  in  Chvostek's  perichondritis  of  the  larynx 

*Weir:    Medical  Record,  1900,  p.  1137. 

t  Gilbert  and  Lippmann:   Soc.  med.  des  Hop.  Paris,  July  17,  1903. 

j  Bertxand  et  Fontan:    L'Hepatite  Suppuree,  Paris,  1895. 

§  Holscher:    Miinchen.  med.  Wochenschrift,  1891,  No.  4,  5. 

!|  Dopfer:    Miinchen.  med.  Wochenschrift,  1888. 
**  Osier:    Edinburgh  Med.  Journal,  1897,  vol.  ii,  p.  427. 

ft  Keen,  W.  W. :    Surgical  CompUcations  and  Sequels  of  Tvphoid  Fever,  1S9S, 
p.  246. 

tt  Osier:   Studies  in  Typhoid  Fever,  Johns  Hopkins  Hospital,  p.  380. 


SINGLE    OR  TROPICAL    ABSCESS.  125 

That  the  typhoid  bacilH  can  give  rise  to  a  sohtary  hejDatic  abscess 
is  supported  by  bacteriological  examination,  but,  as  a  rule,  there  is  a 
mixed  infection. 

In  two  cases  of  solitary  abscess  following  typhoid  fever  bacteriological  examina- 
tion showed  a  pure  culture  of  typhoid  baciUi  in  one,  while  in  the  other  typhoid 
bacilli  and  staphylococci  were  present.     (Cassuto.*) 

I  have  seen  one  case  where  a  single  hepatic  abscess  followed  enteric 
fever. 

An  Imperial  Yeomanry  trooper  aged  thirty  years,  who  had  never  had  dysen- 
tery or  been  previously  out  of  England,  was  inoculated  against  enteric  fever  in 
1900  when  on  his  way  to  South  Africa.  He  had  two  attacks  of  enteric  fever  in  the 
course  of  the  next  twelve  months  in  Africa;  when  convalescent  from  the  second 
attack  he  had  an  attack  of  acute  pneumonia  on  the  right  side,  followed  by  signs  sug- 
gesting empyema.  The  chest  was  aspirated  and  12  ounces  of  sanious  pus  containing 
liver  cells,  but  perfectly  sterile,  was  evacuated.  The  trocar  seemed  to  go  through 
a  tough  membrane.  The  next  day  Mr.  D.  Drew  excised  part  of  the  sixth  rib  and 
freely  opened  an  abscess  in  the  anterior  part  of  the  right  lobe  of  the  liver.  The 
patient  recovered,  was  invalided  home,  and  was  seen  in  December,  1901,  in  perfect 
health. 

Suppurating  Hydatid  Cyst,  etc. — When  a  hydatid  cyst  suppurates  the 
conditions  are  for  all  practical  purposes  the  same  as  a  single  hepatic 
abscess.  In  rare  instances  a  round-worm  in  the  intra-hepatic  bile-ducts 
may  give  rise  to  a  single  small  abscess,  but,  as  a  rule,  there  is  suppurative 
cholangitis  with  multiple  suppurating  foci. 

Single  Pycemic  Abscess. — ^A  single  hepatic  abscess  is  sometimes  due 
to  causes,  such  as  general  hsemic  infection,  or  infection  of  the  portal 
system,  which,  as  a  rule,  give  rise  to  multiple  abscesses.  In  exceptional 
instances  suppuration  or  infection  elsewhere  in  the  body  is  the  onl}^ 
cause  to  account  for  a  single  hepatic  abscess.  Thus  it  has  followed 
cutaneous  abscesses,  whitlow,  suppuration  of  the  parotid,  bronchiectasis 
(Muirf),  parametritis  and  pyosalpinx  (Roughtonf),  prostatic  abscess 
(Lancereaux§),  scarlet  fever,  ||  and  influenza  (Cimbali  **). 

A  single  hepatic  abscess  may  also  occur  as  the  result  of  emboli  de- 
rived from  the  portal  vein  or  its  tributaries.  Thus  in  exceptional 
instances  it  may  follow  gastric  ulcer, ff  appendicitis,  ulcers  in  the  colon, 
or  ligature  of  piles.  But  it  must  be  borne  in  mind  that  in  hepatic  sup- 
puration secondary  to  infection  from  the  alimentary  canal  there  are 
usually  multiple  areas  of  suppuration  and  not  a  solitary  abscess.  This 
is  true  with  the  exception  of  the  single  or  tropical  abscess  following 
amoebic  dysentery. 

A  single  loculated  or  areolar  abscess  may  be  the  late  stage  of  a  number 
of  neighbouring  areas  of  multiple  diffuse  suppuration,  due  to  pyle]ihlebitis 
or  suppurative  cholangitis  affecting  a  comparatively  large  intra-hepatic 
branch  of  the  portal  vein  or  bile-duct.     This  consideration  renders  it 

*  Cassuto:    Th^se  de  Paris,  1900. 
t  Muir:    Edinburgh  Hospital  Reports,  vol.  ii,  p.  100. 
X  Roughton:   St.  Bartholomew's  Hosp.  Reports,  vol,  xxi,  p.  176. 
§  Lancereaux:    Traits  des  Maladies  du  Foie  et  du  Pancreas,  1899. 
II  Guy's  Hospital  Museum,  No.  1294.         **  Cimbali:    Lo  Sperimentale,  1890. 
tt  Daiton,  N.:    Kings  College  Hospital  Reports,  vol.  ii,  p.  25. 


126  DISEASES    OF   THE    LIVEE. 

easj^  to  see  how  a  single  hepatic  abscess  may  occur  as  the  result  of  portal 
infections  which  are  usually  productive  of  multiple  hepatic  abscesses. 

In  appendicitis,  a  single  hepatic  abscess  is  very  rare  indeed;  it  some- 
times happens  that  a  single  abscess  is  diagnosed  and  operated  upon,  but 
the  patient  dies,  and  if  no  postmortem  is  possible,  the  actual  condition 
remains  doubtful;  when  an  autopsy  is  made,  multiple  abscesses  are 
usually  found.  The  two  following  cases  show  the  difficulty  in  forming 
a  positive  opinion  in  some  instances : 

Among  38  cases  of  perityphlitic  abscess  tabulated  by  Hawkins  *  there  was  one 
case  of  hepatic  abscess;  it  was  opened  and  a  half  pint  of  pus  let  out;  the  man  lived 
two  months  longer,  and  as  a  postmortem  was  refused,  there  may  possibly  have  been 
multiple  abscess. 

Stookef  reports  the  case  of  a  marine  aged  twenty-seven  who  had  attacks  of 
diarrhcEa  followed  by  signs  of  hepatic  abscess.  Forty  ounces  of  sweet  pus  were 
evacuated  from  the  liver  abscess,  but  when  the  man  died  nine  days  after  the  opera- 
tion there  were  multiple  abscesses  in  the  right  lobe  and  signs  of  suppuration  around 
the  vermiform  appendix.  Possibly  the  multiple  abscesses  were  secondary  to  the 
larger  abscess. 

In  the  following  case  appendicitis  almost  certainly  gave  rise  to  a 
single  hepatic  abscess : 

MortonJ  recorded  a  case  in  which  a  few  days  after  draining  an  abscess  in  con- 
nexion with  the  appendix,  an  abscess  in  the  liver  was  opened;  the  patient  recovered. 

In  the  following  case  a  large  abscess  due  to  the  union  of  originally 
separate  abscesses  was  clue  to  infection  from  the  appendix : 

A  girl  aged  seven  years  who,  except  for  a  stitch  in  the  right  side  of  the  abdomen 
for  more  than  a  year,  had  never  had  any  signs  of  appendicitis,  came  under  the  care 
of  Dr.  G.  H.  Hames  with  signs  of  right-sided  pleurisy.  Subsequently  hepatic  abscess 
was  diagnosed  and  several  operations  with  the  evacuation  of  pus  from  the  hver 
were  performed  by  Mr.  Charters  Symonds.  At  the  autopsy,  which  I  performed,  § 
the  vermiform  appendix  was  surrovmded  by  old  adhesions  and  recent  lymph,  and 
was  perforated  by  a  pin.  The  portal  vein  was  healthy.  The  Hver,  which  was 
greatly  enlarged,  contained  a  loculated  area  of  suppuration  as  large  as  one's  fist  in 
the  upper  and  back  part  of  the  right  lobe.  It  had  been  partially  opened  during 
life  and  contained  gelatinous  pus.  In  the  immediate  neighbourhood  there  were 
spreading  foci  of  suppuration.  The  rest  of  the  hver  was  of  a  bright  yellow  colour 
resembling  phosphorus  poisoning. 

DISPOSING  FACTORS. 

Geographical  Distribution. — Large  hepatic  abscess  is  a  disease  of 
tropical  climates,  and  cases  seen  in  this  country  are  usually  in  persons 
who  have  been  in  hot  climates  and  suffered  from  dysentery  or  even  from 
a  previous  hepatic  abscess  there.  Although  a  tropical  disease,  hepatic 
abscess  is  not  met  with  uniformly  in  different  parts  of  the  tropics;  thus, 
while  it  is  frequent  in  India,  Senegal,  Ceylon,  Mauritius,  Algiers,  Egypt, 
Java,  Sumatra,  Mexico,  Peru,  Chili,  it  is  much  less  common  in  the 
West  Indies,  China,  Brazil,  Guiana. 

Climate. — A  high   mean  temperature   very  decidedly  favours  the 

*  Hawkins,  H.  P.:    Diseases  of  the  Vermiform  Appendix,  p.  97. 
tStooke:    Brit.  Med.  Journ.,  1901,  vol.  i,  p.  342. 
j  Morton,  C.  A.:    Bristol  Medico-chirurgical  Journ.,  Dec,  1897. 
§  Rolleston:    Trans.  Path.  Soc,  vol.  xlix,  p.  106. 


SIXGLE    OR   TROPICAL    ABSCESS.  127 

occurrence  of  hepatic  abscess.  From  the  incidence  of  chills,  the  com- 
mencement of  the  cold  season  has  been  said  to  be  a  fa"\-oiirite  time  for 
the  development  of  hepatic  abscess.  But  from  an  analysis  of  the  236 
cases  of  hepatic  abscess  in  Calcutta  Rogers  *  found  that  there  was  no 
special  seasonal  prevalence. 

Acclimatisation. — It  would  appear  that  persons  who  have  recently 
become  resident  in  tropical  climates  are  more  likely  to  suffer  from  hepatic 
abscess  than  those  who  have  been  there  some  time. 

In  114  cases  E.  J.  Waringf  found  that  22  per  cent,  of  cases  of  abscess  occurred 
in  India  in  soldiers  who  had  been  less  than  one  j^ear  in  the  country',  10.5  per  cent, 
in  the  second  year,  and  10.5  per  cent,  in  the  third  3-ear.  Brydon's  J  figures,  however, 
tend  to  show  the  reverse,  viz.,  that  long  residence  seems  to  increase  the  Uabihty  of 
Europeans  to  abscess. 

Race. — Europeans  are  much  more  hable  to  hepatic  abscess  in  the 
tropics  than  the  natives. 

In  79,723  cases  of  dysentery  among  the  natives  of  India  collected  by  "\V.  J. 
Buchanan  §  there  were  only  127  cases  of  hepatic  abscess,  or  1  in  628  cases,  while  in 
7972  cases  of  dysentery  among  Europeans  in  India  there  were  441  cases  of  hepatic 
abscess,  or  1  in  18. 

But  when  natives  give  way  to  alcohol  they  are  more  likety  to  be 
attacked  by  abscess.  It  is  said  to  be  commoner  in  the  rich  than  in  the 
poorer  natives  of  India. 

The  greater  susceptibility  of  the  European  male  to  hepatic  abscess 
does  not  depend,  at  any  rate  entirely,  on  the  fact  that  he  is  not  accli- 
mated to  tropical  climates,  for  hepatic  abscess  is  verj^  rare  in  European 
women  and  children  in  the  tropics,  though  they  are  equaU}^  subject  to 
dysentery;  further,  it  does  not  depend  on  a  special  liability  to  dysentery, 
for  in  India  the  natives  are  more  subject  to  dysenter}"  and  less  to  hepatic 
abscess  than  Europeans.  The  important  factors  which  account  for  the 
greater  liabihty  of  European  males  to  hepatic  abscess  will  be  referred  to 
under  the  heading  of  Sex,  page  128. 

Occurrence  in  England. — Residence  in  England  is  not  a  disposing 
factor  to  hepatic  abscess,  but  it  is  convenient  to  refer  to  the  incidence 
of  hepatic  abscess  in  England  here.  As  already  mentioned,  most  of  the 
cases  observed  in  England  have  come  from  tropical  climates,  but  in  a 
certain  number  of  instances  the  patient  has  never  left  this  countr3\  The 
number  of  cases  seen  in  ordinary  hospital  practice  is  smaU,  probably 
not  more  than  two  or  three  a  year  for  each  of  the  large  London  hospitals. 

In  sixteen  years  there  were  1.3  fatal  ca-ses  of  single  hepatic  abscess  at  St.  George's 
Hospital;  in  3  of  these  the  fatal  abscess  was  a  recurrence,  the  patients  having  been 
previously  successfully  operated  upon.  Ten  of  the  cases,  all  men,  had  been  abroad, 
8  in  India,  1  in  China,  and  1  in  South  Africa.  In  15  fatal  cases  at  Guy's  Hos- 
pital in  twenty  years,  5  had  been  in  China,  India,  or  in  the  West  Coast  of  Africa, 
but  in  10  there  was  no  such  history,  and  several  patients  had  never  been  out  of 
England.     (Hilton  Fagge.  H) 

*  Rogers,  L.:    Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  844. 

t  Waring,  E.  J.:    Hepatic  Abscess,  p.  113. 

X  Brydon:    Quoted  by  Davidson,  AUbutt's  System  of  Medicine,  vol.  iv,  p.  139. 

§  Buchanan,  W.  J.:   Journ.  of  Tropical  Medicine,  vol.  i,  p.  173.  1899. 

II  Hilton  Fagge's  Text-book,  edited  by  Pye  Smith,  vol.  ii,  p.  525,  4th  Edit. 


128  DISEASES    OF    THE    LIVER. 

Alcoholism. — By  depressing  the  resistance  of  the  hver  alcohol  dis- 
poses to  hepatic  abscess.  Its  importance  in  this  respect  is  sho\\TL  by  the 
facts  that  abscess  is  seldom  seen  in  total  abstainers,  and  that,  conversely, 
natives  who  drink  may  suffer  from  hver  abscess  while  their  fellows  who 
are  teetotalers  escape. 

According  to  Sandwith,*  hepatic  abscess  is  met  witli  only  in  those  natives  of 
Egypt  who  are  addicted  to  alcohol.  In  40  cases  tabulated  by  E.  J.  Waring  f  only 
13,  or  32  per  cent.,  were  sober  and  temperate;  the  remainder,  67  per  cent.,  were 
intemperate. 

Diet. — ^A  stimulating  and  excessive  diet,  by  giving  rise  to  considerable 
physiological  congestion,  which  under  the  influence  of  the  tropical  chmate 
and  a  sedentary  life  may  become  pathological,  prepares  the  way  for 
hepatitis  and  so  for  abscess.  As  a  disposing  factor  errors  of  diet  are 
probably  A^ery  greatly  inferior  to  alcohohc  excess. 

Malaria. — By  diminishing  the  resistance  of  the  liver  and  producing  a 
certain  amount  of  hepatitis,  malaria  disposes  to  hepatic  abscess  and  in 
a  minor  degree  plays  much  the  same  kind  of  role  as  alcohohsm.  Hepatic 
abscess,  however,  occurs  in  places  where  malaria  is  unknoT\Ta,  as  in  the 
Sej^chelles  group  and  the  island  of  Rodrigues.  (Da"vddson.  j)  Malaria  and 
dysentery  occur  so  frequently  in  the  same  districts  that  malaria  is  often 
an  antecedent  condition  of  hepatic  abscess.  It  is  not,  however,  a  true 
cause  of  hepatic  suppuration. 

Yellow  fever  may  precede  the  development  of  an  hepatic  abscess, 
but  this  is  probably  merely  accidental,  and  there  is  no  reason  to  think 
that  there  is  any  direct  relation  between  them;  though  no  doubt  after 
yellow  fever  the  resistance  of  the  liA'er  is  weakened  and  the  organ  more 
liable  to  infection. 

Sex. — Single  tropical  abscess  is  much  commoner  in  males  than  in 
females.  This  appUes  to  adults,  for  in  children — who  are,  however, 
rarely  the  subjects  of  a  single  hepatic  abscess — the  incidence  is  about 
equal  in  the  two  sexes. 

In  E.  J.  Waring's  300  Indian  cases  291  were  males  and  9  females.  In  13  fatal 
cases  at  St.  George's  Hospital  11  were  males;  in  one  of  the  females  the  abscess  was 
probably  connected  mth  cholelithiasis. 

The  greater  predominance  of  the  male  sex  is  due  to  a  number  of 
factors.  First,  the  larger  number  of  male  Europeans  resident  in  tropical 
chmates  must  be  taken  into  account,  for  Europeans  are  much  more 
subject  to  abscess  than  natives.  But  even  after  allowing  for  this,  males 
are  more  subject  to  abscess  than  women;  for  though  it  appears  that 
dysentery  affects  European  men  and  women  equally,  abscess  seldom 
occurs  in  women.  (Manson.  §)  The  factors  which  have  been  thought  to 
increase  the  tendency  of  European  males  to  abscess  are :  (i)  Alcohohsm, 
which  disposes  to  hepatitis  and  favours  infection  by  reducing  the  resist- 

*  Sandwith:   Quoted  by  Davidson,  AUbutt's  System,  vol.  iv,  p.  136. 
t  Waring,  E.  J.:    Hepatic  Abscess,  p.  114. 
t  Davidson:    AUbutt's  System,  vol.  iv,  p.  137. 
§  Manson,  P.:   Tropical  Diseases,  p.  442. 


SINGLE    OR    TROPICAL    ABSCESS.  129 

ance  of  the  organ;    (ii)  greater  tendency  to  exposure  to  chills,  and  (iii) 
greater  liability  to  blows  in  the  hepatic  region. 

Age. — Hepatic  abscess  is  a  disease  of  adult  life  and  is  rare  in  children 
and  in  old  persons. 

In  227  fatal  cases  tabulated  by  Waring,*  112,  or  48.4  per  cent.,  were  between 
the  ages  of  twenty  and  thirty.  It  must  be  remembered,  however,  that  the  cases 
were  from  the  Indian  army,  which  contained  a  very  large  number  of  men  about 
this  age.  The  oldest  case  met  vnth.  by  Waring  was  a  pensioner  aged  seventy-two 
years,  and  the  youngest  in  a  girl  aged  fifteen  j^ears. 

In  young  children  large  hepatic  abscesses  are  fare,  and  when  the}' 
do  occur,  are  more  often  due  to  worms  in  the  bile-ducts,  to  traumatism, 
or  to  appendicitis.  Cases  of  tj^pical  tropical  abscess  do,  however,  occur 
in  early  life. 

Ambergt  tabulates  12  cases  in  children  due  to  dysentery;  in  only  one  (Slaugh- 
ter's!) were  motile  amoebae  found  in  the  pus,  though  dead  amoebae  were  seen  in 
the  pus  of  Gneftos'§  case.     Amoebic  abscess  is  therefore  very  rare  in  children. 

Moncorvo  i|  records  the  case  of  a  child  aged  two  years  who  recovered  after  500 
grammes  of  pus  had  been  removed  from  the  abscess.  Arnott**  described  a  fatal 
case  in  a  child  aged  two  and  a  half  years,  but  apparently  no  autopsy  was  performed 
Finizioft  reports  a  fatal  case  of  hepatic  abscess  subsequent  to  dj'sentery  in  a  boy 
aged  six  years.  In  a  boy  aged  nine  years  the  abdomen  was  so  distended  that  the 
condition  was  thought  to  be  ascites.     (Hatch.+J) 

MORBID   ANATOMY. 

Situation. — Between  60  and  80  per  cent,  of  large  single  abscesses  are 
in  the  right  lobe  of  the  liver.  Occasionally  a  large  abscess  may  occupy 
parts  of  both  the  right  and  left  lobes. 

Of  E.  J.  Waring's  cases,  67  per  cent,  were  in  the  right  lobe;  6.6  per  cent,  in  the 
left  lobe;  and  14.5  per  cent,  in  both  the  right  and  the  left  lobe.  In  Rouis'§§  series 
78.6  per  cent,  were  in  the  right  lobe,  16.8  per  cent,  in  the  left,  and  4.6  per  cent,  in 
the  Spigelian  lobe. 

From  injection  with  methylene-blue,  Serege  ||  ||  comes  to  the  conclusion  that  the 
blood  from  the  stomach  and  spleen  is  carried  into  the  left  lobe,  while  that  from  the 
pancreas  and  intestines  passes  into  the  right  lobe.  This  theory  ser\^es  in  part  to 
explain  the  greater  frequency  of  abscess  in  the  right  lobe.  In  addition,  the  right 
lobe  is  so  much  the  bigger  of  the  two  that  it  naturally  receives  the  larger  share  of 
blood.  Rogers***  suggests  that  the  frequency  with  which  the  ascending  colon  and 
hepatic  flexure  are  involved  in  amoebic  dysentery,  thus  allowing  amoeba?  to  pass 
across  the  peritoneum  to  the  surface  of  the  liver,  may  also  account  for  the  preponder- 
ance of  abscess  in  the  right  lobe. 

The  abscess  is  often  situated  deeply  in  the  right  lobe  towards  its 
posterior  and  upper  border.  ^Vlien  in  this  situation  it  maj^  work  its 
way  forward  and  present  anteriorly,  but  more  often  it  projects  upwards 

*  Waring,  E.  J.  :  Abscess  in  the  Liver,  p.  112. 
fAmberg:    Johns  Hopkins  Hospital  Bull.,  Dec,  1901. 
i  Slaughter:   Virginia  Med.  Monthlv,  Oct.,  1895. 
lOneftos:    Deutsche  med.  Wochen.,  1891,  S.  853. 
II  Moncorvo:  Rev.  Mensuelle  des  Malad.  de  I'enfance,  Dec,  1899. 
**  Arnott:    Brit.  Med.  Journ.,  1903,  vol.  i,  p.  189. 
ttFinizio:    La  Pediatria,  1896,  p.  310. 
tt  Hatch:    Indian  Med.  Gaz.,  Aug.,  1898. 

§§  Rouis:    Recherches  sur  les  suppurations  endemeques,  1860,  Paris. 
JlllSeregS:  Soc.  Med.  des  Hop.,  April  26,  1901.     Journ.  de    Med.  de  Bordeaux, 
Mav  25,  June  1  and  8,  1902. 
***  Rogers,  L.:    Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  8.50. 
9 


130  DISEASES    OF   THE    LIVER. 

under  the  diaphragm.  In  the  latter  case  the  existence  of  an  abscess  is 
often  very  difficult  to  determine  Tsdth  certainty  by  percussion,  as  it  may 
carry  the  diaphragm  upwards,  and  if  the  lung  is  adherent  to  the  chest 
wall  there  will  be  comparatively  little  duhiess.  In  such  cases  skiagraphy 
is  of  great  service,  by  showing  the  position  and  amount  of  movement 
of  the  right  leaflet  of  the  diaphragm.  The  under  surface  of  the  right 
lobe  of  the  hver  close  to  the  hepatic  flexure  of  the  colon  is  another  favourite 
site  of  abscess.  According  to  Lafieur  *  and  Rogers,  it  is  probable  that 
amcebse  may  pass  through  the  walls  of  the  colon  and  infect  the  surface 
of  the  liver  at  this  point. 

"WTien  an  abscess  is  near  the  surface  of  the  hver  and  close  to  the 
suspensorv^  ligament,  it  may  rupture  into  the  space  between  the  two 
layers  of  that  peritoneal  hgament  and  fonii  an  abscess  between  the  liver 
and  diaphragm.  This  has  been  spoken  of  as  a  supra-hepatic  abscess  by 
Canthe,t  who,  however,  considers  that  this  form  of  abscess  begins  in  the 
lyinphatics  in  the  ligaments  and  not  in  the  liver. 

Number. — ^A  large  abscess  may  be  the  only  focus  of  suppuration  in 
the  liver  or  it  may  be  associated  ■udth  one  or  more  abscesses,  usually 
smaUer. 

In  E.  J.Waring's  300  fatal  cases  177,  or  59  per  cent.,  were  solitary  abscesses, 
and  in  33,  or  11  per  cent.,  there  were  two  abscesses.  Davidsont  gives  75  per  cent. 
as  solitary,  thus  agreeing  with  Rouis,  11  per  cent,  with  two  abscesses,  and  14  per 
cent,  with  more  than  two.  In  13  fatal  cases  at  St.  George's  Hospital  there  was  a 
single  abscess  in  ten. 

The  smaller  abscesses  may  be  secondary'  and  due  to  infection  from 
the  originaUy  single  abscess,  or  they  may  belong  to  a  series  of  small 
abscesses  which  have  imited  to  form  an  areolar  abscess.  Two  or  even 
three  large  abscesses  may  be  independent  in  origin.  Godlee  §  beheves 
that  many  of  the  cases  of  a  second  abscess  fohowing  a  previous  one  are 
due  to  the  drainage-tube  having  been  removed  too  soon,  or  to  some 
diverticulum  of  the  original  abscess  having  been  imperfectly  explored 
and  drained. 

The  shape  of  an  abscess  shows  considerable  variation;  usually  it  is 
round,  but  it  may  be  oval  or  irregular,  and  when  due  to  the  union  of 
pre^dously  separate  abscesses,  may  be  branching  or  areolar. 

The  size  of  a  single  abscess  varies  very  greatly.  Not  uncommonly  it 
contains  three-quarters  of  a  pint  of  pus,  but  as  much  as  16  or  even  19 
pints  have  been  recorded. 

Pathological  Appearances  of  the  Liver. — ^The  surface  of  the  liver 
may  show  recent  inflammation  and  adherent  fibrin  over  the  abscess,  or, 
when  the  process  is  of  some  duration,  fibrous  adhesions  uniting  it  to  the 
diaphragm,  abdominal  wall,  or  adjacent  viscera.  These  are  most  fre- 
quently met  with  between  the  convexity  of  the  right  lobe  and  the  dia- 
phragm;  the  abscess  may  then  project  upwards  under  the  dome  of  the 

*  Lafleur:   Allbutt's  Svstem  of  Medicine,  vol.  iv,  p.  156. 
.  fCanthe,  J.:    Brit.  Med.  Journ.,  1899,  vol.  ii,  p.  646. 
t  Davidson:   Allbutt's  System  of  Medicine,  vol.  iv,  p.  141. 
§  Godlee,  R.  J.:  Medico-chirurg.  Trans.,  vol.  bcxxv,  p.  119,  1902. 


SINGLE    OR    TROPICAL    ABSCESS. 


131 


diaphragm  and  give  rise  to  comparatively  little  enlargement  of  the  liver 
in  a  downward  direction. 

In  its  earliest  stage  a  liver  abscess  appears  as  a  pale,  softened  area, 
sometimes  irregular  in  shape  from  the  union  of  two  or  more  such  foci. 
This  condition  of  commencing  suppuration  if  aspirated  may  be  recog- 
nized by  finding  cylinders  of  liver  cells  in  the  blood-stained  material 
withdrawn,  which,  however,  has  no  naked-eye  resemblance  to  pus.  The 
softened  areas  break  down  into  recent  abscess  cavities  which  have  ragged 
walls  lined  by  necrosing  liver  tissue.  Immediately  around  the  spreading 
abscess  the  liver  substance  is  soft- 
ened, buff-colored  from  swelling, 
degeneration,  and  necrosis  of  the 
liver  cells  and  infiltration  with 
polymorphonuclear  leucocytes.  The 
vessels  contain  emboli  of  pyogenic 
cocci.  As  the  inflammatory  change 
spreads    outwards    it    may    set    up 


Fig.  20. — Single  Abscess  with  a  Definite 
Capsule. 
A  glass  rod  shows  where  it  ruptured  into 
the  inferior  vena  cava.  From  a  specimen 
(series  ix,  171m)  in  St.  George's  Hospital  Mu- 
seum.      (Drawn   by  L.   Jones,    M.B.,   F.R.C.S.) 


Fig.  21.— Sec  I  ion  df  the  Right 
Lobe  of  the  Liver,  showing  the  Union 
OF  A  Number  of  Separate  Abscesses 
INTO  AN  Areolar  Abscess  Cavity. 

From  a  specimen  (series  ix,  171c)  in 
St.  George's  Hospital.  (Drawn  Idv  Dr. 
E.  A.  Wilson.) 


suppurative  thrombosis  in  the  portal  spaces  and  thus  give  rise  to  foci 
of  suppuration  in  the  neighbourhood,  which  may  eventually  open  into  the 
original  abscess. 

In  an  abscess  of  some  standing  there  is  lining  of  granulation  tissue, 
which  is  ragged  at  first,  and  later  becomes  smooth.  Outside  this  there 
is  a  fibrous  capsule  which  runs  into  and  invades  the  surrounding  liver 
substance  for  a  short  distance.  The  internal  lining  of  granulation  tissue 
may  have  debris  and  fibrin  adherent  to  it,  and  often  shows  necrosis 
on  the  internal  surface.  The  granulation  tissue  contains  newly  formed 
vessels  and  in  its  deeper  layers  shows  developing  fibrous  tissue.     In  this 


132  DISEASES    OF   THE    LIVER. 

way  a  capsule  is  formed,  which  in  old  abscesses  is  of  considerable  extent 
and  is  formed  of  dense,  weU-formed  fibrous  tissue.  This  fibrous  tissue 
invades  the  Uver  for  a  short  distance  and  passes  between  the  hver  cells, 
which  are  flattened  and  often  spindle  shaped,  so  as  to  suggest  the  view, 
now  known  to  be  erroneous,  that  they  become  transformed  into  fibrous 
tissue.  The  liver  cells  prohferate  and  give  rise  to  columns  of  smaU 
cubical  cells,- — the  so-caUed  new  bUe-ducts, — and  as  a  result  the  developing 
fibrous  capsule  around  an  abscess  of  some  duration  contains  altered 
liver  cells  and  pseudo-bUe  canalicuU.  In  old  abscesses  the  capsule  is 
often  pigmented  and  ma}'  undergo  calcareous  infiltration.  Occasionally 
suppurating  foci  are  found  outside  the  comparatively  well-formed  wall 
of  a  single  abscess. 

The  rest  of  the  liver  is  usually  enlarged,  and  after  evacuation  of  the 
abscess  heavier  than  in  health.  In  132  cases  tabulated  by  Waring  this 
was  the  condition  of  the  organ  in  113.  The  increase  in  size  is  chiefly  due 
to  parenchymatous  inflammation  and  cloudy  sweUing,  but,  in  addition, 
compensatory  hypertrophy  of  the  remainder  of  the  hver  occurs.  In 
chronic  cases  where  a  flstula  has  existed  increase  in  size  of  the  hver  may 
be  due  to  lardaceous  disease.  In  some  instances  there  may,  in  addition, 
be  pylephlebitic  abscesses  in  the  substance  of  the  liver.  In  rare  instances 
the  liver  substance  may  have  a  striking  appearance,  being  of  a  bright 
yeUow  colour  and  firm  consistence,  resembhng  the  appearances  seen 
in  phosphorus  poisoning. 

I  met  with  this  appearance  in  a  case  of  a  loculated  liver  abscess  due  to  infection 
derived  from  the  appendix,  which  contained  a  pin.*  In  St.  Bartholomew's  Hospital 
Museum  there  is  a  specimen  (2196d)  of  multiple  abscess  showing  this  appearance. 
E.  J.  Waringt  in  113  fatal  cases  mentions  one  where  the  liver  had  this  aspect. 

The  scars  of  former  abscesses  that  have  been  opened  are  sometimes 
seen.  Abscess  is  xery  rarely  found  in  a  genuinely  cirrhotic  hver;  in 
Waring's  113  cases  the  rest  of  the  hver  was  cirrhotic  in  two. 

In  the  so-caUed  amoebic  abscesses  of  the  hver  the  histological  appear- 
ances described  are  so  peculiar  that  special  reference  must  be  made  to 
them.  In  small  and  recent  abscesses  there  is  a  glair\' .translucent  fluid, 
which  when  removed  leaves  a  shreddy,  spongj'  waU.  The  wall  is  irregular 
from  the  remains  of  the  portal  canals,  which  are  left  by  the  necrosis  and 
disintegration  of  the  surrounding  liver  ceUs.  The  liver  ceUs  undergo 
necrosis  probably  as  the  result- of  the  action  of  toxic  substances  manu- 
factured by  the  amcebge,  and  then  liquefy  and  disintegrate.  Amoebae 
are  found  in  the  capillaries  in  the  immediate  neighbourhood  of  the 
abscess. 

There  is  a  remarkable  absence  of  leucocytic  massing  in  the  neighbour- 
hood of  the  small  abscesses  which  is  quite  characteristic  (LafleurJ). 
The  i^rocess  is  one  of  colliquative  necrosis  rather  than  of  inflammation. 
Rogers,  §  however,  who  regards  the  small  multiple  amoebic  abscesses  as 

*  Trans.  Path.  Soc,  vol.  xlix,  p.  106. 

t  E.  J.  Waring:   Abscess  of  the  Liver,  p.  137. 

X  Lafleur:    Allbutt's  System  of  Medicine,  vol.  iv,  p.  15S. 

§  Rogers,  L.:   Brit.  Med.  Journ..  1903.  vol.  i.  p.  131S. 


SIXGLE    OR   TROPICAL    ABSCESS.  133 

due  to  a  mixed  infection  of  amoebae  and  pyogenic  cocci,  figures  small-cell 
infiltration  in  these  minute  abscesses. 

Large  chronic  amoebic  abscesses  differ  little  from  the  appearances  in 
other  chronic  hepatic  abscesses.  Amoebae  are  much  less  numerous  than 
in  the  recent  smaU  amoebic  abscesses,  but  are  found  in  the  same  situation, 
viz.,  in  the  wall  of  the  abscess  cavity. 

Contents  of  the  Abscesses.- — In  large  abscesses  the  character  of  the 
pus  may  vary  very  considerably;  it  may  be  white  and  creamy,  j^ellow, 
brownish  red  or  chocolate  colour,  green;  thick,  mucoid,  or  even  serous. 
The  red  colour  is  due  to  admixture  with  blood  and  the  remains  of  the 
liver  tissue.  In  amoebic  abscess  the  contents  of  the  smaller  abscesses 
are  translucent,  glairy,  and  do  not  flow  easily.  In  larger  amoebic  ab- 
scesses the  fluid  is  very  viscid  and  does  not  resemble  ordinary  pus. 

Microscopically  the  amoebic  abscesses  contain  amoebae,  which  are 
naturally  more  numerous  in  the  recent  abscesses,  necrosing  liver  cells,  and 
red  blood-corpuscles.  Very  few  leucocytes  are  present  and  the  contents 
thus  differ  markedly  from  ordinary  pus.  Charcot-Leyden  crystals  have 
been  found.  (Kruse  and  Pasquale.*)  Amoebic  abscesses  may  also  con- 
tain various  kinds  of  micro-organisms,  such  as  streptococci,  staphylococci. 
Bacillus  coli.  The  pus  is  said  to  have  a  mawkish  taste,  and  is  not,  as  a 
rule,  offensive.  In  abscesses  on  the  under  surface  of  the  liver  in  contact 
with  the  bowel  the  contents  may  have  a  very  faecal  odour,  due  probably 
to  secondary  infection  with  members  of  the  colon  group. 

Bacteriology. — Hepatic  abscesses  may  be  divided  into  (i)  those 
which  contain  amoebae — caUed  dysenteric  by  Kartuhs ;  and  (ii)  the  non- 
amoebic,  due  to  micro-organisms,  usually  absorbed  from  the  alimentarj^ 
tract,  and  termed  by  Kartulis  idiopathic. 

Amoebae. — Since  the  discovery  of  amoebae  in  dysenter}^  and  in  hepatic 
abscesses,  some  uncertainty  has  naturaUy  arisen  as  to  what  proportion 
of  the  cases  of  tropical  liver  abscesses  are  due  to  this  cause  and  to  what 
extent  amoebae  are  concerned  in  the  production  of  suppuration. 

The  Amoeba  coli  described  in  1875  by  Losch  in  dysenteric  dejecta  and  by  Kartulis 
of  Alexandria  in  1887  in  the  contents  of  an  hepatic  abscess,  is  a  unicellular,  motile 
organism.  It  varies  in  size,  its  diameter  being  from  6  to  35  /',  more  commonly 
between  12  and  26  ,«.  It  has  a  nucleus  which  stains  badly,  and  has  an  outer  layer 
or  ectoplasm  and  a  larger  and  inner  portion — entoplasm.  Its  pseudopodial  move- 
ments cease  when  the  temperature  falls  below  75°  Fahr.,  hence  when  stools  or  pus 
are  examined  microscopically  for  amoeba?,  a  warm  stage  is  necessary. 

The  causal  relation  of  amoebae  to  the  amoebic  abscesses  of  the  liver 
has  given  rise  to  a  considerable  amount  of  discussion,  and  the  question 
is  very  far  from  being  settled.     The  following  views  have  been  held. 

(1)  Kartulis,t  who  first  recognized  amcebas  in  the  pus  of  liver  ab- 
scesses, believed  that  they  played  an  important  accessory  part  in  the 
production  of  abscesses,  by  conveying  pus-producing  micro-organisms  to 
the  liver  and  by  rupturing  the  hepatic  capillaries  by  their  active  move- 

*  Kruse  and  Pasquale:  Zeitschrift  f.  Hyg.,  Bd.  xvi,  1894.  Quoted  by  Lafleur, 
AUbutt's  System  of  Medicine,  vol.  iv,  p.  154. 

t  Kartulis:  Centralblatt  f.  Bakt.,  Bd.  ii,  1887.  Virchow's  Archiv,  Bd.  cxviii, 
1889. 


134  DISEASES    OF   THE    LIVER. 

merits;  the  production  of  pus  not  being  due  to  amoebae,  but  to  the  pyo- 
genic micro-organisms. 

(2)  Kruse  and  Pasquale  regarded  the  disintegration  of  the  Hver  and 
abscess  formation  as  due  to  a  direct  co-operation  of  the  amoebae  with 
micro-organisms. 

(3)  Councihnan  and  Lafleur  *  beheve  that  the  amoebae  alone  are 
responsible  for  the  abscess,  since  in  the  smallest  abscesses  bacteria  are 
absent  while  amcebae  are  plentiful.  In  larger  abscesses  bacteria  are  not 
numerous,  and  the  lesions  are  not  like  those  produced  by  bacteria. 
These  lesions  are  largely  necrotic,  and  are  thought  to  be  due  to  a  soluble 
toxine  manufactured  by  the  amoebae. 

(4)  It  has  been  suggested  by  Miss  Sheldon  Amos  f  that  the  presence 
of  amoebae  in  liver  abscesses  is  a  secondary  infection  and  that  the  amoebae 
only  gain  a  footing  in  the  liver  when  it  has  been  damaged  by  bacterial 
invasion.  This  view  is  supported  by  the  fact  that  amoebae  are  absent 
from  cerebral  abscesses  in  cases  where  they  are  found  in  the  pus  from 
the  liver.  Kelsch  and  Nimier  X  deny  that  amoebae  are  responsible  for 
the  production  of  liver  abscess;  and  there  is  rather  a  tendenc}^  at  present 
to  doubt  the  importance  of  amoebae  as  factors  in  the  production  of  hepatic 
abscess,  even  though  they  may  be  found  in  the  pus.  L.  Rogers,  §  from 
observations  in  Calcutta,  has  recently  endorsed  Councilman  and  Lafleur's 
view  that  amoebae  alone  give  rise  to  large  hepatic  abscesses,  and  in  the 
view  that  amoebae  may  work  their  way  froTii  the  bowel  across  the  peri- 
toneum to  infect  the  surface  of  the  liver. 

When  an  abscess  is  opened,  amoebae  may  not  be  found  in  the  pus  until 
some  days  have  elapsed;  this  has  been  explained  by  the  fact  that  the 
amoebae,  are  chiefly  found  in  the  walls  of  the  abscess  and  not  in  its  con- 
tents. In  hepatic  abscesses  examined  in  England,  Manson||  has  found 
amoebae  in  considerably  over  50  per  cent. 

Bacteria. — In  non-amoebic  cases  examination  of  the  pus  bacterio- 
logically  shows  discordant  results.  In  some  instances  the  pus  is  sterile; 
this  has  been  explained  by  supposing  that  in  chronic  cases  the  micro- 
organisms originally  present  have  died  out.  Pus-producing  micro- 
organisms have  frequently  been  found,  such  as  the  Staphylococcus 
pyogenes  aureus,  albus,  citreus,  and  streptococci.  Typhoid  bacilli  have 
been  found  in  pure  culture  (Cassuto  **)  or  in  combination  with  other 
micro-organisms.  Ordinary  pneumococci,  Friedlander's  pneumobaciUus, 
Bacillus  pyocyaneus,  and  the  colon  bacillus  are  also  sometimes  present. 

Condition  of  the  Pleura.: — Inflammation  of  the  pleura  is  a  very 
common  occurrence  in  hepatic  abscess;  it  may  be  due  to  a  spread  of 
infection  along  the  lymphatics  and  may  be  dry,  serous,  or  purulent. 
Pleurisy  may  give  rise  to  universal  adhesions  and  so  prevent  the  abscess 
rupt\iring  into  the  pleura,  but  thus  favour  its  rupture  into  the  lung.     An 

*  Councilman  and  Lafleur:   Johns  Hopkins  Hosp.  Reports,  vol.  ii,  1891. 
t  Miss  Sheldon  Amos:   Journ.  Path,  and  Bacteriolog.,  vol.  viii,  p.  346,  1902. 
i  Kelsch  and  Nimier:   Bull.  Acad,  de  Med.  Paris,  1900,  t.  xliii,  p.  237. 
§  Rogers,  L. :   Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  844;   1903,  vol.  i,  p.  1315. 
II  Manson :  Tropical  Diseases,  p.  456,  1903. 
**Cas.suto:   These  de  Paris,  1900, 


SINGLE    OR   TROPICAL   ABSCESS.  135 

empyema  due  to  this  course  may,  as  in  Duplant's  case,  be  encysted 
between  the  lobes  of  the  huig.  Rupture  or  direct  leakage  of  an  abscess 
into  the  pleura  will  give  rise  to  a  large  empyema.  This  will  be  referred 
to  later. 

Condition  of  the  Lungs. — The  lower  lobe  of  the  right  lung  may  be 
compressed  by  the  upward  pressure  of  the  liver  and  diaphragm,  or  by  a 
pleural  effusion;  or  if  it  is  adherent  to  the  diaphragm  it  may  become 
inflamed  from  direct  extension  of  inflammation  from  the  abscess  through 
the  diaphragm  or  the  abscess  may  burst  into  the  lung.  In  cases  where 
the  abscess  has  leaked  into  the  hepatic  veins  or  into  the  inferior  vena 
cava  there  may  be  secondary  pysemic  abscesses  in  the  lungs.  The 
rupture  of  an  hepatic  abscess  into  the  lung  will  he  referred  to  later. 

CLINICAL   PICTURE. 

SYMPTOMS. 

Latency;  Onset;  Fever;  Sweating;  Rigors;  Pain;  Shoulder  Pain;  Tender- 
ness; Cough;  Digestive  Disturbances;  Arthritis;  Nervous  Disorders. 

There  is  very  great  variety  both  in  the  individual  symptoms  and 
also  in  their  association;  this  is  shown  by  the  number  of  conditions  for 
which  hepatic  abscess  has  been  mistaken.  (Vide  Diagnosis.)  Very  fre- 
quently the  symptoms  suggest  rather  than  definitely  point  to  the  presence 
of  hepatic  abscess. 

Latency, — An  abscess  may  remain  perfectly  latent  and  only  be  found 
at  death;  according  to  Rouis,  this  occurs  in  13  per  cent.  In  some  cases 
there  are  no  definite  symptoms  or  signs  until  the  abscess  ruptures  and 
rapidly  brings  about  a  fatal  result. 

The  onset  of  symptoms  is  gradual,  as  a  rule,  and  is  ushered  in  l^y 
malaise,  languor,  and  general  debility,  and  the  signs  and  symptoms  of 
acute  congestion  of  the  liver  and  acute  hepatitis.  (Vide  p.  117.)  In- 
definite malaise  may  precede  by  many  weeks  any  definite  evidence  of 
abscess.  In  some  instances  there  is  an  acute  onset  with  shivering  or  a 
rigor,  and  the  condition  may  imitate  pneumonia  of  the  right  lower  lobe. 

Fever  is  perhaps  the  most  constant  sign  of  hepatic  abscess.  The 
temperature  varies.  It  may  be  continuous  at  first,  then  remittent,  and 
in  the  later  stages  intermittent.  It  may  closely  imitate  malaria,  or  be 
extremely  irregular.  In  chronic  cases  the  temperature  may  be  normal, 
while  in  severe  and  advanced  forms  of  the  disease  it  may  be  low  and  even 
abnormal.*  In  exceptional  instances  there  may  be  little  or  no  fever, 
even  with  a  large  and  recent  abscess.  Cases  have  been  met  Avith  in 
which  there  is  an  absence  of  pyrexia  from  start  to  finish. 

Moir  t  records  a  case  Avhere  the  abscess  contained  70  ounces  of  pus  while  tiie 
temperature  ranged  between  subnormal  and  99°. 

Sweating. — Nocturnal  sweats  may  be  very  profuse.  Pers])iration 
often  occurs  during  the  day  when  tlie  ])atient  drops  off  to  sloo]).     In 

*  Smith,  .Johnson:   Brit.  Med.  .Jour.,  1900,  vol.  ii,  550. 
t  Moir,  D.  M. :  Indian  Med.  Gaz.,  .June,  1897. 


136  DISEASES    OF   THE    LIVER. 

fact,  the  sweating  is  more  related  to  sleep  than  to  the  night  hours,  and 
is  chiefly  nocturnal  because  sleep  is  more  general  then. 

Rigors  are  often  met  with  in  the  course  of  the  disease.  In  some  cases 
there  is  a  single  rigor  at  the  onset  or  early  in  the  course  of  the  disease; 
in  others  there  are  frequent  rigors,  while  again  they  sometimes  only 
come  on  towards  the  end  of  the  case.  A  feeling  of  chilliness  often  accom- 
panies the  evening  rise  of  temperature. 

Pain  over  the  liver  and  a  sense  of  fulness  in  the  right  hypochondrium 
are  very  commonly  present.  Though  pain  may  be  present  from  the 
start  of  suppuration,  it  is  much  more  in  evidence  when  the  abscess  is 
large  and  approaching  the  capsule  of  the  liver,  than  early  in  the  process 
or  when  the  abscess  is  deeply  situated.  The  pain  may  be  constant  and 
dull,  probably  from  increased  tension  inside  the  liver;  this  is  usually 
early  in  the  course  of  the  disease,  or  intermittent  and  sharp  and  stabbing, 
and,  like  pleuritic  pain,  brought  on  by  respirator}^  movements.  It  may 
be  actually  due  to  pleurisy  or  to  inflammation  of  the  capsule  of  the 
liver,  and  is  then  rather  a  late  symptom.  Pain  on  swallowing,  due  to 
food  disturbing  the  liver,  as  it  enters  the  stomach,  is  mentioned  by 
Manson.* 

Shoulder  Pain. — In  abscess,  as  in  some  other  affections  of  the  liver, 
pain  may  be  referred  to  the  shoulder,  and  may  be  felt  over  the  scapula 
or  at  the  tip  of  the  acromion  process.  It  has  been  suggested  that  this 
localization  may  depend  on  the  communication  between  the  nerve  to 
the  subclavius  muscle  and  the  phrenic  nerve.  According  to  Manson,t 
it  occurs  in  about  one-sixth  of  the  cases.  It  is  most  frequently  present 
when  the  abscess  is  in  the  upper  part  of  the  right  lobe.  In  cases  of 
abscess  in  the  left  lobe  the  pain  may  be  referred  to  the  left  shoulder. 
In  very  rare  instances  the  pain  is  bilateral.     (E.  J.  Waring.J) 

Tenderness. — On  deep  palpation  or  percussion  tenderness  of  the 
liver  is  generally  elicited.  Localized  tenderness  over  some  part  of  the 
surface  of  the  liver  is  perhaps  the  least  unsatisfactory  sign  of  hepatic 
abscess.  §  By  methodical  palpation  over  the  liver  a  localized  tender 
spot  may  be  found  which  serves  as  a  useful  guide  to  the  position  of  the 
abscess.  Occasionally  vomiting  is  constantly  induced  by  pressure  on 
one  spot.     (Smits.  ||) 

Cough. — In  hepatic  abscess  there  is  often  a  spasmodic,  hacking  cough, 
which  is  usuall}"  worse  at  night,  and  may  be  ineffectual  or  unaccompanied 
by  sputum.  It  may  be  due  to  irritation  of  the  pleura  over  the  dia- 
phragm, to  actual  pleurisy,  or  possibly  merely  to  reflex  irritation  from 
the  liver.  It  is  not  peculiar  to  liver  abscess.  Wlien  the  abscess  dis- 
charges through  the  lung,  severe  cough  comes  on  and  expectoration  may 
be  copious.  As  much  as  4  pounds  of  pus  has  been  brought  up  in  twenty- 
four  hours.**    The  colour  of  the  expectorated  matters  differs  greatly  in 

*  Manson,  P. :   Tropical  Diseases,  Ed.  i,  p.  353. 
t  Manson,   P. :    Tropical  Diseases,   p.   448,   1903. 
X  Waring,  E.  J. :   Abscess  of  the  Liver,  p.  147. 
§  Smith,  Johnson:    Brit.  Med.  Journ.,  1900,  vol.  ii,  p.  550. 
li  Smits:   Archiv  f.  klin.  Chirurg.,  Bd.  Ixi,  S.  173,  1900. 
"<    **  Waring:    Abscess  of  Liver,  p.  153. 


SINGLE    OR   TROPICAL    ABSCESS.  137 

different  cases  ;  it  may  be  mixed  with  Ijile.  In  amoebic  abscesses 
amoebsB  may  be  found  in  the  sputum  before  the  abscess  has  burst  into 
the  lung. 

Digestive  Symptoms. — Vomiting  appears  to  be  more  frequent  when 
the  abscess  is  in  the  left  lobe  or  when  there  is  an  abscess  in  the  left  lobe 
together  with  one  in  the  right.  In  very  rare  instances  vomiting  may  be 
due  to  the  abscess  pressing  on  the  pylorus  and  leading  to  pyloric  obstruc- 
tion. Maclean  *  described  pyloric  obstruction  due  to  hepatic  abscess. 
Appetite  is  poor  or  completely  lost,  as  a  rule,  but  sometimes  it  is  well 
13reser\^ed.     Flatulence  may  be  troublesome. 

There  may  be  constipation,  diarrhoea,  or  the  two  may  alternate. 
Septic  absorjDtion  from  the  abscess  may  give  rise  to  ulceration  of  the 
intestine  and  diarrhoea.  A  recrudescence  of  a  former  dysentery  is  not 
imcommonly  described;  while  in  some  cases  there  may  be  a  continuance 
of  chronic  dysentery.  When  the  abscess  bursts  into  the  alimentary 
tract,  large  quantities  of  pus  may  appear  in  the  stools.  In  rare  cases 
there  may  be  considerable  haemorrhage  from  the  bowel.f 

Captain  Weston,  R.A.N.  C,  has  told  me  of  a  case  where  there  were  profuse 
haemorrhages  from  the  bowels  apparently  due  to  an  abscess  in  the  quadrate  lobe  of 
the  liver  pressing  on  the  portal  vein. 

Arthritis,  etc. — Swelling  and  painful  enlargement  of  the  joints,  pre- 
sumably due  to  toxic  products  absorbed  from  the  liver  abscess,  may 
occur,  just  as  in  dysentery.  They  may  be  pysemic,  l^ut  are  prol3ably 
usually  toxic;  at  any  rate,  they  tend  to  disappear  w^ien  the  abscess  is 
opened  or  discharges. 

It  is  interesting  to  note  that  GirardJ  observed  clubbing  of  the  fingers  in  a  case 
of  hepatic  abscess  in  which  there  were  no  pulmonary  lesions.  It  is  possible  that, 
like  arthritis,  this  change  was  of  toxic  origin. 

Nervous  Symptoms. — As  in  most  hepatic  diseases,  there  is  a  good 
deal  of  irritaliility  or  mental  depression,  which  may  even  become  so 
marked  as  to  pass  into  melancholia.  Insomnia  is  very  common.  The 
mental  disturbance  may  be  referred  to  the  action  of  poisons  on  the 
cerebral  cortex.  The  poisons  may  be  absorbed  from  the  liver  abscess 
or  may  be  derived  from  the  alimentary  tract,  the  liver  being  unable  to 
deal  with  them.  Cerebral  symptoms  may  in  rare  instances  depend  on 
pysemic  abscesses  in  the  brain  or  on  septic  meningitis.  In  the  terminal 
stages  delirium,  or  in  rare  instances  convulsions,  ma}''  occur  before  death. 

PHYSICAL  SIGNS, 

Wasting;  Decubitus;    Facial  Aspect;  Jaundice;  Pulse;  Blood;  Respira- 
tory System;    Abdominal  Signs — Painful  Succussion — Skiagraph}' — 
Rigidity    of    Right   Rectus    Muscle — Ballottement — Hepatic  Dul- 
ness — Friction;   GEdema  of  Feet;   Urine. 
Wasting. — Loss  of  flesh  is  progressive  and  may  be  very  considerable. 

The  degree  of  wasting  necessarily  depends  on  the  duration  and  intensity 

*  Maclean:   Brit.  Med.  .Journ.,  April  1,  1874. 

t  Haasler:  Deutsche  med.  Wochen.,  Jan.  16,  1902. 

J  Girard :   La  Semaine  Mcdicale,  1903,  p.  32. 


138  DISEASES    OF   THE    LIVER. 

of  the  disease  and  the  size  of  the  abscess.  In  rare  instances  weight 
may  actually  be  put  on  while  an  abscess  is  maturing.     (Osier.*) 

Decubitus,  or  the  position  assumed  by  the  patient,  is  generally 
dorsal  or  right-sided,  as  being  that  in  which  there  is  greatest  freedom  from 
pain.  When  lying  on  the  back,  the  chest  is  raised  and  the  knees  are 
somewhat  flexed.  When  the  patient  turns  onto  the  left  side,  the  liver  tends 
to  fall  away  from  the  wall  of  the  abdomen  on  the  right  side  and  pain  is 
frequently  felt.  This  is  probably  due  to  stretching  of  adhesions  or  to 
the  separation  of  the  inflamed  capsule  of  the  liver  from  the  parietal  peri- 
toneum. On  the  other  hand,  the  patient  is  sometimes  more  comfortable 
on  the  left  side.  The  differences  in  the  position  assumed  by  the  patient 
may  depend  on  the  increased  size  of  the  hver  and  on  existence  of  adhe- 
sions. Thus,  when  the  liver  is  greatly  enlarged  the  right-sided  position 
is  most  comfortable,  but  if  there  are  peritoneal  adhesions  in  certain 
situations,  the  right-sided  position  may  give  rise  to  tension  on  them  and 
so  to  pain. 

Facial  Aspect. — The  complexion  is  pale  or  sallow  with  a  muddy 
tint,  and  often  slightly  icteric.  The  conjunctivse  if  not  jaundiced  are 
often  of  a  waxy,  white  colour.  The  expression  is  one  of  anxiety  and 
worry,  the  eyes  are  often  sunken,  and  the  general  aspect,  which  is  more 
easily  recognized  than  described,  may  be  peculiarly  suggestive  of  the 
disease.  The  skin  in  the  early  stages  may  be  hot  and  dry,  but  later  it 
becomes  moist  and  clammy. 

A  remarkable  diffuse  cyanosis  for  which  there  was  no  satisfactory  explanation 
was  noticed  by  Osier  t  in  one  case. 

The  tongue  is  usually  furred  along  the  centre  with  a  red  tip.  A 
smooth  red  tongue  with  fissures  running  in  all  directions  is  not  uncommon. 
A  strong  hepatic  odour  from  the  patient  is  described  by  Hatch  J  as  a 
sign  of  hepatic  abscess;  probably  it  is  present  only  when  the  abscess  is 
of  considerable  size. 

Jaundice. — Marked  jaundice  is  very  rare;  a  slight  degree,  probably 
due  to  local  catarrh  of  intra-hepatic  ducts  near  the  abscess,  and  tingeing 
the  conjunctivse  is  sometimes  present. 

_  Definite  jaundice  Avas  seen  in  58  out  of  375,  or  in  16  per  cent.,  cases  quoted  by 
Thierfelder.  § 

In  exceptional  cases  an  abscess  may  exert  pressure  on  the  extra- 
hepatic  ducts'  in  the  portal  fissure! 

In  a  case  reported  by  Moir  !|  a  liuge  abscess  compressed  the  common  hepatic 
duct. 

The  pulse  is  of  low  tension,  full,  and  somewhat  quickened — 80  to  100. 
Exceptionally  it  is  slowed. 

The  blood  may  show  leucocytosis,  and  when  this  is  so,  is  of  great 

*  Osier:  Medical  News  (U.  S.  A.),  April  12,  1902,  p.  673. 

t  Osier:   Medical  News  (U.  S.  A.),  April  12,  1902,  p.  673. 

j  Hatch:  Brit.  Med.  Journ.,  1900,  vol.  ii,  p.  1374. 

§  V.  Ziemssen's  Cycloptedia  of  Practical  Medicine,  vol.  ix,-  p.  126. 

II  Moir:   Indian  Med.  Gaz.,  Oct.,  1902,  p.  391. 


SINGLE    OR   TROPICAL   ABSCESS.  139 

service  in  distinguishing  hepatic  abscess  from  malaria  or  t,yphoid  fever. 
The  existence  of  considerable  leucocytosis — 30,000  to  50,000  per  cubic 
millimeter — has  led  to  the  detection  of  abscess  in  patients  formerty  the 
subjects  of  dysentery  (Boinet  *)  or  thought  to  have  malaria  (Rogers  f)- 
When  leucocytosis  is  present,  it  is  said  to  be  constant  (Boinet),  and  not 
to  appear  and  disappear  as  it  does  in  intermittent  hepatic  fever.  The 
leucocytosis  is  an  ordinary  polymorphonuclear  one,  70  to  80  per  cent, 
of  the  leucocytes  being  of  this  nature.  Leucocytosis,  though  highly 
suggestive  of  hepatic  abscess,  is  by  no  means  found  in  all  cases  of  abscess. 
When  septic  absolution  is  prevented  by  a  thick  capsule  and  in  amoebic 
cases  there  may  be  no  leucocytosis.  It  has  been  thought  that  leucocy- 
tosis is  most  marked  in  small,  deeply  seated  abscesses,  and  less  in  large 
abscesses  bulging  on  the  surface  of  the  liver.     (Rogers.) 

It  was  absent,  or  practically  so,  in  three  out  of  five  cases  recorded  by  Osier,  f 
It  was  absent  in  a  case  examined  by  Cabot, §  and  Rispal||  failed  to  find  more  than 
a  slight  leucocytosis  (15,000  per  cubic  millimeter)  in  three  cases. 

Respiration  is  shallow  and  chiefly  thoracic,  since  movement  of  the 
abdomen  may  be  attended  with  pleuritic  pain.  The  rhythm  is  more 
rapid  than  normal,  both  because  of  the  fever  and  on  account  of  the 
shallow  respirations.  In  cases  of  amoebic  abscess  the  organisms  may  be 
foimd  in  the  expectoration. 

Lung  Signs. — Compression  of  the  lower  lobe  of  the  right  lung  is 
common  and  may  show  itself  by  crepitations  and  dulness.  When  in- 
flammation has  -spread  through  the  diaphragm  to  the  pleura,  friction 
may  be  heard.  Hepatic  abscess  is  therefore  very  likely  to  imitate  pneu- 
monia or  empyema  at  the  right  base;  the  occurrence  of  signs  of  right- 
sided  pleurisy  in  a  patient  who  has  had  dysentery  should  always  suggest 
the  possibility  of  an  abscess  of  the  liver.  The  appearance  of  pleural 
friction  in  a  case  thought  to  be  one  of  hepatic  abscess  is  a  sign  that 
extension  of  the  inflammatory  process  to  the  thorax  is  in  process,  and 
is  therefore  a  signal  for  operative  interference,  so  as  to  prevent  rupture 
of  the  abscess  into  the  pleura  or  into  the  lung.  But  in  some  cases  of 
acute  hepatitis  which  have  been  fruitlessly  explored  and  have  recovered 
some  friction  at  the  base  of  the  right  lung  may  have  been  present. 

An  empyema  may  follow  hepatic  abscess  in  several  ways.  The  ab- 
scess may  burst  directly  into  the  pleura  or  the  infection  may  spread 
thj-ough  the  diaphragm,  or  pus  may  travel  by  the  blood-stream  into 
branches  of  the  pulmonary  artery  and  set  up  abscess  formation  in  the 
lung  with  the  secondary  production  of  an  empyema.  An  empyema  may 
form  between  the  lobes  of  the  lung  and  give  rise  to  great  difficulty  in  its 
evacuation. 

Rupture  of  an  hepatic  abscess  into  the  lung  may  give  rise  to  the  signs 
of  a  cavity  in  the  lower  lobe,  which,  according  to  Godlee,**  are  most 

*  Boinet:   Soc.  de  biolog.,  Paris,  Dec.  29,  1900. 

t  Rogers,  L. :  Brit.  Med".  Journ.,  1902,  vol.  i,  p.  831;   and  1902,  vol.  ii,  p.  844. 
t  Osier:    Medical  News  (N.  Y.),  April  12,  1902,  p.  673. 
§  Cabot :    Clinical  Examination  of  the  Blood,  p.  253 
II  Rispal:   Compt.  rend.  Soc.  de  biolog.,  1901,  p.  862. 
**Godlee:    Medico-chirurg.  Trans.,  vol.  Ixxxv,  p.   119,  1902. 


140  DISEASES    OF   THE    LIVER. 

coiTLULonly  met  with  below  and  to  the  inner  side  of  the  right  ni^Dple,  but 
may  be  present  posteriorly.  "UTien  a  pulmonary  abscess  consequent  on 
an  hepatic  abscess  is  diagnosed,  no  time  should  be  lost  in  operating  upon 
it,  so  as  to  i^revent  extensive  destruction  of  the  lung. 

The  abdomen  is  fuU  and  somewhat  distended;  sometimes  the  dis- 
tension is  general,  as  if  from  tympanites.  There  is  often  definite  fulness 
or  bulging  in  the  right  hjq^ochondrium  or  epigastrium,  and  sometimes 
a  rounded  projection  in  the  position  of,  or  in  connexion  with,  the  liver 
may  be  seen  to  move  with  respiration.  Fluctuation  in  some  cases  can 
be  made  out  over  the  tumor.  'V^Tien  an  abscess  is  situated  near  the 
middle  line  of  the  body  it  may  pulsate  from  the  transmission  of  impulses 
from  the  aorta. 

Carpenter*  describes  a  painful  swelling  the  size  of  a  foetal  head  pulsating  visibly, 
but  not  expansile;  operation  showed  it  to  be  an  hepatic  abscess  containing  two 
pints  of  pus. 

Bulging  of  the  chest  on  the  right  side  as  compared  with  the  left,  and 
in  some  cases  protrusion  and  -^-iclening  of  the  intercostal  spaces,  may  be 
seen.  Redness  of  the  skin  or  localized  oedema  indicates  that  an  abscess 
is  in  close  contact  Tvith  the  affected  cutaneous  area.  Though  a  ver}- 
valuable  sign,  oedema  over  the  abscess  is  only  present  in  about  5  per  cent, 
of  the  cases.  ( Stevenson. f)  Wlien  the  abscess  is  very  large,  it  ma}^  fill 
the  greater  part  of  the  abdomen,  and  has  given  rise  to  an  erroneous 
diagnosis  of  ascites.  Marked  ascites  is  an  extremely  rare  accompaniment 
of  hepatic  abscess. 

Painful  Succussion. — If  the  patient  is  shaken,  much  in  the  same 
manner  as  in  obtaining  ''Hippocratic  succussion"  in  pj^o-pneumothorax, 
pain  is  felt  in  the  liver  M'hich  may  spread  to  the  right  shoulder,  the  pit 
of  the  stomach,  across  the  abdomen,  or  to  the  right  iliac  fossa,  according 
to  the  situation  of  the  abscess.  IMalbott  considers  this  a  certain  sign 
of  abscess. 

Skiagraphy  has  been  applied  to  the  detection  of  hepatic  abscess. § 
In  health  the  shadow  cast  on  the  screen  shows  that  the  right  leaflet  of 
the  diaphragm  is  H  inches  above  the  level  of  the  left  leaflet  and  is  con- 
stantly moving  with  respiration.  In  cases  of  abscess  it  is  displaced 
upwards  and  does  not  move. 

Rigidity  of  the  upper  part  of  the  right  rectus  muscle  may  cer- 
tainly occur  when  an  abscess  is  present,  but  it  is  far  from  constant: 
moreover,  it  is  met  "^dth  in  other  conditions,  such  as  inflammation  of 
the  gaU-bladder,  disease  of  the  pylorus,  duodenal  ulcer,  or  inflammation 
of  the  muscle  itself,  and  therefore  cannot  be  considered  as  a  sign  of  any 
very  special  value.  The  rigidity  of  the  rectus  may  considerably  interfere 
wnth  the  examination  of  the  Hver.  Dalton  ||  refers  to  a  case  in  which 
the  rigidity  did  not  relax  under  an  anaesthetic. 

*  Carpenter:  Brit.  Med.  Joum.,  1899,  vol.  ii,  p.  208. 

t  Stevenson :  Lancet,  1898,  vol.  ii. 

X  Malbot:   Archiv  general  de  Medecine,  August,  1899,  p.  179. 

§  Loison:   Rev.  de  Chirurg.,  1900,  p.  522. 

11  Dalton,  N. :  King's  CoU.  Hosp.  Reports,  vol.  ii,  p.  25. 


SINGLE    OR   TROPICAL    ABSCESS.  141 

Percussion,  besides  eliciting  tenderness  and  causing  pain,  ma}' 
convey  to  the  examiner  a  sensation  of  ballottement,  as  if  he  was  per- 
cussing a  thick-walled  elastic  bag  filled  with  air.* 

Hepatic  Dulness. — -The  area  of  hepatic  dulness  is  increased  both  in 
an  upward  and  in  a  downward  direction.  Though  this  is  the  rule,  it  is  not 
without  exception,  and  in  some  instances  the  underhdng  colon  may  mask 
the  dulness  which  a  collection  of  pus  Avould  naturally  give  rise  to.  The 
dulness  in  extreme  cases  may  reach  as  high  as  the  second  rib.  (Waring. f) 
.^5  the  abscess  is  usually  in  the  right  lobe,  the  enlargement  is  mainl}''  on 
that  side,  and  since  the  abscess  is  most  frequently  near  the  convexity 
of  the  liver,  the  enlargement  is  chiefly  in  an  upward  direction  and  not 
downwards,  as  in  cirrhosis  and  in  lardaceous  and  malignant  disease. 
When  the  abscess  is  deeply  situated,  the  whole  lobe  is  expanded  and 
enlarged,  but  later,  when  the  abscess  reaches  the  surface,  it  may  give 
rise  to  a  definite  projection  from  the  outline  of  the  organ. 

Friction  due  to  perihepatitis,  set  up  by  the  approach  of  the  abscess 
to  the  surface  of  the  organ,  may  be  heard  or  sometimes  even  felt  by  the 
hand.  There  is  commonly  friction  over  the  base  of  the  right  lung,  due 
to  pleurisy  set  up  by  the  spread  of  infection  along  the  lymphatics  of  the 
diaphragm. 

Fine  crepitation,  like  that  obtained  by  pressing  on  frozen  snow, 
may  be  heard  over  the  liver;  it  occurs  with  inspiration  and  expiration. 
Bertrand  regarded  it  as  due  to  perihepatitis,  but  Hassler  and  Boison 
have  heard  it  in  cases  where  laparotomy  showed  that  there  was  no  peri- 
hepatitis, and  believe  it  is  produced  in  the  softened  and  oedematous  liA'cr 
substance  around  the  abscess. 

The  spleen  is  rarely  enlarged.  This  is  of  importance  in  distinguishing 
abscess  from  maldria. 

(Edema  of  the  feet  often  occurs  late  in  the  course  of  the  disease. 

The  urine  is  high-coloured  and  may  be  of  a  high  specific  gravity, 
and  loaded  with  urates.  When  considerable  destruction  of  the  hepatic 
substance  has  taken  place,  the  amount  of  urea  maybe  diminished.  Indi- 
can  may  occur.  Albuminuria  is  sometimes  present.  From  absorption 
of  pus  albumose  may  be  found  in  the  urine;  but  it  has  been  aliscnt  in 
the  cases  I  have  seen. 

In  a  case  of  abscess  foUowinis;  dysentery  crystals  of  leiicin,  tyrosin,  and  clioles- 
terin  were  present  in  the  urine  for  ten  weeks;  on  opening;  the  abscess  the  urine 
became  normal.  J  Crystals  resembling  tyrosin,  but  really  composed  of  a  soap  of 
lime  and  magnesium,  were  found  in  one  case  b}^  Pfiihler.  § 

COURSE  AND  DURATION. 

The  abscess  may  remain  latent  until  it  ruptures  and  gives  rise  to 
acute  symptoms  or  is  revealed  by  a  discharge  of  pus  from  the  alimentary 
or  respiratory  tract.     It  is  difficult  to  say  when  hepatitis  passes  into 

*  Hassler  and  Boison:   Rev.  de  Med.    Oct.,  1896. 
t  Waring,  E.  J. :   Abscess  of  the  Liver,  p.  149. 
i  Lancet,  1900,  vol.  ii,  p.  1729. 
§  Pfiihler:   New  York  Med.  Journ.,  Feb.  15,  1902. 


142  DISEASES    OF   THE    LIVER. 

suppuration,  and  therefore  to  estimate  precisely  the  ckiration  of  an 
abscess  in  the  hver.  An  abscess  may  run  its  course  in  three  weeks  or, 
if  it  gives  rise  to  a  fistula,  especially  in  connexion  with  the  lungs,  may 
drag  on  for  many  months. 

TERMINATION. 

If  not  operated  upon,  an  hepatic  abscess  may  either  remain  intact 
or  may  rupture  into  some  neighbouring  cavity  or  viscus.  An  abscess 
which  remains  intact  may  in  rare  instances  tend  to  dry  up  and  become 
shut  off  and  encysted,  giving  rise  to  a  caseous  mass  surrounded  by  a 
fibrous  capsule.  How  often  this  actually  occurs  it  is  difficult  to  say, 
inasmuch  as  an  abscess  cannot  be  certainly  diagnosed  until  it  has  reached 
a  considerable  size,  and  would  then  be  operated  upon. 

In  25  cases  in  which  recovery  took  place,  there  were  fair  grounds  for  believing 
that  the  abscess  undem-ent  this  spontaneous  cure  in  two.      (E.  J.  Waring.*) 

Possibly  this  spontaneous  cure  is  even  less  frequent  than  is  sometimes 
thought,  since  some  so-called  "  receding ''  abscesses  found  postmortem 
may  in  reality  have  been  gummata.  If  the  abscess  remains  intact  and 
does  not  discharge  its  contents  spontaneous^,  it  usually  leads  to  death. 

In  300  fatal  cases  tabulated  by  Waring  in  1854,  48,  or  16  per  cent.,  only  were 
operated  upon,  while  169,  or  56  per  cent.,  died  with  the  abscess  intact. 

Though  the  abscess  practically  remains  intact,  it  may  give  rise  to 
secondary  abscesses  in  the  lungs  and  to  general  pyaemia.  Death  may 
be  due  to  detachment  of  a  thrombus  formed  in  one  of  the  hepatic  veins 
and  pulmonary  embolism.  In  some  cases  the  destructive  suppurative 
change  in  the  lungs  may  give  rise  to  fatal  haemoptysis.  As  a  rule,  the 
fatal  result  is  due  to  septicaemia,  septic  absorption,  and  exhaustion. 
Diarrhoea  or  an  apparent  recurrence  of  dysentery  may  carry  the  patient 
off.  In  rare  cases  death  may  be  directly  clue  to  intestinal  haemorrhage ; 
this  has  been  observed  by  Hasslerf  and  Duplant.| 


RUPTURE. 

If  undetected  or  not  operated  upon,  an  hepatic  abscess  may  rupture 
internally,  or  in  very  rare  instances  onto  the  surface  of  the  body.  The 
percentage  of  cases  in  which  rupture  occurs  depends  on  the  diagnosis 
and  on  the  frequency  with  which  operative  measures  are  undertaken. 
In  563  cases  of  hepatic  abscess  collected  by  Cyr,  83,  or  15  per  cent.,  only 
were  operated  upon,  and  rupture  occurred  in  159,  or  28.6  per  cent.  But 
it  must  be  remembered  that  interesting  examples  of  perforation  of 
hepatic  abscess  are  more  likely  to  be  put  on  record  than  more  common- 
place cases  where  the  abscess  is  operated  upon  or  not  detected.  More 
than  half  the  cases  of  perforation,  as  will  be  seen  from  Cyr's  and  Thier- 
f elder's  tables,  were  in  an  upward  direction — through  the  diaphragm. 

*  Waring,  E.  J. :  Abscess  of  the  Liver,  p.  195. 
t  Hassler:   Deutsche  med.  Wochen.,  1902. 
t  Duplant :   Lyon  Medical,  Jan.  26,  1902. 


SINGLE    OR   TROPICAL    ABSCESS.  143 

THIEnFELDER,t ' 

Cyr,*  159  Cases.  170  Cases. 

Lung    59]  74] 

Pleura 31  ^57  per  cent.  26  >  59  per  cent. 

Pericardium ij  4j 

Peritoneum 39  23 

Stomach    8  13 

Intestines    13  32 

Kidney    2  1 

Inferior  vena  ca^^a 3 

Bile  passages 4 

Externally    2 

In  both  these  two  series  perforation  occurred  in  two  positions  in 
three  cases,  so  that  the  numbers  of  the  perforations  exceed  the  number 
of  cases. 

The  various  situations  in  which  rupture  occurs  may  conveniently  be 
considered  seriatim  under  the  following  heads:  rupture  into —  (1)  Lung, 
(2)  Pleura,  (3)  Pericardium,  (4)  Peritoneum,  (5)  Stomach  and  duode- 
num, (6)  Intestines,  (7)  Gall-bladder  and  bile-ducts,  (8)  Kidney,  (9) 
Hepatic  veins  and  Inferior  Vena  Cava,  (10)  Portal  Vein,  (11)  Onto  the 
surface  of  the  body. 

(1)  Rupture  into  the  Lung. — This  is  the  most  frequent  method  by 
which  an  hepatic  abscess  spontaneously  discharges.  In  an  overwhelming 
majority  of  cases  it  is  the  right  lung  into  which  the  abscess  opens.  Before 
the  abscess  can  extend  into  the  lung  the  liver  must  become  adherent  to 
the  diaphragm,  and  the  diaphragm  to  the  base  of  the  lung.  The  inflam- 
matory processes  necessarily  give  rise  to  pain  and  usually  to  signs  of 
basal  pleurisy  and  to  cough.  Inflammation  spreads  into  the  lung  and 
consolidation  with  suppuration  ensues ;  the  communication  between  the 
abscess  cavity  in  the  liver  and  that  in  the  lower  lobe  of  the  right  lung  is 
usually  somewhat  small,  like  a  shirt-stud  abscess,  and  may  be  missed; 
in  some  instances  no  naked-eye  perforation  of  the  diaphragm  is  forth- 
coming. In  rare  cases  there  may  be  a  small  collection  of  pus  betw^een 
the  diaphragm  and  lung  as  well  as  an  abscess  in  the  lower  lobe  of  the 
lung.  The  formation  of  an  abscess  in  the  lower  lobe  is,  according  to 
Lafleur,  due  to  an  extension  of  inflammation  and  infection  by  continuity 
from  the  liver,  and  not  hsematogenous  and  due  to  embolism  through 
the  pulmonary  artery.  On  the  other  hand,  amoebae  have  been  found  in 
the  small  branches  of  the  pulmonary  artery,  so  that  hsematogenous  in- 
fection is  quite  conceivable.  The  suppurative  process  in  the  lo^Ver  lobe 
spreads  into  the  surrounding  pulmonary  tissue  and  tends  to  produce 
fistulous  passages  in  the  lung,  which  as  a  result  becomes  much  disorgan- 
ized. The  abscess  discharges  into  one  of  the  bronchi  in  the  lower  lobe 
of  the  lung  and  characteristic  sputum  mixed  with  blood  is  coughed  up. 
The  sputum  contains  ]nis,  blood,  and  often  fragments  of  hepatic  and 
pulmonary  tissue,  fat  glolniles,  micro-organisms,  and  amoebae.  Occasion- 
ally a  fistulous  communication  between  the  bronchi  and  a  bile-duct  in 
the  liver  may  be  established  and  bile  may  be  brought  up  from  the  lungs. 

*Cyr:   Traito,  Practique  des  Maladies  du  foie,  1887. 

t  'riHcrfcldcr:  Cyclopiodia  of  ihc  Practice  of  Medicine,  a-.  Ziemssen,  vol.  ix,  p. 
13S. 


144  DISEASES    OF   THE    LIVER. 

The  pulmonary  abscess  may  progress,  and,  indeed,  prove  fatal  from 
exhaustion  or  haemoptysis,  when  the  original  hepatic  abscess  has  under- 
gone complete  cure.  Since  the  pus  is  like  that  brought  up  from  the  liver 
and  may  contain  amcebse,  the  expectoration  of  chocolate-coloured  pus 
does  not  prove  that  the  original  liver  abscess  has  not  healed.  (Godlee.*) 
Lafieur,f  writing  on  amoebic  abscess  of  the  liver,  gives  a  very  unfavorable 
prognosis  in  cases  of  rupture  into  the  lung.  Other  writers,  however, 
take  a  very  different  view;  Decastro,J  for  example,  estimating  that 
recovery  occurs  in  76  per  cent,  of  the  cases. 

(2)  Rupture  into  the  Pleura. — Rupture  into  the  pleura,  though 
much  the  same  process,  is  less  frequent  than  rupture  into  the  lung.  This 
depends  on  the  fact  that  the  abscess  as  it  advances  through  the  dia- 
phragm tends  to  set  up  adhesive  pleurisy  and  so  glues  the  lower  lobe 
of  the  lung  to  the  diaphragm.  When  the  abscess  opens  into  the  pleura, 
the  signs  are  those  of  an  empyema.  The  effusion  may  reach  a  very  large 
size  with  great  rapidity  and  seriously  endanger  the  patient's  life. 

(3)  Rupture  into  the  Pericardium. — Rupture  into  the  pericardium 
is  very  rare,  since  this  is  likely  to  occur  only  when  the  abscess  is  in  the 
left  lobe  of  the  liver — a  rare  situation. 

Waring!  quotes  6  recorded  cases  and  I  have  notes  of  9  others,  making  15  in 
all.  In  a  very  remarkable  case  recorded  by  Bentley  ||  there  were  four  pints  of 
sero-purulent  fluid  in  the  pericardium  which  communicated  with  an  abscess  in  the 
left  lobe  of  the  liver. 

An  abscess  in  the  left  lobe  may  leak  onto  the  surface  of  the  liver  and 
set  up  a  subphrenic  abscess  which  may  subsequently  perforate  into  the 
pericardium.  Tolot**  reports  a  case  of  this  kind.  The  clinical  evidence 
of  rupture  into  the  pericardium  is  severe  pain,  dyspnoea,  and  the  rapid 
development  of  a  pericardial  effusion.  Death  follows  very  soon  after 
this  accident. 

(4)  Rupture  into  the  Peritoneum. — This  is  a  comparatively  com- 
mon form  of  rupture.  It  may  occur  freely  into  the  general  peritoneal 
cavity  or  may  give  rise  to  a  localized  intraperitoneal  abscess  which  may 
subsequently  burst  into  the  general  cavity  of  the  peritoneum  or  may 
discharge  into  the  bowel  or  even  externally.  Rupture  of  an  abscess 
into  the  general  cavity  of  the  peritoneum  may  be  due  to  traumatism  or 
to  muscular  exertion,  while  the  danger  of  leakage  must  always  be  borne 
in  mind  when  the  question  of  aspiration  with  a  trocar  through  the  ab- 
dominal wall  is  contemplated.  Perforation  into  the  general  peritoneal 
cavity  is  more  likely  to  follow  sudden  exertion  or  traumatism  than  to 
occur  spontaneously,  as  an  abscess  pointing  on  the  surface  of  the  liver 
tends  to  set  up  local  peritonitis  and  adhesions  before  actually  rupturing. 
When  rupture  occurs  into  the  general  cavit}^  of  the  peritoneum  there 

*  Godlee:  Medico-chirurg.  Trans.,  vol.  Ixxx,  p.  119,  1902. 
t  Lafleur :  AUbutt's  System,  vol.  iv. 

IDecastro:  Des  abscess  du  foie  des  Pays  Chauds,  Paris,  1870.  Quoted  by 
H.  J.  Waring:    Diseases  of  Liver. 

§  Waring,  H.  J. :  Abscess  of  the  Liver  in  the  East  Indies,  1854,  p.  133 
II  Bentley:  Trans.  Path.  Soc,  vol.  ii,  p.  70. 
**  Tolot:  Lyon  Medical,  1902,  p.  51. 


SINGLE    OR   TROPICAL    ABSCESS.  145 

are  symptoms  of  severe  collapse,  and  if  the  patient  survives  long  enough, 
acute  septic  peritonitis  results,  which  is  nearly  always  fatal.  In  cases 
where  the  existence  of  an  hepatic  abscess  has  not  been  recognized,  the 
sudden  onset  of  acute  symptoms  may  imitate  perforation  of  an  intes- 
tinal ulcer  in  ambulatory  t5rphoid  fever. 

A  soldier  aged  twenty-seven  years  who  had  contracted  dysentery  in  the  Trans- 
vaal War  of  1900  was  admitted  into  St.  George's  Hospital  in  a  moribund  condition. 
At  the  autopsy  he  was  found  to  have  several  pints  of  turbid  fluid  in  the  peritoneal 
cavity  and  general  peritonitis  due  to  leakage  from  an  abscess  in  the  left  lobe  of  the 
liver.  The  ruptured  abscess  was  thin-walled  and  quite  small,  it  communicated 
with  a  large  abscess  the  size  of  a  foetus'  head,  which  occupied  the  whole  of  the  left 
lobe  of  the  liver,  and  had  walls  composed  of  glistening  fibrous  tissue  about  ^  inch 
thick.  The  right  lobe  of  the  hver  was  greatly  scarred  from  cicatrices  but  did  not 
contain  any  gummata;  it  showed  early  lardaceous  change.  The  portal  vein  was 
thrombosed;  there  had  prolaably  been  ascites  before  the  onset  of  acute  peritonitis. 

Hulke  *  has  recorded  a  remarkable  example  of  recovery  from  rupture  of  a 
hepatic  abscess  into  the  general  peritoneal  cavity  which  was  flushed  out  some 
twenty-four  hours  after  rupture  occurred.  In  this  patient  an  hepatic  abscess  had 
previously  ruptured  through  the  lung,  and  rather  more  than  a  year  after  recovery 
from  the  operation  for  rupture  into  the  peritoneum,  a  third  abscess  in  tlie  liver  was 
successfully  operated  upon. 

(5)  Rupture  into  Stomach  and  Duodenum. — When  rupture  occurs 
into  the  stomach  or  duodenum  pus  is  vomited,  sometimes  in  very  con- 
siderable quantities,  and  is  passed  by  the  bowel,  but  from  the  distance 
which  it  has  to  travel  the  pus  may  not  be  detected  in  the  faeces.  After 
rupture  the  size  of  the  liver  may  be  perceptibly  diminished,  and  in  some 
instances  a  tympanitic  note  has  resulted  from  entrance  of  air  into  the 
abscess  cavity.  The  n.ipture  into  the  stomach  is  preceded  by  dyspepsia 
and  discomfort,  and  accompanied  by  vomiting  and  severe  epigastric  pain. 

(6)  Rupture  into  the  Intestines. — An  hepatic  abscess  very  seldom 
opens  into  any  ipart  of  the  small  intestine  except  the  duodenum.  Rup- 
ture into  the  colon  is  not  uncommon;  it  is  accompanied  by  colicky  pain 
and  a  feeling  of  collapse  and  is  followed  by  the  passage  of  pus  by  the 
bowel. 

(7)  Rupture  into  the  Gall-bladder  or  Bile-ducts. — This  is  a  very 
rare  event.  The  pus  may  pass  down  the  common  bile-duct  into  the 
duodenum  and  so  imitate  rupture  of  an  abscess  into  the  bowel.  Symp- 
toms of  biliary  colic  have  been  noted  in  this  rare  form  of  fistula. 

(8)  Rupture  into  the  pelvis  of  the  right  kidney  is  very  rare.  H. 
J.  Waring  f  estimates  the  recorded  cases  at  about  10. 

(9)  Rupture  into  the  Hepatic  Veins  and  Inferior  Vena  Cava. — 
From  the  fact  that  the  hepatic  veins  are  not  surrounded  by  any  fibrous 
sheath  at  all  comparable  to  Glisson's  capsule  around  the  jiortal  canals, 
an  hepatic  abscess  is  more  likely  to  leak  or  rupture  into  them  than  into 
the  branches  of  the  portal  vein.  The  abscess  may  burst  into  one  of 
the  hepatic  veins  quite  close  to  the  inferior  vena  cava.  In  a  few  cases 
an  hepatic  abscess  has  been  found  to  perforate  directly  into  the  inferior 
^'ena  cava  and  not  into  the  hepatic  veins. 

*  Hulke:  Medico-chirurg.  Trans.,  vol.  Lxxvi,  p.  81. 
t  Waring,  H.  J. :  Diseases  of  the  Liver,  p.  98. 
10 


146  DISEASES    OF   THE    LIVER. 

Cyr's  list  contains  3  cases,  and  since  then  Flexner  *  (1897)  has  given  an  account 
of  two  cases  in  which  amoebic  hepatic  abscesses  perforated  the  inferior  vena  cava. 
A  case  occurred  in  St.  George's  Hospital  which  is  figured  on  page  131;  the  abscess 
occupied  a  third  of  the  liver  and  had  set  up  parietal  thrombosis  in  the  inferior 
vena  cava.  The  pulmonarj^  artery  contained  firm  thrombi  and  there  was  pneu- 
monic consolidation  of  the  right  lower  lobe. 

When  the  abscess  begins  to  penetrate  the  wall  of  the  hepatic  veins 
or  inferior  vena  cava  parietal  thrombosis  may  be  set  up,  and  thus  for  a 
time  prevent  the  pus  entering  freely  into  the  circulation,  but  eventually 
pus  passes  into  the  blood-stream  and  tends  to  give  rise  to  secondary 
abscesses  in  the  lungs.  Detachment  of  a  large  piece  of  clot  may  give 
rise  to  pulmonary  embolism. 

(10)  Rupture  into  the  Portal  Vein.— Rupture  into  the  portal  vein 
is  extremely  rare.  Occasionally  the  abscess  is  in  contact  with  the  wall 
of  the  vein  and  sets  up  thrombosis  in  the  vein  which  would  prevent  the 
contents  of  the  abscess  from  passing  into  the  vein. 

(11)  Rupture  Externally  onto  the  Surface  of  the  Body.— A  hver 
abscess  is  very  seldom  allowed  to  rupture  spontaneously  on  the  surface 
of  the  body,  though  it  would  do  so  in  a  certain  number  of  cases  if  not 
anticipated.  Most  frequently  the  abscess  points  anteriorly,  but  occa- 
sionally it  presents  in  the  loin. 


COMPLICATIONS. 

Apart  from  manifest  rupture  hepatic  abscess  may  give  rise  to  second- 
ary inflammation  and  suppuration,  especially  in  the  thorax.  From  the 
spread  of  inflammation  through  the  diaphragm  there  may  be  a  simple 
serous  pleurisy  on  the  right  side.  Infection  may  travel  through  the 
diaphragm  and  set  up  an  empyema  on  the  right  side,  which  may  be  en- 
cysted between  the  lobes  of  the  lung,  as  in  Duplant's  f  case.  Infection 
may  spread  through  the  diaphragm,  produce  pleurisy  and  adhesions 
between  the  base  of  the  lung  and  the  diaphragm,  and  then  extend  into 
the  substance  of  the  lower  lobe,  setting  up  pneumonic  consolidation,  in 
^  the  middle  of  which  an  irregular  abscess  may  develop.  Rupture  of  the 
abscess  into  the  lung  and  pleura  and  broncho-biliary  fistula  have  already 
been  described. 

Cerebral  Abscess. — One  of  the  dangers  of  an  empyema  or  a  pul- 
monary abscess  is  that  a  cerebral  abscess  may  follow. 

Godlee  J  describes  an  instructive  case  where  the  liver  abscess  was  completeh' 
healed  but  there  were  nmnerous  abscesses  in  the  right  lung  and  one  as  large  as  an 
orange  in  the  left  lung:  death  was  due  to  an  abscess  in  the  right  occipital  lobe  of  the 
brain. 

Abscesses  in  the  brain  which  do  not  contain  amoebse  may  occur  in 
cases  where  the  hepatic  abscess  contained  them;  this  is  comparable  to 
what  sometimes  occurs  in  actinomycosis,  pysemic  abscesses  only  con- 
taining pyogenic  cocci. 

*  Flexner:  American  Journal  of  Medical  Sciences,  vol.  cxiii,  p.  553,  May,  1897. 
^  t  Duplant :  Lyon  Medical,  .Jan.  26,  1902. 
'  X  Godlee:  Medico-chirurg.  Trans.,  vol.  Ixxxv,  p.  119,  1902. 


SINGLE    OR  TROPia\L   ABSCESS.  147 

As  a  result  of  firm  adhesions,  associated  ^vith  an  old  amoebic  abscess 
in  the  left  lobe  of  the  liver,  fatal  strangulation  of  the  small  intestine 
has  been  recorded.  (Rogers.*)  From  adhesions  on  the  under  surface 
of  the  Uver  around  the  portal  fissure,  in  cases  where  an  abscess  has  been 
successfully  operated  upon  and  contraction  has  followed,  compression  of, 
and  traction  on,  the  bile-ducts  giving  rise  to  jaundice,  or  on  the  colon 
or  pvlorus,  producing  kinking  and  dilatation  of  the  stomach,  mav  occur. 
(Godlee.t) 

Thrombosis  of  the  inferior  vena  cava  is  a  very  rare  complication; 
a  parietal  thrombus  may  form  when  an  abscess  bursts  into  the  inferior 
vena  cava,  which  itself  is  very  rare. 

In  one  case  of  hepatic  abscess  with  extreme  marasmus  under  the  care  of  my 
colleague.  Dr.  Ewart,  there  was  extensive  thrombosis  of  the  inferior  vena  cava, 
which  appeared  to  have  spread  from  the  ihac  veins ;  tliere  was  no  focus  of  suppura- 
tion in  tlie  pelvis  to  account  for  it.  In  this  instance  there  was  some  oedema  of 
the  feet  and  legs,  but  this  may  occur  late  in  the  course  of  hepatic  abscess  without 
thrombosis  of  the  inferior  vena  cava. 

Escape  of  bile  from  the    fistula  of   the  operation  wound  is  not 

very  uncommon,  but  it  is  rare  for  all  the  bile  to  pass  in  this  way,  as  in 
three  cases  mentioned  by  Godlee.J 

Lardaceous  disease  may  supervene  as  the  result  of  long-continued 
discharge  of  pus  from  a  fistulous  passage,  such  as  a  hepato-bronchial 
fistula. 

DIAGNOSIS. 

There  is  no  one  sign  or  symptom  which  may  not  be  absent  in  tropical 
abscess.  The  most  frequent  indications  of  liver  abscess  are  pain  in  the 
region  of  the  liver,  progressive  enlargement  of  the  organ,  and  fever;  but 
these  may  be  present  in  congestion  or  acute  hepatitis  as  well  as  in  other 
conditions.  The  presence  of  a  fluctuating  swelling  or  oedema  of  the 
abdominal  wall  over  the  liver  make  the  diagnosis  almost  certain,  but 
unfortunately  they  are  so  often,  or  in  the  case  of  oedema  generally, 
absent.  The  history  that  the  patient  has  had  dysentery  or  has  been  in 
tropical  countries,  the  fact  that  the  patient  is  manifestly  ill,  and  the 
presence  of  some  of  the  commoner  signs  and  symptoms  of  abscess,  such 
as  hepatic  pain,  enlargement,  and  tenderness,  and  continued  fever  in 
the  absence  of  an}"  evidence  of  malaria  or  other  sufficient  cause,  are  strong 
grounds  for  suspecting  a  tropical  abscess. 

Boinet  §  has  recently  laid  stress-  on  the  value  of  a  considerable  leuco- 
cj^tosis  in  cases  where  there  is  no  other  proof  of  abscess,  but  other  ob- 
sers'ations  show  that  the  leucocytosis  may  be  comparatively  slight  or 
absent.  (Osier.  ||)  Leucocytosis  in  a  doubtful  case  is  in  favour  of 
abscess,  but  its  absence  does  not  exclude  abscess. 

Puncture  of  the  liver  with  a  fine  trocar  in  order  to  determine  whether 

*  Rogers,  L. :  Brit.  Med.  Joum.,  1903,  vol.  i,  p.  1316. 

t  Godlee,  R.  J.:  Medico-chirurg.  Trans.,  vol.  Ixxxv,  p.  121. 

t  Godlee:  Medico-chirurg.  Trans.,  vol.  ixxxv,  p.  123. 

§  Boinet:  Soc.  de  biolog.  Paris,  Dec.  29,  1900. 

II  Osier:  Medical  News  (N.  Y.),  April  12,  1902,  p.  673. 


148  DISEASES    OF   THE    LIVER. 

pus  is  present,  is  a  means  of  settling  the  diagnosis  which  is  often  em- 
plo3^ed.  It  is  not,  however,  in  spite  of  statements  to  the  contrar}-,  free 
either  from  fallacy  or  from  danger.  The  trocar  may,  of  course,  miss  the 
abscess  or  may  pass  through  it,  or  may  get  blocked  and  not  bring  any 
pus  away.  Death  has  been  known  to  follow  exploratory  puncture  from 
haemorrhage  (Hatch,*  Maitland  t);  in  order  to  diminish  the  risk  of  this, 
Maitland  urges  that  when  a  fruitless  puncture  has  been  made,  a  second 
puncture  in  another  direction  should  not  be  made  while  the  end  of  the 
trocar  is  still  in  the  liver,  since  this  manoeuvre  tends  to  enlarge  the 
orifice  and  so  favours  haemorrhage;  if  necessar}^,  an  entirely  fresh  punc- 
ture should  be  made.  Cantlie,:]:  who  is  a  strong  advocate  of  the  use  of 
the  aspirating  syringe,  considers  that  the  inferior  vena  cava  is  the  only 
vessel  likely  to  be  wounded,  and  that  if  the  needle  is  not  introduced  for 
more  than  3^  inches,  this  danger  can  be  ehminated.  The  risk  from 
haemorrhage  is  said  to  be  greatest  in  those  cases  where  there  is  no  abscess. 
Further,  a  puncture  may  lead  to  peritonitis  or  may  be  the  means  of 
spreading  infection  in  the  liver  by  passing  through  the  abscess  and 
■carrying  the  pus  into  other  parts  of  the  organ. 

DIFFERENTIAL  DIAGNOSIS. 

Suppurating  Hydatid;  Subdiaphragmatic  Abscess;  Pylephlebitis  and 
Multiple  Abscess;  Suppurative  Cholangitis;  Intermittent  Hepatic 
Fever;  Pancreatic  Qs^st,  Acute  Pancreatitis;  Suppuration  in  Rectus 
Muscle;  Acute  Hepatitis;  Typhoid  Fever;  Malaria;  New-growth; 
Lymphadenoma ;  Gumma;  Ascites;  Dilated  Gall-bladder;  Pleural 
Effusion  and  Empyema  on  Right  Side;  Tuberculosis. 

Suppurating  Hydatid  Cysts. — In  simple  hydatid  disease  the  liver 
is  enlarged  but  the  general  health  and  nutrition  are  good,  there  is  no 
fever,  and  there  is  a  general  absence  of  symptoms,  such  as  pam,  which 
form  a  striking  contrast  to  the  prominent  local  physical  signs.  No  diffi- 
culty is  therefore  likely  to  arise  in  distinguishing  between  an  ordinary 
hydatid  cyst  and  abscess  of  the  liver.  When,  however,  a  hydatid  cyst 
becomes  infected  and  suppurates,  a  condition  of  affairs  exactly  the  same 
as  abscess  is  brought  about.  In  such  cases  the  historj^  that  there  had 
been  a  quiescent  tumor  in  the  position  of  the  liver  for  a  considerable  time 
before  the  development  of  symptoms  would  suggest  the  exact  state  of 
affairs;  otherwise  it  will  be  impossible  to  make  an  absolutely  accurate 
diagnosis  until  the  suppurating  cyst  is  operated  upon  and  its  contents 
examined.  Difficulty  might  conceivably  arise  in  distinguishing  between 
a  simple  hydatid  complicated  by  fever,  such  as  typhoid,  and  abscess  of 
the  liver. 

Subphrenic  Abscess. — ^A  sub^Dhrenic  abscess  may  be  due  to  various 
causes,  such  as  leakage  of  an  hepatic  abscess  or  suppurating  hydatid 
cyst,   suppurative   cholecystitis,   perforation   of  a  gastric   or  duodenal 

*  Hatch:  Indian  Med.  Gaz.,  April,  1898. 

t  Maitland:  Brit.  Med.  Journ.,  1902,  vol.  i,  458. 

t  Cantlie,  J. :  Brit.  Med.  Journ.,  1903,  vol.  ii,  p.  656. 


SINGLE    OR  TROPia\L   ABSCESS.  149 

ulcer,  appendicitis,  calculous  or  tuberculous  disease  of  the  kidney,  and 
in  rare  cases  from  suppuration  in  the  spleen  or  in  connexion  with  malig- 
nant disease  of  the  large  intestine.  In  cases  where  an  abscess,  either 
tropical  or  one  of  the  multiple  abscesses  seen  in  suppurative  pylephlebitis 
or  cholangitis,  leaks  on  to  the  convexity  of  the  liver  and  gives  rise  to  a 
localized  abscess  between  the  diaphragm  and  the  liver,  the  condition  of 
affairs  is  for  all  practical  purposes  much  the  same  as  the  original  intra- 
hepatic disease.  ^Mien  a  localized  peritoneal  abscess  is  due  to  perfora- 
tion of  a  gastric  or  duodenal  ulcer,  the  cavity  contains  air  and  is  often 
termed  a  subphrenic  pj^opneumothorax.  The  physical  signs — resonance 
on  percussion,  a  bell  note,  and  succussion — distinguish  it  from  hepatic 
abscess,  which  it  does  not  so  much  resemble  as  a  real  pneumothorax. 
TMien  a  subphrenic  abscess  does  not  contain  gas,  it  may  be  extremely 
difficult  to  differentiate  it  from  an  abscess  in  the  liver.  Thus  in  cases 
of  neglected  appendicitis  a  large  abscess  may  pass  upwards  from  the 
right  iliac  fossa,  displace  the  right  lobe  of  the  liver  forT\'ards,  and 
give  rise  to  increase  in  the  hepatic  dulness  and  to  apparent  enlargement 
of  the  liver.  It  should  be  differentiated  from  a  hepatic  abscess  by  the 
history,  the  signs  of  appendicular  mischief  in  the  right  iliac  fossa,  and 
by  its  tendency  to  bulge  more  into  the  right  loin.  The  histoiy  or  evi- 
dence of  recent  appendicitis  are  of  some  importance,  for  subphrenic 
abscess  is  commoner  than  hepatic  abscess  as  a  result  of  appendicitis. 
(Elsberg.*) 

Suppurative  Pylephlebitis  or  Multiple  Abscesses.— The  general 
resemblance  of  single  and  of  multiple  abscesses  is  often  ver}"  marked, 
and  an  absolute  diagnosis  between  them  is  not  always  justified.  The 
points  on  which  a  distinction  can  be  based  are  (i)  local  signs  of  abscess, 
such  as  fluctuation  over  a  prominent  sweUing,  or  oedema  of  the  body 
wall  over  the  liver;  (ii)  the  histor\'  of  dysenten,^  in  the  case  of  single 
abscess,  or  of  appendicitis  in  multiple  pylephlebitic  abscesses.  It  must 
be  remembered,  however,  that  dysentery  may  be  followed  by  multiple 
abscesses.  This  was  seen  in  the  dysentery-  affecting  the  British  troops  in  the 
Boer  War  of  1899-1902.  In  a  patient  who  has  had  dysenteiy,  agglu- 
tination of  the  Shiga-Flexner  bacillus  would  point  to  bacillar}'-  dysentery 
and  to  the  intra-hepatic  suppuration  being  multiple  rather  than  single. 

In  the  following  case,  seen  on  March  22,  1903,  at  Coltishall  with  Dr.  Burton 
Fanning,  multiple  abscesses,  secondary  to  appendicitis,  verj'-  closely  resembled  a 
single  abscess.  A  man  aged  forty-eight  was  seized  seven  weeks  before  with  pain 
at  the  umbilicus  which  had  continued  ever  since.  There  were  dulness,  friction,  and 
distant  bronchial  breathing  at  the  right  base,  but  no  enlargement  of  the  liver  in 
front.  His  temperature  had  fallen  that  morning  to  96.4°,  he  was  collapsed,  looked 
almost  moribund,  and  had  a  pulse  of  140.  Mr.  H.  A.  Ballance  did  a  transpleural 
operation,  letting  out  serous  fluid  from  the  pleura,  and  opened  an  abscess  about 
the  size  of  a  teacup  m  the  back  of  the  right  lobe  of  the  liver;  no  other  abscesses 
could  be  seen.  The  man  seemed  much  better  and  the  temperature  remained  below 
normal  for  four  days;  it  then  became  hectic  and  he  died  on  April  2d.  Dr.  Burton 
Fanning  did  a  postmortem  examination  and  found  the  vermiform  appendix  gan- 
grenous and  the  right  lobe  of  the  liver  riddled  with  multiple  abscesses.  There 
was  a  good  deal  of  serous  fluid  in  the  right  pleural  cavity. 

*Elsberg:  Subphrenic  Abscess  after  Appendicitis.  Annals  of  Surgery,  vol. 
xxxiv,  p.  729,  1901. 


150  DISEASES    OF   THE   LIVER. 

Intermittent  Hepatic  Fever. — In  intermittent  hepatic  fever  de- 
pending on  infective  cholangitis  due  to  calculi  in  the  ducts  periodical 
attacks  of  fever,  jaundice,  pain,  and  hepatic  enlargement  occur.  The 
history  in  such  cases  would  probably  point  to  cholelithiasis,  while  the 
variation  in  the  size  of  the  liver  or  absence  of  enlargement,  and  the 
intervals  of  fair  health,  would  tend  to  eliminate  hepatic  abscess.  It  is, 
however,  well  to  bear  in  mind  that  infective  cholangitis  may  go  on  to 
suppuration  and  that  the  temperature  is  then  continuously  raised. 

Pancreatic  Cyst. — A  pancreatic  cyst  lifting  up  the  left,  or  less  often 
the  right,  lobe  of  the  liver  may  imitate  an  abscess  in  the  substance  of 
that  viscus.  A  pancreatic  cyst  is  not  accompanied  by  fever  and  often 
appears  after  a  blow.  But  in  very  exceptional  instances  an  abscess  in 
the  liver  is  not  accompanied  by  pyrexia  and  may  of  course  supervene 
after  traumatism.  As  a  rule,  a  pancreatic  cyst  forms  a  definite  tumor 
in  the  left  hypochondrium  of  large  size  and  does  not  imitate  an  abscess 
even  in  the  left  lobe  of  the  liver. 

Acute  pancreatitis  with  the  production  of  an  abscess  limited  to  the 
cavity  of  the  lesser  sac  of  the  peritoneum  may,  as  shown  in  the  following 
case,  resemble  an  abscess  in  the  left  lobe  of  the  liver. 

A  man  aged  forty  came  into  St.  George's  Hospital  on  September  15,  1899, 
having  been  ill  sixteen  days,  with  a  fluctuating  tumor  in  the  epigastrium  which 
had  been  noticed  four  days  before.  It  was  in  the  position  of  the  left  lobe,  but  tlie 
rest  of  the  liver  showed  no  enlargement  and  the  patient  had  never  been  oiit  of 
England.  A  tentative  diagnosis  of  suppurating  hydatid  cyst  or  of  a  pancreatic 
cyst  was  made.  Mr.  G.  R.  Turner  operated  the  same  day  and  opened  a  large 
abscess  which  was  not  in  the  Uver  but  occupied  the  sac  of  the  lesser  omentuna  and 
went  back  to  the  spine.  The  patient  did  well  for  a  time,  but  in  October  fever 
returned,  he  had  rigors,  and  eventually  died  on  November  8th.  At  the  necropsy 
there  was  an  abscess  cavity  in  the  lesser  sac  of  the  peritoneum  with  gangrene  of 
the  tail  of  the  pancreas.  There  were  suppurative  pylephlebitis,  multiple  abscesses 
in  the  liver,  and  a  left-sided  empyema. 

Suppuration  in  the  Rectus  Muscle. — Suppuration  in  the  sheath  of 
the  rectus  abdominis  muscle  is  rare,  and  when  it  does  occur,  as  it  has 
been  known  to  do  after  typhoid  fever,  is  usually  below  the  umbilicus. 
An  abscess  in  the  rectus  muscle  above  the  umbilicus  might  imitate  a 
pointing  hepatic  abscess,  but  there  is  not  complete  dulness  over  the 
swelling  and  the  liver  is  not  enlarged.  A  needle  introduced  into  an 
abscess  in  the  abdominal  wall  remains  stationary,  while  a  needle  project- 
ing into  an  abscess  in  the  liver  should  move  with  respiration.  (Middel- 
dorff's  method.)  This  test  may  fail  when  the  Uver  is  firmly  adherent 
to  the  abdominal  wall  (Osier  *),  and  is  not  devoid  of  danger,  since  leakage 
may  take  place  from  the  puncture  in  the  liver. 

A  phantom  tumor  is  likely  to  be  mistaken  for  an  abscess  only  when 
the  patient  has  been  in  the  tropics  or  has  been  exposed  to  dysentery. 
The  gradual  disappearance  of  a  phantom  tumor  under  a  general 
anaesthetic  is  important  in  the  diagnosis  from  hepatic  abscess.  Sir  W. 
Bennett  f  has  described,  in  a  man  who  had  had  dysentery,  a  phantom 
tumor  which  was  operated  upon. 

*  Osier:  Practice  of  Medicine,  p.  581,  4th  ed.,  1901. 
t  Bennett,  W.  H. :  Lancet,  1902,  vol.  i,  p.  3. 


SINGLE    OR   TROPICAL   ABSCESS.  151 

Since  acute  hepatitis  j)recedes  and  may  be  considered  an  early 
stage  of  abscess,  the  question  often  arises  whether  suppuration  has  actu- 
alh'  developed  or  not  in  a  patient  who  has  had  dysenters^  and  presents 
symptoms  suggesting  suppuration  in  the  liver. 

In  a  case  of  this  kind  operated  upon  by  B«rard  *  on  the  assumption  that  there 
was  an  abscess,  the  patient  was  reheved  considerably  by  the  four  punctures  made 
into  the  liver. 

In  obscure  forms  of  septicemia  the  association  of  fever  and  enlarge- 
ment of  the  liver  from  cloudy  swelling  may  easilj^lead  to  a  diagnosis 
of  abscess.  Remlinger  f  and  Bozzolo  have  described  a  form  of  acute 
hepatitis  as  the  infectious  liver  which  imitates  abscess  very  closely.  In 
typhoid  fever  considerable  hepatic  enlargement  sometimes  occurs  and 
may  give  rise  to  a  diagnosis  of  hepatic  abscess.  J  This  difficulty  is  more 
likely  to  arise  in  warm  climates,  where  the  two  diseases  are  both  preva- 
lent.' 

The  presence  or  absence  of  the  agglutination  reaction  should  be  of 
Yery  great  assistance,  but  it  might  be  present  in  a  patient  with  hepatic 
abscess  who  had  previously  had  enteric  fever.  An  examination  of  the 
blood  should  always  be  made,  since  there  is  no  leucocytosis  in  uncom- 
plicated tyi^hoid  fever,  while  in  abscess  it  may  be  present  and  be  verA^ 
considerable. 

From  malaria  a  diagnosis  of  hepatic  abscess  may  be  made  b}'  ex- 
amination of  the  l^lood  and  a  search  for  the  parasite.  In  malarial 
cases  treated  with  quinine  the  blood  does  not  show  the  parasite;  in 
such  cases  leucopenia  points  to  malaria,  §  while  in  hepatic  abscess  there 
may  be  a  high  degree  of  leucocytosis.  Cases  of  hepatic  abscess  vnth 
little  enlargement  of  the  liver  may  easily  be  regarded  as  malarial  in  the 
absence  of  a  blood  exaixdnation,  while,  conversely,  chronic  malaria  with 
hepatitis  may  imitate  hepatic  abscess,  in  the  enlargement,  pain  both  in 
the  liver  and  the  right  shoulder,  and  the  general  ill  health.  In  malaria 
the  hepatic  enlargement  is  more  uniform  and  is  accompanied  by  en- 
largement of  the  spleen. 

New-growth. — Confusion  sometimes  arises  when  rapidly  growing 
malignant  disease  in  the  liver  is  associated  with  a  raised  temperature. 
A  soft  groA\i:h,  especially  when  in  the  left  lobe,  may  cause  a  bulging  of 
the  abdominal  wall  and  give  rise  to  a  sense  of  fluctuation  more  or  less 
obscure.  In  such  cases,  of  which  examples  are  given  in  the  section  on  mal- 
ignant disease  of  liver,  exploration  is  the  onty  sure  method  of  coming  to 
a  diagnosis.  It  is  veiy  rare  indeed  for  the  converse  to  occur,  viz.,  for 
an  abscess  to  be  regarded  as  a  new-growi^h.  It  is  more  likely  to  occur  in 
cases  where  the  patient  is  extremely  cachectic  and  deeply  jaundiced. 

In  the  following  case  of  Osier's  ||  the  condition  was  thought  to  be  probably 
gall-stones  with  cancer.     Summar}-:  Woman,  sixty-four  years,  dyspepsia  for  two 

*  Bc'rard:  Tiyon  Medical,  May  8,  1902. 
t  Remlinger:  La  Presse  Mddicale,  1903,  p.  80. 

t  Bozzolo:  Rivista  Critica  di  Clinica  Medica,  Marcli,  1902.  H.  .Jones:  1^-it. 
Med.  .Tourn.,  1897,  vol.  ii,  p.  1581. 

'^  Vide  L.  Rosrers:  Brit.  Med.  Journ.,  1902,  vol.  i,  p.  S.31. 
II  Osier:  Medical  News,  April  12,  1902,  p.  073. 


152  DISEASES    OF   THE    LIVEE. 

years,  loss  of  weight,  pain  in  right  side  at  intervals  for  three  months,  attacks  of 
vomiting,  slight  jaundice,  progressive  weakness,  no  rigors,  no  leucocytosis,  increase 
in  size  of  liver,  slight  fever.  Death.  Amoebic  abscess  in  right  lobe  of  liver.  No 
ulceration  of  intestines. 

Lymphadenoma. — In  generalized  lymphadenoma  the  temperature 
may  closely  resemble  that  of  suppuration,  and  in  rare  instances  there 
is  very  considerable  enlargement  of  the  liver. 

Some  years  ago  a  man  was  under  my  care  with  a  pedunculated  mass  in  the  left 
groin  of  many  years'  standing,  which  turned  out  to  be  lymphadenoma;  he  devel- 
oped a  hectic  temperature  and  considerable  enlargement  of  the  liver.  The  condi- 
tion was  not  unlike  hepatic  abscess  and  the  question  of  operation  was  raised  during 
life.  He  died  at  his  home  and  a  postmortem  examination  was  performed  by  Mr. 
Archer  of  Vincent  Square,  who  kindly  sent  me  portions  of  the  liver  which  showed 
lymphadenoma. 

As  a  rule,  there  is  not  much  enlargement  of  the  liver  in  generalized 
lymphadenoma.  In  the  blood  examination  of  lymphadenoma  there  is 
usually  no  leucocytosis,  while  in  abscess  there  may  be  a  polymorpho- 
nuclear leucocytosis.  Further,  in  lymphadenoma  the  superficial  glands 
are  usually  affected. 

Syphilitic  Disease. — In  some  cases  of  syphilis  there  is  continued 
fever  and  very  considerable  hepatic  enlargement,  and  when  this  is  met 
with  in  patients  who  have  been  in  India  or  other  countries  where  hepatic 
abscess  is  common,  the  resemblance  to  abscess  is  very  likely  to  lead  to  a 
mistake.  This  is  shown  by  the  fact  that  cases  of  hepatic  gummata  have 
been  operated  upon  under  the  idea  that  an  abscess  was  present. 

Ascites. — In  a  few  cases  an  abscess  has  been  so  large  as  to  imitate 
ascites,  and  the  abdomen  has  been  tapped  on  this  assumption.  This  is 
more  likely  to  occur  in  young  subjects.  Cases  have  been  recorded  by 
Hatch*  and  Powell. f 

Dilated  Gall-bladder. — Though  it  seems  unhkely,  a  greatly  dilated 
gall-bladder  has  been  tapped  under  the  idea  that  it  was  an  hepatic 
abscess.  There  is  a  specimen  (No.  1381)  in  St.  Thomas'  Hospital  Museum 
illustrating  this. 

Right-sided  Pleural  Effusion. — There  may  be  a  very  close  resem- 
blance between  hepatic  abscess  and  a  right-sided  pleural  effusion.  An 
abscess  in  the  upper  and  back  part  of  the  right  lobe  of  the  liver  will  push 
the  diaphragm  up  and  give  rise  to  dulness  at  the  base  of  the  lung.  The 
dulness  is  said  to  be  curved  and  to  be  higher  in  front  and  in  the  axilla 
than  behind,  but  this  is  not  always  the  case,  as  there  may  be  a  smaU 
concomitant  pleural  effusion  in  the  right  pleura  due  to  the  spread  of 
inflammation  through  the  diaphragm.  The  upward  displacement  of 
the  diaphragm  does  not  lead  to  displacement  of  the  heart  to  the  left  in 
the  same  way  that  a  large  pleural  effusion  does,  but  this  is  not  of  much 
use,  as  an  hepatic  abscess  rarely  imitates  a  large  pleural  effusion.  In  a 
case  of  hepatic  abscess  the  patient's  general  condition  is  worse  than  it 
would  be  in  a  comparatively  small  empyema  or  pleural  effusion;  further, 
the  liver  is  usually  enlarged  downwards  in  abscess,  while  a  pleural  effu- 

*  Hatch :  Indian  Med.  Gaz.,  Aug.,  1898. 
t  Powell:  Indian  Med.  Gaz.,  Feb.,  1898. 


SINGLE   OR  TROPICAL   ABSCESS.  153 

sion  of  the  size  which  an  hepatic  abscess  imitates  would  not  displace 
the  liver  downwards.  As  has  been  pointed  out,  hepatic  abscess  often 
gives  rise  to  pleurisy  and  pleuritic  pain,  so  that  the  question  to  be  decided 
is  whether  there  is  an  abscess  in  the  liver  or  whether  the  whole  disease 
is  intrapleural.  In  a  case  of  tropical  abscess  foUo'^dng  typhoid  fever 
{vide  p.  125)  the  resemblance  to  an  empyema  was  considerable. 

Tuberculosis. — Cases  of  pulmonary  tuberculosis  with  hectic  tem- 
perature and  with  an  enlarged  fatty  liver  in  which  the  physical  signs  of 
pulmonary  disease  are  not  prominent  or  have  not  been  detected,  have 
been  diagnosed  as  hepatic  abscess.*  In  hepatic  abscess  without  any 
hepatic  enlargement  in  patients  who  have  never  been  out  of  England 
the  continued  temperature  may,  in  the  absence  of  any  other  signs,  suggest 
generalized  tuberculosis. 

PROGNOSIS. 

The  prognosis  of  hepatic  abscess,  though  always  serious,  and  specially 
severe  in  the  presence  of  complications,  which  will  be  referred  to  later, 
is  by  no  means  necessarily  bad. 

In  a  collection  of  1094  cases  the  mortality  was  30  per  cent.  (Solonofff)- 

Lafleur  J  considers  the  prognosis  more  unfavourable  in  amoebic  than 
in  other  forms  of  hepatic  abscess,  but  Manson  §  joins  issue  with  him  on 
this  point.  The  prognosis  is  considerably  modified  by  the  period  at 
which  operative  interference  takes  place.  If  the  case  is  operated  upon 
early,  the  outlook  is  favourable.  Operation  in  private  practice  in  India 
is,  probably  for  this  reason,  much  more  successful  than  in  hospital 
practice. 

According  to  Moorhead,  ||  75  per  cent,  of  private  cases  and  50  per  cent,  of  hos- 
pital cases  recover.  Hatch**  found  that  in  some  years  90  per  cent,  of  the  hospital 
cases  terminated  fatally,  while  in  private  practice  the  mortality  was  about  20  per 
cent. 

When  operative  measures  are  only  undertaken  late,  the  prognosis 
is  bad.  Inasmuch  as  extensive  destruction  of  the  liver  substance  has 
taken  place,  the  patient's  strength  is  exhausted  by  the  continued  fever, 
and  secondary  results,  such  as  pyaemia,  have  had  time  to  develop. 

Rupture  of  the  abscess  externally  is  favourable;  rupture  into  the 
lung  is  generally  regarded  as  fairly  favourable,  though  convalescence 
may  be  tedious;  thus,  De  Castroff  estimates  that  75  per  cent,  recover, 
but  Lafleur  and  Godlee  take  an  unfavourable  view  of  this  complica- 
tion. Rupture  into  the  colon  is  usually  followed  by  recovery.  On  the 
other  hand,  rupture  into  the  general  peritoneal  cavity  and  into  the 
pericardium  are  nearly  always  fatal.     The  presence  of  active  dysenter}- 

*  .Josserand:  Joum.  de  M6d.,  July  25,  1898. 

t  Solonoff:  Brit.  Med.  Journ.,  190.3,  vol.  i,  p.  262. 

t  Lafleur:  AUbutt's  System  of  Med.,  vol.  iv,  p.  168. 

!^  Manson,  P. :  Tropical  Diseases,  1903,  p.  457. 

I|  Moorhead:  Brit.  Med.  .lourn.,  1899.  vol.  i,  p.  1032. 
**  Hatch:  Lancet,  1902,  vol.  ii,  p.  1543. 
ft  De  Castro:  Les  Maladies  du  Foie  dans  les  pays  c-liaud,  Paris,  1870. 


154  DISEASES    OF   THE    LIVER. 

is  unfavourable.  The  existence  of  more  than  one  abscess  makes  the 
prognosis  bad;  this  is  difficult  to  diagnose  with  certainty,  but  it  should 
be  suspected  when  the  temperature  remains  raised  in  a  case  where  an 
abscess  has  been  opened  and  is  discharging  quite  freely.  Wlien  the  ab- 
scess continues  to  discharge  for  a  long  time  and  signs  of  lardaceous 
disease — albuminuria,  oedema  of  the  feet,  and  diarrhoea — appear,  the 
outlook  becomes  grave. 

After  hepatic  abscess  and  apparent  reco\'ery  there  is  a  danger  of 
recurrence.  Recurrence  is  more  likely  to  occur  if  the  patient  remains 
in  a  tropical  country  or  returns  to  it  too  soon  after  recover}^  Marshall  * 
advises  that  no  patient  should  be  allowed  to  return  to  a  dangerous  cHmate 
until  two  years  have  elapsed  since  the  abscess  was  opened;  and  it  is 
wiser  that  the  patient  should  remain  in  England  or  a  temperate  climate 
])ermanently. 

TREATMENT. 

The  treatment  of  hepatic  abscess  is  essential^  surgical  and  consists 
in  removal  of  the  pus  and  free  drainage  of  the  abscess  cavity  at  the 
earliest  opportunity.  Medical  treatment  is  only  justifiable  when  there 
is  doubt  whether  an  abscess  has  formed,  and  during  the  period 
when  acute  hepatitis  will  explain  the  condition  of  affairs.  During  this 
period  of  uncertainty  the  medical  treatment  is  the  same  as  in  acute 
hepatitis  {vide  p.  118).  Probably  before  long  it  will  be  possible  to  treat 
this  condition  by  the  hypodermic  injection  of  a  bactericidal  serum  which 
is  polyvalent  and  able  to  counteract  the  forms  of  micro-organisms  most 
probably  present,  as  shown  by  an  investigation  of  the  agglutinating 
properties  of  the  patient's  blood-serum. 

In  the  stage  when  it  is  doubtful  whether  an  abscess  has  actually 
formed  and  it  is  justifiable  to  hope  that  there  is  merely  acute  hepatitis, 
the  patient  should  be  kept  in  bed  on  a  light  diet.  The  bowels  should  be 
kept  open,  if  necessary  by  mild  laxatives,  and  local  pain  relieved  by 
leeches,  cupping,  the  application  of  an  ice-bag,  and  other  methods  men- 
tioned in  the  treatment  of  acute  hepatitis.  Chloride  of  ammonium  in 
twenty-grain  doses  three  times  a  day  should  be  tried,  but  its  value  is 
somewhat  problematical.  Aspiration  of  the  liver  and  removal  of  blood 
from  the  congested  organ  has  been  thought  to  be  of  use  in  preventing 
inflammation  going  on  to  suppuration,  but,  as  already  pointed  out,  it 
is  not  entirely  free  from  risk.     (Vide  Acute  Hepatitis.) 

Aspiration. — Tapping  the  liver  through  the  abdominal  walls  with 
a  Dieulafoy's  aspirator  has  been  commonly  advocated  and  is  often 
successful.  It  is,  however,  dangerous,  and  should  not  be  attempted. 
The  abscess  may  leak  into  the  general  peritoneal  cavitj^  and  set  up  gen- 
eral peritonitis ;  severe  haemorrhage  may  occur  if  the  aspirator  wounds  a 
large  branch  of  the  hepatic  arteiy,  or  possibly  the  aspirator  may  perforate 
one  of  the  hollow  abdominal  viscera,  such  as  the  stomach  or  intestines. 

In  England  Manson  and  Cantlie  t  have  enthusiasticalty  ad\-ocated 

*  Marshall:  Brit.  Med.  Journ.,  1899,  vol.  i,  p.  1387. 
t  Cantlie,  .J.:  Brit.  Med.  Journ.,  1903,  vol.  ii,  p.  656. 


SINGLE    OR  TROPICAL   ABSCESS.  155 

drainage  of  the  abscess  b}^  means  of  a  trocar  and  cannula,  and  estab- 
lishing a  S3'phon  drainage.  This  method  has  not  found  favour  with 
Indian  surgeons,  who  have  had  the  greatest  experience  in  the  treatment 
of  hepatic  abscess.  It  is  urged  that  this  method  is  faulty  in  that  it  does 
not  provide  thorough  drainage,  that  if  the  tube  becomes  displaced  there 
is  great  difficulty  in  replacing  it,  and  that  if  the  tube  gets  out  the  pus  may 
escape  into  the  j^eritoneal  cavity.  After  an  abscess  has  been  emptied 
by  the  cannula  the  liver  may  become  so  nmch  smaller  and  altered  in 
position  that  the  cannula  cannot  be  introduced. into  the  abscess  and 
drainage  is  prevented,  while  leakage  may  take  place  into  the  peritoneal 
cavity. 

The  most  satisfactory  treatment  of  an  abscess  is  free  opening  and 
drainage.  The  surgical  procedure  I  cannot  attempt  to  deal  with,  and 
the  reader  should  refer  to  surgical  text-books  or  to  special  works,  such 
as  Waring's  "Surgical  Diseases  of  the  Liver."  The  position  of  the 
abscess  must  be  first  determined,  and  though  it  is  not  a  harmless  pro- 
cedure, this  must  often  be  done  by  exploration  with  an  aspirator  under 
an  ansesthetic.  The  abscess  should  be  freely  opened  so  as  to  aUow  of  its 
interior  being  explored  and  any  adjacent  abscess  opened.  It  is  essential 
that  adequate  provision  for  free  drainage  should  be  made. 

In  cases  where  an  abscess  bursts  into  the  lung,  pleura,  or  peritoneum 
operation  should  be  undertaken,  and  in  the  case  of  the  peritoneum  of 
course  without  any  delay.  (Vide -p.  144.)  In  rupture  into  the  colon  no 
operation  is  necessary  unless  there  are  signs  of  peritonitis.  Operative 
interference  should  be  undertaken  in  the  rare  cases  where  rupture  occurs 
into  the  pericardium  or  pelvis  of  the  kidney,  but  in  the  former  event  death 
may  be  A'ery  rapid. 

During  convalescence  from  hepatic  abscess  tonics,  fresh  air,  and 
nourishing  food  are  necessary.  Change  of  air  to  the  seaside  should  be 
recommended,  and  if  possible,  the  patient  should  not  return  to  a  tropical 
climate,  and  in  any  case  not  until  two  years  have  elapsed. 


MULTIPLE  ABSCESS  IN  THE  LIVER. 

The  infection  leading  to  multiple  abscesses  in  the  liver  may  reach 
the  organ  in  several  ways.  The  method  of  production  provides  a  means 
of  classifying  multiple  hepatic  abscess. 

(1)  Ordinary  pysemic  abscesses,  in  which  the  infection  arrives  by  the 

hepatic  arter\^ 

(2)  Abscess  due  to  portal  vein  infection.      (a)    Multiple    abscesses  in 

bacHIar}'  and  amoebic 
dj'sentery,  in  appendi- 
citis, etc.,  due  to  infec- 
tive emboli. 
(h)  Suppurative  pylephle- 
bitis.    (Vide  p.  67.) 

(3)  Suppuration  in  and  spreading  from  the  bile-ducts.     This  is  described 

under  "Suppurative  Cholangitis,"  and  includes  verminous  ab- 
scesses due  to  worms  which  haA^e  travelled  up  the  conmion  bile- 
duct. 

(4)  Secondary  abscesses  due  to  the  spread  of  infection  from  a  large  single 

abscess. 

PYEMIC  ABSCESSES. 

In  general  pygemia  numerous  minute  abscesses  may  be  found  in  the 
liver. 

In  24  cases  of  general  pysemia  that  were  examined  in  the  postmortem  room 
of  St.  George's  Hospital,  1890-1896,  abscesses  were  found  in  the  liver  in  4  cases, 
multiple  in  3,  while  in  1  there  were  two  abscesses. 

In  infective  endocarditis  secondar}^  abscesses  in  the  liver  are  rare; 
thus,  in  65  fatal  cases  of  infective  endocarditis  collected  by  Kelynack* 
there  was  only  one  case  in  which  the  liver  was  affected. 

An  hepatic  abscess  may  be  secondary'  to  suppuration  anywhere  in 
the  body,  even  when  there  is  no  generalized  pyeemia.  In  such  cases  the 
liver  is  probably  in  a  state  of  diminished  resistance,  so  that  micro-organ- 
isms which  would  be  destroyed  elsewhere  are  able  to  flourish  there. 
Percival  Pott  long  ago  stated  that  multiple  abscesses  in  the  liver  were 
especially  apt  to  follow  injuries  and  suppuration  in  the  head. 

At  the  present  time,  when  pysemia  is  a  comparatively  infrequent 
disease,  its  commonest  causes  are  acute  infective  periostitis  and  middle- 
ear  disease.  In  cases  of  middle-ear  disease  multiple  hepatic  abscesses 
may  be  merely  pygemic.  But  it  is  noticeable  that  sometimes  abscesses 
are  not  found  in  any  other  organ.  This  is  difficult  to  explain.  It  might 
be  said  that  the  micro-organisnxs  manage  to  get  through  the  lungs  with- 
out being  arrested  there  and  that  the  liver  is  the  place  of  least  resistance, 

*  Kelvnack :  Encvclopsedia  Medica,  vol.  iv,  p.  365. 
156 


MULTIPLE   ABSCESS   IN  THE   LIVER.  157 

the  other  organs  in  the  body  destroying  the  micro-organisms.  Another 
though  rather  unhkely  explanation  is  that  the  micro-organisms  pass 
down  from  the  head  and  drop,  so  to  speak,  through  the  right  auricle  into 
the  hepatic  veins.  This  passage  of  micro-organisms  against  the  current 
of  blood  is  termed  retrograde  embolism:  It  is  rare,  but  it  undoubtedly 
occurs.* 

It  is  a  very  speculative  point,  but  it  is  possible  that  in  the  pre-anses- 
thetic  days  of  Pott,  retrograde  infection  of  the  liver  from  suppuration 
about  the  head  was  commoner  than  at  the  present  time,  when  opera- 
tions are  quietly  performed  under  an  anaesthetic.  Thus  retrograde 
embohsm  is  favoured  by  violent  expiratory  efforts  which  may  result  in 
blood,  and  the  pus  or  micro-organisms  in  it,  being  driven  out  of  the  right 
auricle  into  the  hepatic  veins.  Such  expiratory  efforts  would  be  likely 
to  occur  at  the  time  of  any  operation  in  the  pre- anaesthetic  days,  and 
any  pus  or  micro-organisms  in  the  right  auricle  might  thus  be  driven 
into  the  hepatic  veins  and  infect  the  liver. 

MULTIPLE  ABSCESS  IN  CONNEXION  WITH  PORTAL  VEIN  INFECTION. 

Multiple  abscesses  may  occur  as  the  result  of  widespread  embolism 
of  the  intra-hepatic  branches  of  the  portal  vein.  Where  this  occurs 
without  any  pylephlebitis  of  the  extra-hepatic  parts  of  the  portal  vein, 
the  process  in  the  liver  may  be  regarded  as  due  to  "portal  pyaemia."  In 
reahty  no  hard-and-fast  line  can  be  drawn  between  such  cases  and  typical 
pylephlebitis  with  multiple  foci  of  suppuration  in  the  liver. 

Multiple  abscess  may  occur  in  dysentery.  It  is  rare  in  the  form  de- 
scribed as  amoebic,  rather  less  so  in  non-amoebic,  dysentery.  In  both  these 
forms  of  dysentery  there  may  be  a  number  of  small  abscesses  all  of  about 
the  same  size  and  due  to  multiple  embolism  of  the  intra-hepatic  branches 
of  the  portal  vein.  There  may  be  a  single  large  abscess  which  has,  by 
infection  of  the  branches  of  the  portal  vein,  given  rise  to  secondary  and 
multiple  foci  of  suppuration. 

In  amoebic  dysentery  the  contents  of  the  small  multiple  abscesses 
are  barely  liquid.  The  walls  are  formed  of  necrotic  liver  tissue  and  the 
abscesses  have  evidently  originated  in  a  portal  space.  There  is  usually 
absence  of  the  ordinary  small-cell  infiltration  seen  in  other  forms  of 
suppuration.  (Lafleur.t)  According  to  Rogers,J  the  small  multiple  ab- 
scesses are  due  to  a  mixed  infection  of  amoebae  and  pyogenetic  cocci,  while 
the  large  abscesses  are  solely  due  to  amoebae.  Rogers  figures  small-cell 
infiltration  in  the  small  multiple  abscesses.  Multiple  abscesses  contain- 
ing amoebae  have  been  found  in  cases  where  the  intestines  appeared 
normal.     (Buxton.  §) 

In  non-amoebic  dysentery  the  multiple  abscesses  are  like  those  seen 
in  pylephlebitis.     In  the  non-amoebic  dysentery  seen  in  South  Africa 

*  For  a  number  of  examples  wde  Welch :  AUbutt's  System  of  Medicine,  vol.  vi, 
p.  233. 

t  Lafleur:  AUbutt's  System,  vol.  iv,  p.  158. 

i  Rogers,  L. :  Brit.  Med.  Joum.,  1903,  vol.  i,  p.  1317. 

§  Buxton:  Proc.  Philadelphia  Path.  Soc,  Jan.,  1899. 


158  DISEASES    OF   THE    LIVER. 

in  the  War  of  1899-1902  hepatic  suppuration,  when  it  occurred,  was  in 
the  form  of  multiple  liver  abscesses  without  any  evidence  of  pylephlebitis. 
Multiple  abscesses  from  portal  vein  infection  are  most  commonly 
secondary  to  appendicitis.  The  hepatic  abscesses  may  be  clue  to  multiple 
emboli  of  pus-ceUs  and  ixdcro-organisms  which  have  passed  up  from  a 
small  abscess  in  connexion  with  the  appendix,  the  intervening  part  of 
the  portal  and  superior  mesenteric  veins  being  normal;  or  there  may  be 
suppurative  pylephlebitis  with  multiple  abscesses  in  the  liver.  In  some 
instances  there  is  a  large  abscess  with  smaller  ones  around  it;  the  large 
abscess  may  be  due  to  smaller  and  originally  separate  abscesses  running 
together.  From  leakage  or  rupture  of  a  small  abscess  general  or  locahzed 
peritonitis  will  result;  in  the  latter  case  there  may  be  an  abscess  between 
the  convex  surface  of  the  liver  and  the  diaphragm.  Either  an  empyema 
on  the  right  side  or  merely  pleurisy  with  effusion  is  a  frequent  complica- 
tion. Luckily  hepatic  suppuration  is  not  a  common  complication  of 
appendicitis;  it  is  more  likely  to  occur  with  a  small  abscess  under  con- 
siderable tension. 

In  112  cases  of  appendicitis  examined  after  death  there  were  2  cases  of  abscess 
of  liver,  2  cases  of  suppurative  hepatitis,  and  2  of  perihepatitis.      (Langheld.*) 

The  following  is  a  good  example  of  what  Dieulafoy  calls  the  "appen- 
dicular liver  " : 

A  woman  aged  twenty-four  with  a  history  of  appendicitis  presented  signs  of 
a  local  abscess  in  the  right  iHac  fossa;  the  appendix,  which  was  thickened,  and  an 
ounce  of  pus  in  its  neighbourhood  were  removed.  Tlie  patient  went  on  Avell  for  a 
week,  when  the  discharge  from  the  wound  became  very  profuse ;  exploration  showed 
that  there  was  a  suppurating  cavity  Hned  by  coils  of  intestines.  Her  condition 
became  one  of  chronic  pj'semia,  and  in  tlie  last  seven  weeks  of  life  the  temperature 
was  only  normal  on  four  occasions.  At  the  autopsy  the  right  lobe  was  riddled 
with  abscesses;  there  was  no  general  pylephlebitis  or  thrombosis  of  the  portal  vein, 
but  a  few  intra-hepatic  branches  of  the  portal  vein  in  the  right  lobe  were  throm- 
bosed. 

Sometimes  the  existence  of  the  primary  source  of  infection  in  the 
appendix  is  entirely  latent  and  the  patient  comes  under  obser^'ation 
with  a  hectic  temperature,  rigors,  and  an  enlarged  liver. 

Infection  of  the  liver  with  the  production  of  multiple  abscesses  is 
very  seldom  secondary  to  gastric  ulceration.  Murchison  f  recorded  two 
cases  of  this  kind.  It  is  noticeable  that  suppurative  pylephlebitis  is 
also  extremely  rare  after  gastric  ulcer.  As  a  curiosity  Lambert's  J  case, 
in  which  a  pin  passed  from  the  stoniach  into  the  right  lobe  of  the  liver 
and  set  up  multiple  abscesses,  may  be  mentioned.  In  very  rare  instances 
multiple  abscesses  occur  in  the  liver  after  tj-'phoid  fever;  Gibbon  §  has 
collected  nine  examples.  They  may  be  secondary  to  intercurrent  appen- 
dicitis and  pylephlebitis,  as  in  a  case  of  Osier's,  ||  due  to  embolism  of  the 
small  branches  of  the  portal  vein,  or  to  infection  through  the  hepatic 
artery  and  secondary  to  an  abscess  elsewhere  in  the  body. 

*  Langheld:  Quoted  by  Loison,  Rev.  de  Chirurg.,  1900,  p.  522. 

t  Murchison:  Trans.  Path.  Soc,  vol.  xvii,  p.  145. 

t  Lambert:  New  York  Med.  Journ.,  Feb.  5,  1898. 

§  Gibbon,  J.  H. :  American  Journ.  Med.  Sciences,  vol.  cxxv,  p.  592. 

II  Osier:  Trans.  Associat.  American  Physicians,  vol.  xii,  p.  380. 


MULTIPLE    ABSCESS    IN   THE    LIVER.  159 

111  a  case  of  primary  ulceration  of  the  lower  part  of  the  rectum  multiple  abscesses 
in  tlie  liver,  containing  the  Bacillus  influenzae  similis,  were  found  by  Ophiils.*  There 
was  no  septic  thrombosis  in  the  hasmorrhoidal  or  portal  veins. 

Suppuration  in  the  pelvis  may  give  rise  to  multiple  abscesses  in  the 
liver,  infection  of  the  portal  vein  having  occurred  by  means  of  the  com- 
munications between  the  superior  hsemorrhoidal  branch  of  the  inferior 
mesenteric  vein  and  the  branches  (middle  and  inferior  hremorrhoidal) 
of  the  internal  iliac  veins. 

Thus  a  prostatic  abscess  (Lancereaux  f),  gonorrhceal  salpingitis  (Handford  $), 
perimetric  abscess  (Roughton  §),  and  a  suppurating  submucous  fibromyoma 
(Delestre  1|)  have  been  known  to  give  rise  to  multiple  abscesses  in  the  liver. 


SECONDARY  ABSCESSES  DUE  TO  THE  SPREAD  OF  INFECTION  FROM 
A  LARGE  SINGLE  ABSCESS. 

A  number  of  small  abscesses  are  often  found  associated  with  a  large 
single  abscess  cavity.  In  some  instances  the  large  abscess  is  due  to  a 
number  of  small  abscesses  becoming  confluent.  In  other  instances  the 
small  abscesses  are  secondary  to  infection  from  the  originally  single 
abscess,  and  are  usually  found  in  its  neighbourhood.  They  are  described 
by  Davidson**  under  the  name  of  "  secondary  pyo-septicseinic  abscess." 

The  clinical  features,  diagnosis,  and  prognosis  in  cases  with  the 
larger  multiple  abscesses  in  the  liver  are  practically  the  same  as  in  sup- 
purative pylephlebitis,  to  which  the  reader  should  refer.  The  miliary 
abscesses  in  the  liver  in  general  pysemia  do  not  give  rise  to  any  special 
symptoms. 

*  Ophiils:  American  Joum.  Med.  Sciences,  vol.  cxxii,  p.  797,  1901. 
t  Lancereaux:  Traite  des  Maladies  du  Foie  et  des  Pancreas,  p.  231. 
t  Handford:  Trans.  Path.  Soc,  vol.  xxxvii,  p.  267. 
§  Roughton :  St.  Bartholomew's  Hosp.  Reports,  vol.  xxi,  p.  173. 
II  Delestre:  Bull.  Soc.  Anat.,  Paris,  1898,  p.  219. 
**  Davidson:  Allbutt's  System  of  Med.,  vol.  iv,  p.  133. 


PERIHEPATITIS, 

Perihepatitis,  or  inflammation  of  the  peritoneal  capsule  of  the  liver, 
mav  be  acute  or  chronic. 


ACUTE  PERIHEPATITIS. 

Causation. — In  temperate  climates  acute  inflammation  of  the  peri- 
toneum covering  the  liver  and  the  underlying  capsule  is  not  a  primary 
and  independent  condition,  in  the  same  way  that  pericarditis  and  pleurisy 
often  are,  but  is  secondary  to  disease  in  the  Hver  or  in  the  neighbourhood, 
and  is  usually  quite  subordinate  to  the  primary  affection.  The  only 
exception  to  this  is  the  occurrence  of  traumatic  perihepatitis  such  as 
follows  fracture  of  the  ribs  on  the  right  side;  in  such  cases  acute  inflam- 
mation of  the  peritoneum  covering  the  bruised  or  wounded  areas  of  the 
Uver  may  be  found  if  there  is  a  fatal  termination.  It  has  been  thought 
(Canthe  *)  that  in  the  tropics,  where  acute  perihepatitis  is  much  com- 
moner than  in  this  country,  it  may  be  a  primary  affection  Hke  acute 
pleurisy;  but  it  is  reasonable  to  beheve  that  its  frequency  in  hot  climates 
depends  on  the  fact  that  active  congestion  of  the  liver  and  acute  hepa- 
titis, which  are  common,  often  extend  to  the  surface  of  the  liver  and 
thus  set  up  perihepatitis. 

Acute  perihepatitis  may  be  secondary  to  acute  hepatitis,  suppuration 
inside  the  liver,  such  as  abscess,  suppurating  hydatid  cyst,  pylephlebitis, 
and  cholangitis.  It  may  also  be  seen  over  rapidly  growing  nodules  of 
new-growth  involving  the  surface  of  the  hver. 

Acute  inflammation  of  the  peritoneal  surface  of  the  liver  necessarily 
occurs  in  general  peritonitis  and  in  some  forms  of  localized  peritonitis 
due  to  inflammation,  ulceration,  and  perforation  of  adjacent  viscera; 
for  example,  in  pancreatitis  and  inflammation  locahzed  to  the  lesser  sac 
of  the  peritoneum,  in  cholecystitis,  and  in  subphrenic  abscess  and  sub- 
phrenic pyopneumothorax  due  to  perforation  of  a  gastric  or  duodenal 
ulcer,  to  appendicitis,  or  other  causes.  In  such  conditions  where  the 
surface  of  the  liver  happens  to  form  the'  waU  of  an  abscess  cavity  there 
is  really  no  need  to  speak  of  pyoperihepatitis  or  pyopneumo-perihepa- 
titis.f  The  first  symptoms  of  a  subphrenic  abscess  due  to  appendicitis 
may  be  those  of  acute  perihepatitis. 

In  acute  pleurisy,  pneumonia,  and  pericarditis,  inflammation  may 
spread  through  the  diaphragm  and  set  up  local  peritonitis  over  the  con- 
vexity of  the  liver.  Occasionally  it  develops  in  the  course  of  chronic 
venous  engorgement  of  the  liver,  either  as  part  of  a  passing,  or  of  a  terminal, 

*  Cantlie,  J. :  Encyclopaedia  Medica,  vol.  vii,  p.  2. 

t  Vide  Chauffard,  in  Traite  de  M^decine  (Bouchard-Brissaud),  tome  v,  p.  154. 
1902. 

160 


PERIHEPATITIS. 


161 


infection  of  the  liver.     Acute  perihepatitis  is  more  often  partial  than 
universal. 

Morbid  Anatomy. — The  surface  of  the  liver  in  the  affected  area  shows 
the  dulling,  loss  of  gloss,  and  slight  granular  appearance  seen  in  acute 
peritonitis  elsewhere.  The  vessels  of  the  capsule  are  injected  with  blood 
and  the  parenchyma  of  the  liver  immediately  under  the  capsule  may 
show  cloudy  sweUing. 

At  a  later  date  organization  of  the  fibrinous  lymph  takes  place  and 
filamentous  adhesions  are  left  as  a  memorial  of  past  acute  peritoneal 
inflammation,  uniting 
the  liver  to  the  dia- 
phragm, abdominal 
wall,  and  the  adjacent 
viscera.  These  adhe- 
sions are  not  progres- 
sive and  must  not 
be  considered  as  evi- 
dence of  chronic  peri- 
hepatitis. Such  adhe- 
sions are  very  com- 
monly found  in  the 
postmortem  room, 
and  in  the  great  ma- 
jority of  instances 
have  given  rise  to  no 
symptoms  during  life. 
Exceptionally  they 
may,  however,  induce 
pain  and  a  sense  of 
dragging  in  the  right 
hypochondrium.  If 
the  adhesions  involve 
the  stomach,  its  move- 
ments may  be  so  interfered  with  that  dyspepsia  of  a  very  obstinate 
nature  (adhesion  dyspepsia)  may  be  produced. 

Mr.  AUingham  performed  laparotomy  on  a  patient  with  very  severe  dyspepsia, 
under  the  care  of  Dr.  Vernon  Jones,  and  found  firm  adhesions  between  the  stom- 
ach and  liver;  these  were  divided  and  the  symptoms  were  reheved.  There  was 
a  history  of  acute  perihepatitis  twelve  years  before  in  India. 

As  an  example  of  perihepatitis  due  in  all  probability  to  a  terminal 
infection  the  following  case  is  of  interest : 

A  boy  aged  ten  years  died  in  St.  George's  Hospital  with  adherent  pericardium, 
a  dilated  and  hypertrophied  left  ventricle,  and  signs  of  backward  pressure.  In  the 
last  few  days  of  life  he  had  pain  over  the  liver  and  a  raised  temperature,  but  no 
jaundice.  At  the  autopsy  tliere  was  recent  lymph  on  the  surface  of  the  liver,  which 
weighed  29  ounces.  On  section  the  liver  was  swollen,  of  a  mottled  yellow  colour, 
not  nutmeggy.  Unfortunately  none  of  the  liver  was  preserved  for  more  minute 
examination,  but  its  description  .suggests  that  a  terminal  infection  had  fallen  on 
tlie  liver  and  given  rise  to  acute  inflammation  of  its  capsule  and  degenerative 
changes  in  the  liver  cells. 
11 


Fig.  22. — Lymph  in  Acute  Perihepatitis  on  the  Surface 
OF  A  Cirrhotic  Liver  which  Shows  Some  Little 
Thickening  of  the  Capsule. 

The  lymph  appears  opaque.  Some  separation  has  taken 
place  between  the  layers  of  the  thickened  capsule.  (Photo- 
micrograph by  S.  G.  Penny,  Esq.) 


162  DISEASES    OF   THE    LIVER. 

Signs  and  Symptoms. — There  is  pain  over  the  Kver,  which  is  made 
worse  on  respiration  and  is  accompanied  by  a  friction  rub.  The  right 
side  of  the  chest  moves  Httle  and  the  Hver  is  tender  to  the  touch,  and 
when  an  attempt  to  examine  it  is  made,  the  overlying  abdominal  muscles 
at  once  become  rigid.  If  the  liver  is  grasped  between  the  two  hands, 
placed  in  front  and  behind,  and  moved  backwards  and  forw^ards,  acute 
pain  is  elicited,  which  may  run  up  to  an  area  between  the  clavicle  and 
the  acromion  process  of  the  scapula  on  the  front  of  the  chest  (Cantlie), 
thus  differing  from  the  shoulder  pain  of  intra-hepatic  disease.  Dry 
cough  may  occur  and  be  readily  induced  by  examination  of  the  liver. 
Fever,  sense  of  weight  in  the  hypochondrium,  and  other  symptoms  may 
be  due  to  accompanying  and  underlying  hepatitis  and  active  congestion. 
Local  acute  perihepatitis  may  give  rise  to  some  ascites,  but  very  rarely 
to  a  sufficient  amount  to  be  detected  clinically.  I  am  convinced  that 
slight  ascites  may  be  thus  produced  from  observation  during  laparotomy 
on  a  case  of  pylephlebitis  with  local  involvement  of  the  capsule  of  the 
liver. 

Diagnosis. — It  must  be  remembered  that  perihepatitis  is  j^ractically 
always  due  to  some  underlying  condition,  and  that  diligent  search  must 
always  be  made  for  the  primary  disease,  such  as  abscess  and  other  forms 
of  intra-hepatic  suppuration,  hepatitis,  new-growth,  chronic  venous 
engorgement,  etc.  Acute  perihepatitis  is  very  likely  to  be  confused  with 
acute  pleurisy  on  the  right  side;  indeed,  in  many  cases  the  two  condi- 
tions may  co-exist,  the  inflammation  spreading  from  one  serous  surface 
to  the  other.  In  differentiating  these  two  conditions  Cantlie  lays  stress 
on  grasping  the  li^^er  between  the  hands  and  moving  it ;  the  pain  running 
up  into  the  supraclaAdcular  fossa  is  regarded  as  diagnostic  of  perihepa- 
titis. 

Treatment. — Rest  and  warmth  in  bed  are  important,  while  the  under- 
lying cause  is  sought  for  and  treated.  Treatment  of  the  inflamed  capsule 
of  the  liver  wiU  consist  chiefly  in  the  relief  of  pain.  If  severe,  half  a 
dozen  leeches  may  be  applied  and  be  followed  by  a  poultice;  in  slighter 
cases  hot  fomentations  over  the  liver,  or  counterirritation  in  the  form 
of  a  mustard  poultice  or  leaf,  will  be  sufficient.  Dry  cupping  often  gives 
considerable  rehef .  Strapping  the  side,  as  in  the  method  emploj^'ed  for 
fractured  ribs,  will  minimize  movement  and  pain.  A  light  milk  diet 
should  be  given  at  first  until  the  patient  feels  able  to  take  solid  food. 

CHRONIC  PERIHEPATITIS. 
Under  this  heading  two  conditions  of  very  different  importance  are 
included — (i)  local  and  (ii)  universal  perihepatitis. 

LOCAL  CHRONIC  PERIHEPATITIS. 

This  condition  nia}^  be  due  to  a  number  of  different  causes.  In  its 
slighter  degrees  it  is  seen  as  the  result  of  pressure  in  tight-laced  livers, 
when  a  belt  has  l^een  worn,  or  may  result  from  the  conununicated 
pulsations  of  a  large  heart.     The  thickening  of  the  capsule,  often  asso- 


PERIHEPATITIS.  163 

ciated  with  some  atrophy  of  the  hver  substance  immediately  subjacent, 
is  analogous  to  the  milk  spots  so  commonly  seen  on  the  surface  of  the 
heart.  In  many  cases  this  local  thickening  of  the  capsule  is  associated 
with  backward  pressure  due  to  obstructive  heart  or  lung  disease;  in 
such  cases  the  distension,  and  perhaps  pulsation,  of  the  liver,  by  giving 
rise  to  increased  friction  and  attrition,  helps  to  call  forth  the  capsulitis. 
In  IS  cases  of  Hale  Wliite's  *  backward  pressure  was  present  in  10. 
In  87  cases  of  tricuspid  stenosis  recorded  by  Pitt  f  perihepatitis  was 
present  in  11.  The  local  perihepatitis  is  occasionally  part  of  cancerous 
or  tuberculous  peritonitis,  or  may  be  found  over  a  gumma  or  hydatid 
cyst  embedded  in  the  liver;  it  may  also  be  clue  to  the  irritation  of  a 
calculous  gall-bladder  or  to  a  gastric  ulcer.  Capsulitis  of  the  spleen  is 
frequently  associated  with  it  (in  9  out  of  18  of  Hale  White's  cases). 

Local  perihepatitis  very  seldom  goes  on,  so  far  as  is  known,  to  the 
diffuse  or  universal  form.  NichoUs  {  records  a  case  of  local  perihepatitis 
clue  to  cholecystitis  in  which  this  transformation  was  in  progress.  The 
thickened  portion  of  the  capsule  of  the  liver  does  not  peel  off,  but  is 
firmly  adherent;  it  thus  contrasts  with  the  "false  membranes"  seen  in 
universal  perihepatitis,  which  lie  on  the  surface  of  and  not  in  the  sub- 
stance of  the  capsule  of  the  liver.  The  local  thickenings  on  the  liver 
resemble  anatomically  the  milk  spots  on  the  heart  and  the  corneal  fibro- 
mata on  the  capsule  of  the  spleen.  Microscopically  they  show  parallel 
strands  of  well-formed  fibrous  tissue  with  cells  between  them,  but  do  not 
contain  blood-vessels.  The  fibrous  tissue  shows  hyaline  change.  These 
local  areas  of  chronic  capsulitis  may  be  adherent  to  adjacent  parts,  but 
usually  they  are  free. 

Local  chronic  perihepatitis  may  account  for  some  pain  and  tenderness 
over  the  liver  and  may  possibly  give  rise  to  a  friction  rub  over  the  organ. 
Strictly  localized  perihepatitis  does  not  give  rise  to  ascites;  but  in  some 
cases  where  areas  of  chronic  perihepatitis  are  scattered  over  the  surface 
of  the  liver  so.  as  to  give  rise  to  a  transition  between  local  and  universal 
chronic  perihepatitis,  ascites  may  possibly  be  due  to  this  cause.  The 
cases  of  ascites  in  cirrhosis  of  the  liver  which  are  frequently  tapped  may 
be  due  to  this  form  of  chronic  peritonitis.  Strictly  localized  chronic 
perihepatitis  is  of  little  or  no  clinical  importance  apart  from  the  asso- 
ciated morbid  conditions  of  the  liver. 

Treatment. — If  the  condition  is  suspected  and  there  is  pain,  it  may 
be  treated  by  local  applications,  such  as  poultices,  hot  compresses,  or 
belladonna  plasters,  but  usually  no  special  treatment  is  required. 

*  Hale  White:  Trans.  Clin.  Soc,  vol.  xxi,  p.  219.  AUbutt's  System  of  Medicine, 
vol.  iv,  p.  lis. 

t  Pitt :  Allbutt's  System,  vol.  vi,  p.  23. 

j  Nicholls,  A.  G. :  Studies  from  the  Royal  Victoria  Hospital,  Montreal,  vol.  i, 
No.  3,  p.  41,  1902. 


164  DISEASES   OF  THE   LIVER. 


UNIVERSAL  CHRONIC  PERIHEPATITIS. 

Synonyms:  Diffuse  Chronic  Hyperplastic  Perihepatitis,  Chronic  Hyaline  Perihepa- 
titis, Chronic  Deforming  Perihepatitis,  Icing  Liver  (Zuckergussleber) . 

History,  etc. — ^The  condition  was  observed  by  Budd  *  in  1852. 
Curschmann  f  in  1884  described  the  morbid  changes  in  detail  and  in- 
v^ented  the  graphic  name  of  sugar-iced  hver  (Zuckergussleber).  The 
writings  of  Hilton  Fagge  %  and  Hale  Wliite  §  of  Guy's  Hospital  have  been 
of  great  value  in  distinguishing  the  clinical  aspects  of  perihepatitis  from 
those  of  cirrhosis,  and  in  drawing  attention  to  the  relationship  between 
chronic  interstitial  nephritis  and  chronic  perihepatitis.  Nicholls||  of 
Montreal  has  recently  (1902)  published  a  monograph  of  80  pages,  and 
Kelly  **  has  written  an  exhaustive  paper  on  this  subject. 

This  condition  has  received  a  number  of  rather  cumbrous  names,  but 
is  usually  only  a  local  manifestation  of  diffuse  chronic  peritonitis.  It 
is  in  fact  artificial  to  separate  chronic  universal  perihepatitis 
from  diffuse  chronic  peritonitis.  The  chronic  inflammatory  change 
may  begin  in  the  peritoneal  coat  of  the  liver  and  subsequently 
involve  the  adjacent  peritoneum,  or  it  may  extend  to  the  serous  covering 
of  the  organ  in  cases  of  more  or  less  general  chronic  peritonitis.  As  a 
matter  of  fact,  the  name  chronic  perihepatitis  suggests  a  more  intimate 
relationship  to  the  Uver  than  actually  exists.  A  more  accurate  though 
longer  descriptive  title  would  be  chronic  peritonitis  with  perihepatitis, 
or  chronic  peritonitis  involving  the  liver. 

Pathogeny. — ^The  chronic  peritonitis,  of  which  chronic  perihepatitis 
is  part,  is  usually  that  form  spoken  of  as  simple,  since  it  is  not  mani- 
festly due  to  tuberculosis  or  to  new-growth.  It  is  characterized  by  a 
widespread  fibrosis  with  cicatricial  contraction,  so  that  the  mesentery 
and  omentum  are  shortened  and  the  viscera  become  inclosed  in  a  firm 
casing  which  contracts  upon  and  compresses  them.  In  considering  the 
question  of  causation,  it  wiU.  be  convenient  to  divide  cases  of  chronic 
perihepatitis  and  peritonitis  into  three  groups : 

(I)  When  associated  with  varying  degrees  of  chronic  inflammation 
of  the  pericardium  and  pleurae  (multiple  serositis). 

(II)  When  associated  with  arteriosclerosis  and  granular  kidneys. 

(III)  When  associated  with  other  conditions. 

I.  When  Associated  with  Varying  Degrees  of  Chronic  Inflammation  of 
the  Pericardium  and  Pleurce  (Multiple  Serositis). — Chronic  peritonitis  and 
chronic  universal  perihepatitis  may  be  associated  with  varying  degrees  of 
the  same  change  in,  or  in  connexion  with,  the  serous  membranes  in  the 
thorax — ^the  pericardium  and  pleura.     The  combined  changes  in  more 

*  Budd:  Diseases  of  Liver,  p.  139. 

t  Curschmann:  Deutsche  med.  Wochensch.,  1884,  S.  564. 

X  Hilton  Fagge:  Principles  and  Practice  of  Med.,  vol.  ii,  p.  294. 

§  Hale  White:  Trans.  Clin.  Soc,  vol.  xxi,  p.  219.  Guy's  Hosp.  Reports,  vol. 
xlix,  p.  1. 

II  NichoUs,  A.  G. :  Studies  from  the  Royal  Victoria  Hospital,  Montreal,  \o\.  \, 
No.  3,  April,  1902. 

**  Kelly,  A.  O.  J. :  American  Jour.  Med.  Sciences,  vol.  cxxv,  p.  116.  Jan.,  1903. 


PERIHEPATITIS.  165 

than  one  serous  membrane  are  spoken  of  as  multiple  serositis,  polyorro- 
menitis,  or  Concato's  disease.  There  may  be  a  descending  scale  in  the 
extent  of  the  associated  intrathoracic  changes.  Thus,  there  may  be 
extensive  fibrosis  of  the  mediastina  with  adherent  pericardium  and 
pleurae  (indurative  mediastino-pericarditis),  adherent  pericardium  with 
thickening  and  obliteration,  partial  or  complete,  of  both  or  of  only  one 
pleura,  or  only  a  calcified  and  adherent  or  an  adherent  pericardium.  In 
this  class  the  inflammatory  change  is  most  intense  on  each  side  of  the 
diaphragm,  and  fades  off  in  the  more  distant  parts  of  the  peritoneum 
and  pleurae;  probably  the  constant  movement  of  the  diaphragm  assists 
in  keeping  up  the  morbid  process  when  once  it  has  been  started.  The 
inflammatory  change  beginning  on  one  side  of  the  diaphragm  readily 
spreads  through  the  lymphatics  to  the  neighbouring  serous  membrane. 
In  most  of  the  cases  the  inflammatory  change  is  primary  in  the  pericar- 
dium or  pleura  and  spreads  to  the  convexity  of  the  liver,  but  in  some  it 
is  probable  that  it  begins  as  an  acute  inflammation  close  to  the  convexity 
of  the  liver  and  subsequently  becomes  chronic  and  extends  to  the  right 
pleura  and  pericardium.  In  chronic  perihepatitis  associated  with  intra- 
thoracic changes  of  the  same  kind  the  kidneys  are,  as  a  rule,  healthy, 
or  merely  show  chronic  venous  engorgement.  But  in  some  instances 
they  are  granular  and  thus  merge  into  the  next  group. 

A  well-marked  example  of  chronic  proliferative  peritonitis  and  perihepatitis 
associated  with  chronic  indurative  mediastino-pericarditis  was  seen  in  a  man  aged 
fifty-five  years,  an  in-patient  at  St.  George's  Hospital  in  1896.  He  presented 
ascites,  which  required  tapping  26  times,  and  oedema  of  the  legs ;  during  life  miedi- 
astinal  growth  appeared  probable  from  the  existence  of  post-stemal  dulness.  At 
the  autopsy  the  pericardium  was  firmly  adherent  to  the  heart  and  to  all  the  sur- 
rounding parts,  especially  to  the  region  of  the  thymus  gland,  which  was  occupied  by 
very  dense  firm  fibrous  tissue  (microscopically  only  fibrosis).  There  were  very 
dense  pleural  adhesions,  J  an  inch  thick  on  the  left  side,  and  universal  chronic  perito- 
nitis and  perihepatitis.  The  liver  weighed  72  oimces  and  microscopically  showed 
early  cirrhosis,  though  to  the  naked  eye  it  appeared  normal.  The  kidneys  weighed  8 
ounces  each  and  were  healthy. 

A  number  of  cases  of  universal  chronic  perihepatitis  associated  with 
adherent  pericardium  have  been  recorded  and  the  condition  is  not  in 
reality  rare. 

Gilbert  and  Gamier  *  described  11  cases  under  the  name  of  symphyse  pericardio- 
perih^patique.  Heidemann,t  in  a  paper  on  the  results  of  adherent  pericardium, 
collected  7  fresh  cgises.  Kelly, J  in  his  elaborate  account  of  multiple  serositis, 
referred  to  27  cases  of  universal  perihepatitis  associated  with  adherent  pericardium. 

I  have  seen  2  cases  in  which  chronic  perihepatitis  was  associated  with,  and 
probably  due  to,  extension  of  inflammation  through  the  diaphragm,  form  an  ad- 
herent pericardium  that  had  undergone  calcification. 

A  closely  allied  condition  to  universal  chronic  perihepatitis  associated  with 
adherent  pericardium  was  described  by  Pick  §  as  pericarditic  pseudo-cirrhosis  of  the 
liver,  in  which,  together  with  latent  adherent  pericardium,  there  was  ascites  due  to 
fibrous  hyperplasia  and  circulatory  disturbance  in  the  liver.  Any  evidences  of 
chronic  inflammation  of  the  peritoneum  were  regarded  by  Pick  as  accidental  or 
secondary  to  ascites  and  chronic  venous  engorgement.  Cases  of  this  kind  without 
chronic   universal  perihepatitis   or  chronic   peritonitis   certainly   occur,   and  ha^'e 

*  Gilbert  and  Gamier:  Soc.  de  biolog.,  Jan.  15,  1893. 

t  Heidemann:  Berlin,  klin.  Wochen.,  1897. 

X  Kelly,  A.  O.  J.:  American  Journ.  Med.  Sciences,  vol.  cxxv,  p.  116,  1903. 

§  Pick:  Zeitschrlft  f.  klin.  Med.,  1896,  Bd.  xxix,  S.  385. 


166  DISEASES    OF   THE    LIVER. 

already  been  described  as  exaggerated  cases  of  chronic  venous  engorgement  of  the 
liver.  {Vide  p.  97.)  Kelly,*  on  the  other  hand,  groups  together  under  the  head- 
ing of  "multiple  serositis"  these  cases  of  pericarditic  pseudo-cirrhosis  and  the  cases 
of  "iced  liver,"  or,  as  they  are  usually  called  in  England,  chronic  universal  peri- 
hepatitis, and  while  admitting  some  anatomical  distinctions,  regards  them  as  very 
much  alike  clinically. 

(II)  Chronic  Perihepatitis  Associated  with  Arteriosclerosis  and  Granular 
Kidneys. — Chronic  perihepatitis  is  frequently  associated  with  arterio- 
sclerosis and  granular  kidneys;  this  was  so  in  19  out  of  Hale  White's  f 
22  cases.  In  this  group  there  is  not  the  same  intimate  relationship 
between  chronic  perihepatitis  and  thoracic  lesions  as  in  the  previous 
category,  though  the  two  conditions  may  be  found  together. 

There  appears  to  be  some  connexion  between  arteriosclerosis  and 
fibrosis  of  the  serous  membranes  (perivisceritis). J  It  is  conceivable  that 
arteriosclerotic  change  in  the  kidneys  is  a  disposing  cause  of  chronic 
inflammation  in  the  body  generally.  As  Flexner  §  has  shown,  the  bac- 
tericidal power  of  the  blood  is  reduced  in  chronic  renal  disease  and  so 
allows  microbic  infections  to  occur.  It  is  reasonable  to  believe  that 
chronic  perihepatitis  and  peritonitis  might  be  produced  by  micro-organ- 
isms of  no  great  virulence  but  capable  of  inducing  considerable  fibrosis. 
It  is  more  probable  that  the  process  is  microbic  than  that  it  is  purely 
toxic  and  due  to  an  altered  (ursemic)  condition  of  the  blood.  In  either 
case  the  influence  of  arteriosclerosis  and  granular  kidneys  should  lead 
to  a  similar  change  in  the  other  serous  cavities,  the  pleura  and  peri- 
cardium. This  condition  of  combined  inflammation  of  several  serous 
membranes — 'polyorromenitis  ||  or  multiple  serositis — does  sometimes 
occur  in  cases  of  granular  (arteriosclerotic)  kidneys,  but  it  is  by  no  means 
constant  to  find  another  serous  membrane  involved  as  well  as  the  peri- 
toneum. In  order  to  explain  cases  where  the  peritoneum  alone  is  attackec,! 
or  is  much  more  affected  than  any  of  the  other  serous  membranes,  it  may 
be  suggested  that  the  facilities  for  infection  are  greater  in  the  abdomen 
and  that  the  resistance  of  the  peritoneum  has  been  specially  lowered  in 
these  cases.  It  has  been  thought  that  arteriosclerosis  of  the  small 
vessels  of  the  peritoneum  may  produce  chronic 'peritonitis** — a  fibrosis 
due  to  impaired  nutrition. 

As  an  example  of  this  form  the  following  case  may  be  quoted :  A  woman  aged 
sixty-nine  years  had  ascites  requiring  paracentesis;  eventually  she  died  in  an 
extremely  thin  and  cachectic  state.  The  autopsy  revealed  granular  kidneys, 
universal  chronic  peritonitis,  a  liver  which  weighed  only  23  ounces,  and  on  section 
looked  cirrhotic,  iDut  not  in  the  least  nutmeggy.  Microscopically  the  liver  was 
typically  nutmeggy  and  only  showed  slight  replacement  fibrosis.  The  heart  weighed 
8  ounces,  and  was  dcA^oid  of  epicardial  fat;  on  section  it  showed  brown  atroj^hy  of 
the  myocardium. 

A  well-marked  example  of  chronic  universal  perihepatitis  with  similar  changes 

*  Kelly,  A.  O.  J.:  American  Jour.  Med.  Sciences,  vol.  cxxv,  p.  116,  Jan.,  1903. 

t  Hale  White:  Trans.  Clin.  Soc,  vol.  xxi,  p.  221. 

t  Labadie,  Lagrave  et  Deguy:  Archiv.  General,  de  MM.,  1898,  p.  411  (Perivis- 
ceritis). §  Flexner:  Journ.  Experimental  Medicine,  vol.  i,  1S96. 

II  For  an  account  of  this  condition  see  Taylor,  F. :  Brit.  Med.  Journ.,  1900,  vol. 
ii,  p.  1698;  Kelly,  A.  O.  J.:  American  Journ.  of  the  Medical  Sciences,  vol.  cxxv, 
p.  116,  1903. 

**  Delpeuch :  Archives  Centrales  de  Medecine,  1884.  Quoted  by  Tabadie,  Lagrave 
and  Deguy:  Archives  G^nerales  de  Medecine,  1898,  p.  411. 


PERIHEPATITIS. 


167 


in  the  pleura  and  pei'icardium,  and  granular  kidneys  occurred  in  a  woman  who  died 
in  St.  George's  Hospital  in  coma  in  1898.  She  had  often  been  treated  for  myx- 
cedema.  She  had  ascites,  universal  chronic  perihepatitis,  perisplenitis,  and  peri- 
tonitis with  a  number  of  fibrous  nodules  in  the  peritoneum  near  the  umbilicus 
(peritonitis  fibrosa).  Both  layers  of  the  pericardium  were  much  thickened,  and 
the  cavity  contained  excess  of  fluid.  The  pleurae  were  both  thickened,  showed 
adhesions,  and  contained  about  8  ounces  each  of  clear  fluid.  The  liver  (60  ounces) 
was  nutmeggy  and  free  from  cirrhosis.  Microscopically  there  was  a  dense  layer  of 
fibrous  tissue  on  the  surface  of  the  liver  replacmg  the  capsule.  There  was  sub- 
capsular atrophj'^  of  the  liver  cells,  while  the  branches  of  the  hepatic  artery  and 
portal  vein  appeared  as  ]3rominent  objects  from  a  very  peculiar  swelling  of  their 
coats.  (Vide  Fig.  23.)  This  change  seemed  to  be  due  to  mj^xomatous  degeneration 
and  to  be  connected  with  the  primary  disease — myxcedema.  The  kidneys  (right, 
3^  ounces;  left,  3^  ounces)  were-  red  and  granular.     The  heart  weighed  14  ounces. 


Fig.  23. — Microscopic  Section  showing  Homogeneous  Hyaline  Membrane  on  the  Sur- 
face OF  the  Liver  with  a  Similar  Hyaline  Change  in  the  Fibrous  Tissue  of 
the  Portal  Spaces  in  the  Underlying  Liver  Substance.  From  a  Case  of  Myx- 
cedema. 


The  thymus  gland  could  not  be  found,  and  the  pituitary  body  was  not  enlarged. 
The  thyroid  gland  was  very  atrophied  and  of  a  pale  yellow  colour.  There  was  some 
obsolete  tubercle  in  the  lungs. 

(Ill)  Universal  Chronic  Perihepatitis  Due  to  Other  or  Obscure  Causes. 
— In  a  few  instances  perihepatitis  may  be  associated  with  sj'phihtic 
lesions  of  the  Hver,  but,  as  a  rule,  hepatic  gunuuata  only  give 
rise  to  a  local  thickening  of  the  capsule  of  the  hver. 

Cheadle  *  expresses  his  belief  that  perihepatitis  is  more  marked  and  frequent 
in  association  with  syphilitic  disease  of  the  liver  tlian  in  any  otliei-  condition.  In 
22  cases  of  universal  perihepatitis  collected  by  Hale  White  t  there  ^\■ere  3  in  Avhich 
syphilis  was  the  apparent  factor.     Niunerous  small  syphilitic  gummata  may  so 

*  Cheadle.  W.  B.:  Some  Cirrhoses  of  tlie  T>iver,  1900,  i>p.  41,  43. 
t  Hale  White:  Allbutt's  System,  vol.  iv,  p.  121. 


168  DISEASES    OF   THE    LIVEE. 

extensivel.y  involve  the  capsule  as  to  set  up  universal  perihepatitis.      (Sharkej^,* 
N.  Moore. t) 

In  the  following  case  universal  perihepatitis  and  chronic  peritonitis  were  asso- 
ciated with  the  presence  of  three  old  and  several  recent  gummata  in  the  liver. 
The  patient,  a  man  aged  thirty-seven  years,  who  denied  syphihs,  but  drank  3 
pints  of  beer  daily,  had  been  well  imtil  three  and  a  half  months  before  his  death, 
when  he  began  to  suffer  from  morning  sickness  and  abdominal  pain.  A  month 
later  he  became  jaundiced,  ascitic,  oedematous  as  to  his  legs,  and  vomited  a  little 
bipod.  He  was  tapped  twice,  40  pints  being  removed.  The  urine  was  free  from  albu- 
min. After  death  there  was  general  chronic  peritonitis  of  not  very  marked  degree 
and  universal  chronic  perihepatitis;  the  liver  weighed  56  ounces  and  contained  3 
gummata  ha  the  right  lobe  and  several  scars  and  recent  gummata  in  the  left  lobe; 
there  was  no  general  fibrosis  of  the  liver.  There  appeared  to  be  kinking  of  the 
portal  vem  and  bile-duct  in  the  portal  fissure,  but  on  cutting  away  the  adhesions 
around  them  the  vein  and  duct  were  foimd  to  be  unobstructed.  The  kidneys 
weighed  6  ounces  each  and  were  healthy  and  free  from  lardaceous  change.  The 
heart  weighed  8  ounces  and  was  healthy. 

In  rare  instances  universal  chronic  periliepatitis  may  be  associated 
with  intra-abdominal  malignant  disease  or  be  due  to  tuberculosis.  In  the 
latter  case  the  lesions  are  those  of  chronic  fibrosis  and  are  very  different 
from  those  of  ordinarj^  tuberculous  peritonitis. 

Hale  White  expressed  a  very  definite  opinion  that  imiversal  chronic  perihepa- 
titis was  never  due  to  tuberculous  or  malignant  peritonitis.  This  is  probably  too 
dogmatic  a  statement.  Xicholls  after  discussion  of  the  available  data  concludes 
that  some  cases  are  undoubtedlj^  due  to  tuberculosis. 

Chronic  peritonitis  and  perihepatitis  may  be  associated  with  and 
possibly  due  to  that  rare  condition— cirrhosis  of  the  stomach — the  fibrotic 

process  extending  from  the  stomach  to  the  peritoneum.     This  association 
was  well  illustrated  by  the  f oUowing  case : 

A  man  aged  forty-eight  was  under  my  care  in  St.  George's  Hospital  in  November 
and  December,  1899,  with  a  well-marked  alcoholic  history  and  the  facies  of  hepatic 
cirrhosis.  _  He  was  tapped  twice  for  the  relief  of  ascites  in  those  two  months,  and 
the  question  pi  operative  interference,  with  the  object  of  setting  up  artificial  peri- 
toneal adhesions,  was  being  considered  when  he  suddenly  died.  The  autopsy 
showed  dilatation  of  the  left  ventricle  of  the  heart,  perUiepatitis,  chronic  peritonitis, 
extreme  cirrhosis  of  the  stomach,  and  hypertrophy  of  the  muscular  coat  of  the 
oesophagus.  There  was  extreme  thickening  of  the  submucous  coat  of  the  stomach, 
but  no  trace  microscopicall}^  of  carcinoma.  The  substance  of  the  liver  was  healthy, 
and  the  kidneys  were  normal.  I  have  seen  one  other  case  of  this  kind.  Most 
authorities,  however,  regard  "cirrhosis  of  the  stomach"  as  a  diffuse  carcinomatous 
infiltration. 

It  may  also  be  found  in  cases  of  backward  pressure  without  any  ad- 
herent pericardium.  In  other  instances  alcoholism  has  been  thought  to 
be  the  only  antecedent  condition,  while  sometimes,  as  in  the  very  ex- 
treme condition— systematic  hypertrophic  cirrhosis  of  the  peritoneum 
described  by  Du  Pacquier  J — no  cause  is  forthcoming. 

It  is  conceivable  that  in  some  instances  chronic  perihepatitis  and 
peritonitis  may  start  from  foci  of  local  irritation  which  usually  only 
give  rise  to  circumscribed  perihepatitis.  In  such  cases  the  widespread 
effect  is  analogous  to  the  development  of  a  keloid  in  the  skin  after  a  slight 
injury. 

*  Sharkey,  S.  J.:  Trans.  Path.  Soc.  vol.  xxxiv,  p.  118. 

t  Moore,  N. :     idem,  p.  133. 

j  Du  Pacquier:  Archiv.  General,  de  Medecine,  Dec,  1897. 


PERIHEPATITIS.  169 

NichoUs  *  recorded  in  full  detail  a  case  of  widespread  chronic  hyperplastic 
inflammation  of  the  serous  membranes  (including  perihepatitis)  in  a  woman  aged 
forty-eight  with  a  chronic  duodenal  ulcer  and  sliglit  chronic  interstitial  nephritis. 
The  changes  in  the  serous  membranes  Avere  referred  to  irritation  and  possibly 
infection  from  the  duodenal  ulcer. 

Morbid  Anatomy. — The  surface  of  the  hver  is  covered  over  by  a 
crust  or  coating  of  fibrous  tissue  of  cartilaginous  consistence.  It  is 
ghstening  and  white,  resembles  the  icing  of  confectioners,  and  thus 
accounts  for  the  name  "sugar-iced  liver"  (Zuckergussleber)  which  has 
been  applied  to  this  condition  by  Curschmann.  The  surface  of  this 
casing  is  pitted  or  fenestrated,  probably  as  a  result  of  rupture  during  its 
spontaneous  shrinking  and  contraction.  This  coat  can  be  peeled  off, 
leaving  the  peritoneal  surface  in  a  fairly  healthy  state.  The  liver  is 
compressed  and  deformed  by  the  constant  traction  which  the  cicatricial 
tissue  exerts  upon  it.  Thus  the  anterior  margin  may  be  bent  upwards 
and  over  so  as  to  touch  the  convex  surface.  The  convexity  of  the  liver 
is  usually  much  more  affected  than  the  under  surface,  and  of  course  the 
portions  uncovered  by  peritoneum  are  free  from  the  change.  The  gall- 
bladder is  nearly  always  collapsed  and  buried  under  thick  membrane 
and  is  with  difficulty  discovered,  its  position  being  sometimes  merely 
indicated  by  a  depression. 

In  the  one  case  where  I  have  seen  it  dilated  there  was  malignant  disease  of  the 
peritoneum  in  addition  to  chronic  periliepatitis  and  peritonitis. 

Even  when  the  portal  fissure  is  invaded  by  the  perihepatitis  the 
portal  vein  hardly  ever  becomes  compressed  as  might  be  expected.  Hale 
White  t  points  out  that  if  the  portal  vein  were  compressed  or  kinked 
the  bile-duct  would  also  be  affected,  and  that  this  must  be  very  rare 
from  the  clinical  absence  of  jaundice.  His  point  is  that  ascites  is  due  to 
the  chronic  peritonitis  and  not  to  mechanical  interference  with  the  portal 
vein,  for  in  two  cases — very  exceptional  ones — where  universal  chronic 
perihepatitis  existed  without  any  chronic  peritonitis  there  was  no  ascites. 
In  the  case  given  on  page  168,  however,  there  appeared  to  be  kinking  of 
the  portal  vein  and  bile-duct.  There  may  be  adhesions  between  the 
surface  of  the  liver  and  the  diaphragm,  abdominal  walls,  and  adjacent 
organs. 

The  liver  is  usually  soft,  fatty,  and  shows  chronic  venous  engorgement 
with  general  atrophy.  Multilobular  cirrhosis  is  very  rarely  combined 
with  well-marked  perihepatitis  of  the  kind  now  under  discussion.  It  is 
true  that  adhesions  and  opacity  with  thickening  of  the  capsule  are  often 
seen  in  advanced  cirrhosis,  but  the  combination  of  the  "iced  liver"  and 
cirrhosis  is  so  rare  that  in  Nicholls'  %  monograph  only  one  example  is 
admitted.  Superficial  fibrosis  spreading  in  from  the  surface  (Ghssonian 
cirrhosis)  is  not  uncommon,  l)ut  it  docs  not  extend  for  any  distance. 

Microscopically  the  thickened  membrane  is  seen  to  lie  on  Glisson's 
capsule,  which  is  thrown  into  wavy  folds.     This  "icing"  membrane  is 

*  NichoUs,  A.  G. :  Loc.  cit. 

t  White,  Hale:  Allbutt's  System  of  Medicine,  vol.  iv,  p.  120. 

X  Nicholls:  Studies  from  Royal  Victoria  Hospital,  Montreal,  vol.  i,  No.  3,  p.  26. 


170 


DISEASES    OF   THE    LIVER. 


composed  of  well-formed  fibrous  tissue  arranged  in  horizontal  laminae 
with  a  few  nuclei  between  them.  The  structure  is  like  that  of  a  lamel- 
lar fibroma  of  the  spleen.  The  fibrous  tissue  has  undergone  hyaline 
degeneration.  From  the  presence  of  this  change  NichoUs-  speaks  of  the 
condition  as  hyaloserositis.  The  membrane  does  not  contain  blood- 
vessels and  there  is  usually  a  distinct  line  of  separation  between  the 

membrane  and  the  underlying 

capsule  of  the  liver.     In  the 

^::-..  deeper  layers  and  between  it 

and    the    underlying    capsule, 
•  which    is    thrown    into    folds, 

there  are  collections  of  leuco- 
cytes and  mast  cells ;  there  is  no 
reaction  for  fibrin.  (Nicholls.)- 
The  condition  of  the  un- 
derlying liver  varies  a  little; 
it  is  rarely  absolutely  normal, 
being  generally  atrophied,  with 
fatty  and  pigmentary  change 
in  the  liver  cells,  while  chronic 
''  venous    engorgement    is   very 

common.  Not  very  rarely 
there  is  slight  Glissonian  cir- 
rhosis or  fibrosis  spreading  a 
short  way  into  the  substance 
of  the  liver.  The  underlying 
liver  tissue  may  show  a  similar 
hyaline  change  in  the  fibrous 
septa.     (Fig.  23.) 

The  spleen  is  usually  rather 
larger  than  natural,  and  its 
capsule  shares  in  the  chronic 
thickening  of  the  peritoneum. 
It  is  often  firmly  adherent  to 
the  diaphragm  and  abdominal 
wall. 

The  kidneys  in  cases  asso- 
ciated with  indurative  medi- 
astino  -pericarditis,  adherent 
pericardium,  and  chronic  pleu- 
risy may  show  little  change 
except  chronic  venous  en- 
gorgement. When  chronic  perihepatitis  is  associated  with  arterioscler- 
osis, the  kidneys  usually  share  in  the  change  and  are  red  and  granular. 
The  peritoneum  shows  the  same  fibroid  and  hyaline  change  as  the  cap- 
sule of  the  liver,  and  undergoes  the  same  cicatricial  contraction  and  pucker- 
ing. The  great  omentum  is  rolled  up  and  transformed  into  a  hard  cord,  the 
mesentery  is  thickened,  and  by  its  retraction  tethers  the  intestines,  which 


Fig.  24. — Photomicrograph   showing  the   Thick 
"Icing"  in   Chronic    Universal   Perihepa- 
titis. 
The  line  of  distinction  between   it  and  the  liver 
is  well  seen.     The  liver  showed  some   fibrosis  and 
chronic    venous    engorgement.      (Photomicrograph 
by  Dr.  H.  Spitta.) 


PERIHEPATITIS.  171 

are  much  shortened,  to  the  spine,  so  that  they  cannot  reach  to  the  front 
of  the  abdominal  -vvalL  As  a  result  of  this  the  abdomen  may  be  uni- 
formly dull  in  front. 

The  right  pleura  is  more  often  affected  by  the  chronic  fibroid  change 
than  the  left.  The  body  as  a  whole  is  thin  and  may  be  extensively 
oedematous. 

Clinical  Picture. — Sex. — The  sexes  are  about  equally  affected,  thus 

contrasting  with  cirrhosis,  in  which  the  male  sex  provides  a  large  majorit}^ 

of  the  patients. 

In  Hale  White's  *  21  cases  there  were  13  males  and  8  females.  In  20  cases  that 
I  have  tabulated  the  sexes  were  equally  affected. 

Age. — The  age  varies  considerably,  but  is  generally  about  the  same 

as  in  cirrhosis. 

In  Hale  White's  cases  the  average  age  was  forty-seven  and  a  half  years,  the 
youngest  being  twenty-nine  and  the  oldest  sixty-nine  years.  In  my  20  cases  the 
average  age  was  42.6  years,  being  practically  the  same  in  the  two  sexes;  the  ex- 
tremes were  fourteen  and  sixty-nine  years. 

Heredity  does  not  appear  to  have  any  influence  in  the  development 
of  the  disease,  in  spite  of  the  fact  that  arteriosclerosis,  which  appears 
to  play  some  part  in  the  production  of  chronic  perihepatitis  and  chronic 
peritonitis,  is  to  some  extent  hereditary. 

Onset. — Usually  the  development  of  ascites  is  gradual,  but  in  some 
instances  is  acute;  this  was  so  in  6  out  of  14  cases  selected  by  Nicholls. 
The  condition  has  been  thought  to  date  back  to,  and  be  started  by,  an 
acute  inflammatory  change  involving  the  pericardium  or  liver. 

Course. — The  course  of  the  disease  is  slow  and  extends  over  years. 

Nicholls  finds  that  the  duration  of  the  disease  is  from  two  to  sixteen  years. 

Ascites,  which  constantly  recurs,  is  the  main  symptom,  but  the  general 

health  and  strength  are  fairly  maintained  for  a  long  time.     Emaciation 

gradually  appears  and  death  occurs  from  some  intercurrent  disease  or 

secondary  infection,  such  as  acute  peritonitis,  or  pneumonia. 

In  one  case  under  my  care  death  was  due  to  influenza,  and  at  the  autopsy  there 
were  two  small  recent  ulcers  in  the  first  part  of  the  duodenum  with  acute  inflam- 
mation of  the  duodenum. 

Signs  and  Symptoms. — ^The  condition  is  practically  always  accom- 
panied by  ascites,  and  thus  contrasts  with  cirrhosis,  which  may  be 
quite  latent.  Ascites  is  the  chief  physical  sign  and  requires  frequent 
tapping.  Thus,  Osier  |  refers  to  a  child  in  whom  this  operation  was 
performed  121  times.  As  time  goes  on  tapping  becomes  necessary  at 
shorter  intervals  and  may  be  called  for  every  fortnight  or  even  sooner. 
Ascites  is  compatible  with  fair  health  and  strength  during  the  earlier 
part  of  the  disease,  and  in  the  intervals  between  the  tappings  the  patient 
may  be  up  and  about. 

A  woman  suffering  from  universal  chronic  perihepatitis,  secondary  to  calcifica- 
tion of  the  pericardium,  who  eventually  died  after  her  sixtieth  tapping,  was  married 
after  being  tapped  twenty  times.  She  was  under  the  care  of  my  colleague,  Dr. 
Ewart,  in  St.  George's  Hospital. 

The  recurrence  of  ascites  combined  with  fair  health,  or  at  any  rate 

*  Hale  White:  Allbutt's  System  of  Medicine,  vol.  iv.  p.  121. 
t  Osier:  Practice  of  Medicine,  p.  576,  4th  ed.,  1901. 


172  DISEASES    OF   THE    LITER. 

freedom  from  toxsemia,  are  important  points  in  the  diagnosis  from  cir- 
rhosis. The  ascitic  fluid  is  clear  and  straw-colored,  but  contains  a  high 
percentage  of  albumin  (3  per  cent.),,  -which  alhes  it  T\-ith  inflammatory 
exudations  rather  than  with  passive  transudations.  If  allowed  to  stand, 
threads  of  fibrin  may  be  formed.  OccasionaUy  the  ascites  is  encj^sted 
from  the  presence  of  adhesions.  The  hver  may  be  enlarged  and  palpable  in 
the  earUer  stages,  but  becomes  smaller  as  time  goes  on.  Ascitic  distension 
of  the  abdomen  may  interfere  with  the  estimation  of  the  size  of  the  liver 
and  spleen.     Some  enlargement  of  the  spleen  is  usual  in  3^oung  subjects. 

The  omentum  may  be  felt  as  a  transverse  band  passing  across  the 
abdomen,  and  must  not  be  regarded  as  the  lower  border  of  the  liver. 
The  subcutaneous  abdominal  veins  (superior  and  inferior  epigastric  veins) 
are  sometimes  enlarged  and  are  seen  to  form  a  collateral  circulation 
between  the  superior  and  inferior  venge  cavae.  These  veins  do  not  con- 
verge towards  the  umbihcus,  as  is  the  case  in  the  collateral  circulation  of 
portal  obstruction.  Jaundice  is  almost  always  absent;  it  was  present 
in  only  one  of  the  22  cases  analysed  by  Hale  White,  and  when  it  occurs 
is  probably  due  to  some  independent  or  concomitant  factor.  The  urine 
is  diminished  in  amount  and  may  contain  albumin,  either  from  chronic 
venous  engorgement  or  from  arteriosclerotic  change  in  the  kidneys. 

In  addition  to  ascites  there  may  be  signs  of  the  conditions  specially 
associated  with  chronic  perihepatitis:  Adz.,  (i)  adherent  pericardium, 
chronic  mediastinitis,  dense  pleural  adhesions,  or  (ii)  arteriosclerosis  and 
granular  kidney.  (Edema  of  the  legs  is  often  seen  late  in  the  disease  and 
may  extend  to  the  trunk  and  upper  extremities. 

Since  the  liver  substance  is  weU  preser^'ed,  there  is  little  constitu- 
tional disturbance  and  no  tendency  to  hepatic  inadequacy  or  to 
haemorrhages,  drowsiness,  and  the  other  toxsemic  manifestations  seen  in 
cirrhosis.  If  such  symptoms  do  develop,  they  are  to  be  referred  to  con- 
comitant renal  disease.  It  must  be  remembered  that  in  many  cases 
which  chnicaUy  present  themselves  as  faihng  heart  from  granular  kidnej^s, 
Tvith  ascites  and  general  dropsy,  there  is  universal  perihepatitis.  There 
may  be  loss  of  appetite  and  dyspepsia,  while,  from  the  relaxed  and  flabby 
condition  of  the  abdominal  waUs,  constipation  is  often  induced.  Gastro- 
intestinal haemorrhage  does  not  occur  unless  there  is  some  comphcation, 
such  as  gastric  or  duodenal  ulcer  or,  ia  rare  instances,  cirrhosis. 

Diagnosis. — ^The  presence  of  long-continued  ascites  not  manifestly 
due  to  obstructive  heart  or  lung  disease,  or  to  chronic  parenchymatous 
nephritis,  points  ver}'-  strongly  to  universal  chronic  perihepatitis  and 
peritonitis. 

Differential  Diagnosis. — From  Cirrhosis  of  the  Liver. — When  ascites 
develops  in  cirrhosis  the  end  is  usually  near  and  paracentesis  is  not  likely 
to  be  often  required  unless  the  ascites  is  due  to  associated  chronic  peri- 
tonitis. Repeated  tappings  therefore  are  strongly  in  favour  of  chronic 
peritonitis  and  perihepatitis;  evidence  of  arteriosclerotic  kidney  disease 
would  also  strengthen  this  view.  Jaundice,  grave  constitutional  and 
toxsemic  symptonxs,  haematemesis,  melaena,  haemorrhages,  and  an  enlarged 
liver  and  spleen  are  in  favour  of  cirrhosis. 


PERIHEPATITIS.  173 

From  the  effects  of  backward  'pressure  due  to  dilatation  of  the  right  side 
of  the  heart,  mitral  disease,  etc.,  the  diagnosis  depends  on  the  recogni- 
tion of  the  underlying  cause  and  on  the  good  effects  of  treatment  by- 
cardiac  tonics.  In  cases  of  adherent  pericardium  and  advanced  nutmeg 
liver  (compare  " Pericarditic  Pseudo-cirrhosis  of  the  Liver,"  p.  97)  the 
resemblance  to  chronic  perihepatitis  associated  with  adherent  pericar- 
dium is  very  close,  but  cardiac  treatment  is  much  more  effective  in  the 
former  condition,  which  occurs  mainly  in  the  young,  while  universal 
chronic  perihepatitis  is  little  affected  by  this  treatment  and  usually 
occurs  in  adults. 

In  malignant  disease  of  the  liver  with  ascites  there  is  considerable 
enlargement  of  the  liver,  with  perhaps  some  palpable  nodules  of  new- 
growth,  and  the  course  of  the  disease  is  much  more  rapid. 

Syphilitic  gummata  in  the  liver  may  closely  imitate  perihepatitis  by 
giving  rise  to  recurrent  ascites,  and  the  distinction  between  them  is  often 
very  difficult.  Outward  signs  of  sy]3hilis  may  be  entirely  absent,  even 
when  there  are  numerous  gummata  in  the  Hver.  The  only  reliable  means 
of  making  a  diagnosis  is  by  giving  the  patient  a  vigorous  antisyphilitic 
course  of  iodides. 

Chronic  Tuberculous  Peritonitis. — In  this  condition  the  effusion  is 
seldom  very  large  and  lumps  may  be  felt  in  the  abdomen.  Induration 
around  the  umbilicus,  concomitant  pleurisy,  and  fever  are  points  in 
favour  of  tuberculous  peritonitis.  In  cases  of  doubt  the  tuberculin  test 
can  be  employed. 

Prognosis. — The  prognosis  is  most  unfavourable:  death  always 
occurs  eventually,  though  it  may  be  postponed  for  a  long  period.  Thus 
a  patient  may  live  to  be  tapped  60  or  even  100  times.  But  as  time  goes 
on  the  tappings  become  necessary  at  shorter  intervals,  and  the  patient 
gradually  gets  weaker.  The  disease  has  been  said  to  be  more  rapidly  fatal 
in  cases  associated  with  adherent  pericardium. 

Treatment. — Treatment  is  only  palliative.  Dry  diet,  viz.,  limiting 
the  intake  of  fluid,  and  diuretics,  such  as  citrate  of  caffeine,  diuretin,  stro- 
phanthus,  digitalis,  apocynum,  may  be  tried.  Iodide  of  potassium  is 
usually  given  a  trial,  but  it  is  very  doubtful  whether  it  has  any  effect 
except  when  there  is  syphilitic  disease  of  the  liver.  However,  as  the 
diagnosis  between  gummata  involving  the  portal  vein  and  universal 
perihepatitis  may  be  difficult,  it  is  well  to  give  iodides  on  the  chance  of 
an  error  in  diagnosis.  Paracentesis  should  be  performed  when  necessary . 
a  permanent  drain  is  somewhat  dangerous  from  the  risk  of  infection  and 
subsequent  peritonitis,  and  it  should  therefore  not  be  employed.  Hale 
White  *  speaks  of  having  tried  it  without  any  benefit  in  one  case. 

Dissecting  off  a  small  piece  of  the  membrane  covering  the  liver  and 
uniting  the  liver  with  the  abdominal  wall,  as  in  Drummond  and  Morison's 
operation  for  cirrhosis,  was  tried  in  one  case  of  Dr.  Ewart's  t  by  Mr. 
Warrington  Howard  in  St.  George's  Hospital,  and  I  believe  by  others,  but 
without  any  permanent  benefit. 

*  Hale  White :  Allbutt's  System,  vol.  iv,  p.  123 
t  Brit  Med.  Journal,  1899,  vol.  i,  p.  908. 


CIRRHOSIS  OF  THE  LIVER. 

CLASSIFICATION  OF  THE  VARIOUS  FORMS  OF  CIRRHOSIS. 

Cirrhosis  of  the  liver  has  been  classified  in  various  ways,  according 
to  its  causes,  according  to  the  methods  by  which  the  cirrhosis  is  brought 
about,  according  to  the  anatomical  changes  and  lesions,  and  according  to 
the  distinctive  clinical  features.  Some  writers,  such  as  Lancereaux* 
and  Hawkins,!  consider  cirrhosis  under  the  headings  of  alcohohc,  mala- 
rial, and  syphilitic.  But  as  there  are  other  factors  which  may  lead  to 
cirrhosis,  this  classification,  though  in  some  ways  convenient,  is  not 
sufficiently  broad. 

Classification  According  to  the  Methods  by  which  Cirrhosis  is 
Induced. — The  following  classification  of  the  cirrhoses  has  been  drawn 
up  by  Chauffard  J  and  is  based  on  the  ^'arious  methods  b}^  which  the 
changes  in  the  liver  are  brought  about : 

I.  Vascular,     (a)  Toxic.  (i)  Poisons  taken  by  the  mouth. 

(ii)  Poisons   manufactured   in  the 
intestinaltract. 
(6)   Infective.  (i)  The    direct    action   of    micro- 

organisms, 
(ii)  The  action  of  bacterial  toxines, 
either  produced  by  bacteria 
in  the  liver  itself  or  manu- 
factured elsewhere  in  the 
body  and  carried  to  the  Kver. 
■   (c)  Dystrophic.      (i)  Due    to    arteriosclerosis;     this 

kind  of  cirrhotic  liver  would 
be  homologous  to  a  granular 
or    arteriosclerotic    kidney, 
the  fibrosis  being  a  replace- 
ment fibrosis, 
(ii)  Due  to  chronic  venous  conges- 
tion, the  fibrosis  of  a  nutmeg 
liver. 
IT.  Biliary.        (a)  Secondary  to  obstruction  of  the  larger  bile-ducts. 
(&)   Primarily  an  inflammation  of  the  smallest  bile- 
ducts,    leading    to    a    monolobular    cirrhosis. 
Hanot's   hypertrophic    cirrhosis   with   chronic 
jaundice. 
HI.  Capsular      cirrhosis  or  perihepatitis, 
(a)  Chronic  localized. 
(h)  Chronic  universal. 

*  Lancereaux :  Traits  des  Maladies  du  Foie  et  du  Pancreas,  1899. 
t  Hawkins,  H.  P. :  Allbutt's  System  of  Medicine,  vol.  iv. 

j  Cliauffard,  A.:  Trait6  de  M'^d^cine  [Charcot,  Bouchard,  Brissaud],  vol.  iii,  p. 
827,  1892 

174 


CIRRHOSIS    OF   THE   LIVER.  175 

This  classification  is  too  elaborate,  for  even  from  a  theoretical  point 
of  view  the  toxic  and  infective  forms  overlap,  while  from  a  clinical 
standpoint  some  of  these  subdivisions  are  too  minute  to  l^e  of  much 
practical  value. 

Anatomical  Classifications. — Adami  *  has  proposed  a  division  of 
cirrhosis  on  anatomical  grounds. 

(I)  Portal  cirrhosis. 

(II)  Biliary  cirrhosis,  (a)  beginning  around  the  larger  ducts. 

(h)  beginning  around  the  smallest  bile-ducts 
and  capillaries. 

(III)  Pericellular  cirrhosis. 

(IV)  Arterial  cirrhosis;  caused  by  arteriosclerosis  inducing  a  dys- 
trophic cirrhosis  or  fibrous  replacement. 

In  a  microscopic  examination  of  the  liver  in  100  consecutive  cases  Adami  t 
found  that  hepatic  arteriosclerosis  was  by  no  means  uncommon,  although  it  was 
never  marked.  Arteriosclerotic  fibrosis  of  the  hver  might  naturally  be  expected 
in  the  aged,  and  a  statement  to  this  effect  is  sometimes  made.  Personally  from  a 
microscopic  examination  of  a  large  number  of  livers  I  consider  it  to  be  very  rare,  and 
when  present  of  very  slight  degree.  I  have  often  seen  considerable  atrophy  of  the 
liver  cells  without  any  replacement  fibrosis. 

(V)  Centrilobular  cirrhosis  consisting  in  fibrous  replacement  around 
the  intralobular  veins  and  due  to  chronic  venous  engorgement. 

It  has  often  been  assumed  that  chronic  venous  engorgement  is  a  cause  of  fibrosis, 
and  though  it  is  true  that  some  atrophy  of  the  liver  cells  with  a  little  secondary 
fibrous  replacement  is  met  with,  there  seems  to  be  no  proof  at  all  that  chronic  venous 
engorgement  of  the  liver  alone  gives  rise  to  anything  resembling  ordinary  cirrhosis. 
Other  factors,  such  as  the  action  of  toxines  absorbed  froni  the  intestines,  which  are 
specially  prone  to  catarrh  in  chronic  venous  engorgement,  may  increase  this  amount 
of  fibrosis.  But  for  practical  uses  it  is  safe  to  state  dogmatically  that  chronic 
venous  engorgement  is  not  a  cause  of  hepatic  cirrhosis.  This  question  is  discussed 
under  the  heading  of  "Chronic  Venous  Engorgement"  (p.  88). 

(VI)  Secondary  or  centripetal  cirrhosis  is  the  same  as  capsular  or 
Glissonian  cirrhosis  or  perihepatitis,  which  is  described  elsewhere 
and  is  really  quite  distinct  from  cirrhosis  of  the  liver. 

It  is  true  that  a  certain  amount  of  fibrosis  may  spread  into  the  liver  substance 
from  the  capsule,  but  the  most  marked  perihepatitis  may  exist  without  any  trace 
of  hepatic  fibrosis;  when  an  extension  inwards  does  occur,  the  sequence  of  events 
is  analogous  to  what  occurs  in  cases  of  interstitial  pneumonia  secondary  to  chronic 
pleurisy  (pleurogenous  pneumonia).  It  has  been  suggested  that  toxic  bodies 
manufactured  in  connexion  with  the  process  of  perihepatitis  may  be  absorbed  by 
the  lymphatics,  pass  into  the  liver,  and  set  up  fibrosis.  If  this  does  occur,  its 
results  are  comparatively  slight  and  of  no  practical  importance. 

(VII)  Sporadic  cirrhosis.  This  group  includes  (i)  the  fibrosis  that 
occurs  locally  round  miliary  or  larger  granulomata,  such  as  tuber- 
cles or  gummata,  (ii)  the  fibrosis  developing  around  focal  necroses, 
(iii)  fibrosis  associated  with  anthracosis  or  silicosis.  {Vide  "Pig- 
mented Cirrhosis.")  This  class  is  chiefly  interesting  from  an 
anatomical  and  pathological  standpoint;  clinical  manifestations 
are  exceptional,  but  when  they  are  present  they  resemble  those  of 
portal  cirrhosis. 

*  Adami,  J.  G. :  Sajous'  Annual,  vol.  ii,  p.  284,  1899. 
t  Adami:  Montreal  Med.  Jour.,  Jan.    1897. 


176  DISEASES    OF   THE    LIVER. 

The  Author's  Anatomical  Classification, — A  purely  structural  classi- 
fication may  be  drawn  up  from  the  microscopic  appearances  as  fol- 
lows: 

(I)  Multilobular  cirrhosis  in  which  a  varying  number  of  lobules  are 
enclosed  in  a  fibrous  ring ;  the  following  sub-varieties  may  be  rec- 
ognized : 

(a)  With  fatty  change  in  the  liver  cells. 

(6)  With  hypeiplasia  of  the  liver  cells  to  such  an  extent  that 
nodular  cirrhosis,  or  cirrhosis  with  adenoma,  results. 

(c)  With  pigmentation  of  the  liver  cells  and  also  of  the  fibrous 
tissues  (hsemochromatosis). 

(d)  Mixed,  with  pericellular  infiltration  of  the  hepatic  lobules. 
This  is  sometimes  seen  in  rapidly  advancing  cirrhosis. 

Multilobular  cirrhosis  is  almost  always  due  to  poisons  brought  by 
the  portal  vein,  and  is  therefore  spoken  of  as  periportal  or  venous  cir- 
rhosis, but  it  may,  in  exceptional  instances,  be  associated  with  changes 
in  the  larger  bile-ducts. 

(II)  Monolobular  cirrhosis;  each  lobule  is  separated  from  its  fellows 
by  a  delicate  fibrosis.  The  arrangement  thus  far  imitates  that 
normally  seen  in  the  pig's  liver.  Monolobular  cirrhosis  is  specially 
related  to  inflammation  of  the  minute  bile-ducts,  but  is  sometimes 
described  as  a  result  of  cholangitis  of  the  larger  ducts.  Mono- 
lobular cirrhosis  is  often  complicated  by  multilobular  cirrhosis 
and  is  frequently  associated  with  pericellular  cirrhosis,  so  that  a 
mixed  form  of  cirrhosis  results. 

(III)  Pericellular  cirrhosis;  each  hepatic  cell  is  separated  by  young 
connective  tissue  from  its  fellows. 

(IV)  Mixed  cirrhosis;  in  which  there  are  various  combinations  of  the 
three  preceding  main  types,  the  multilobular,  monolobular,  and 
pericellular.  This  is  met  with  in  many  cases  of  portal  cirrhosis, 
especially  when  the  course  of  the  disease  has  been  rapid,  and  is  also 
seen  at  the  termination  of  long-standing  cases  of  hypertrophic 
biliary  cirrhosis.  Mixed  cirrhosis  is  a  common  anatomical  form, 
but  has  no  claims  to  be  considered  as  a  clinical  type  of  cirrhosis. 

(V)  Sporadic  fibrosis,  in  which  there  are  isolated  patches  of  fibrosis 
not  corresponding  with  any  of  the  preceding  categories.  Under 
this  heading  come  local  fibrosis  around  parasites,  cysts,  granulo- 
mata,  the  results  of  small  areas  of  focal  necrosis,  and  the  replace- 
ment fibrosis  seen  in  chronic  venous  engorgement. 

In  the  foregoing  anatomical  classifications  the  portal  and  bihary 
forms  of  cirrhosis  are  of  great  clinical  importance,  the  others,  with  the 
exception  of  pericellular  cirrhosis  of  congenital  S5^philis  and  the  cirrhosis 
of  hsemochromatosis  (p.  300),  are  chiefly  of  pathological  interest. 

Clinical  Classification. — If  any  formal  classification  be  adopted,  it 
should  be  one  that  can  be  used  at  the  bedside.  A  large  number  of 
different  varieties  of  hepatic  cirrhosis  have  been  described,  and  in  many 
cases  the  probable  causes  of  the  cirrhosis,  or  associated  conditions,  such 


CIRRHOSIS   OF  THE   LIVER.  177 

as  alcohol,  malaria,  S3q3hilis,  tubercle,  diabetes,  dyspepsia,  biliary  ob- 
struction, have  been  taken  as  grounds  for  estabhshing  different  tj^pes  of 
the  disease.  Again,  cirrhosis  has  been  classified  according  to  the  size  of 
the  liver  or  of  the  spleen.  A  large  (hypertrophic)  cirrhotic  liver  and  a 
small  (atrophic)  cirrhotic  liver  are  often  spoken  of;  while  the  French 
school  has  distinguished  different  types  of  biliary  cirrhosis  not  only 
according  to  the  relation  in  size  between  the  liver  and  spleen,  but  also 
according  to  the  time  incidence  of  enlargement  of  the  two  organs.  Thus, 
the  liver  may  be  much  larger  (hepatomegalic),  of  relatively  much  the 
same  size  (splenomegahc)  or  even  smaller  (hypersplenomegahc  bihary 
cirrhosis)  than  the  spleen;  or  the  liver  may  be  enlarged  before  (pre- 
splenomegalic),  at  the  same  time  (splenomegalic),  or  after  (metaspleno- 
megalic  hypertrophic  bihary  cirrhosis)  the  enlargement  of  the  spleen  is 
detected.  These  titles  serve  to  show  the  minute  and  elaborate  character 
of  the  classification  attempted. 

A  practical  classification,  which  can  to  some  extent  be  utilized  in 
clinical  practice,  is  that  proposed  by  Senator. 

I.  Portal  Cirrhosis,     (a)  The  hobnailed  hver,  cUminished  in  size. 

(6)  With  jaundice,  which  is  either  due  to  gastro- 
intestinal catarrh  obstructing  the  common 
bile-duct,  or  to  pressure  exerted  on  the 
intra-hepatic  radicles  of  the  bile-ducts. 

(c)  With  increased  size  of  the  liver,  which  may 
subsequently  be  followed  by  a  diminution 
in  bulk. 

II.  Biliary  Cirrhosis,     (a)  Due  to  calculous  obstruction  of  the  ducts. 

No  splenic  enlargement,  no  ascites. 
(&)  With  an  enlarged  spleen.     This  is  a  tran- 
sitional form  to  the  next. 

III.  Hypertrophic  biliary  cirrhosis  with  chronic  jaundice. 


From  a  practical  point  of  view  it  seems  to  me  to  be  best  to  make,  in 
the  first  instance,  a  broad  division  of  cirrhosis  into  two  principal  t}'pes 
as  shown  by  their  clinical  features: 

(a)  Ordinary  or  common  cirrhosis  (portal), 

in  which  hsematemesis  is  an  early  symptom  and  ascites  a  terminal 
incident.  Jaundice  is  not  prominent;  death  may  be  preceded 
by  a  toxsemic  state  without  much  or  any  ascites.  The  liver  may 
be  either  large  or  small,  but  shows  multilobular  fibrosis ;  the  spleen 
is  enlarged,  but  not  so  constantly  or  markedly  as  in  the  second 
category. 
(&)  The  biliary  type.  Jaundice  is  the  most  prominent  feature  and 
may  be  constant  for  long  periods;  hsematemesis  and  ascites  are 
only  met  with  exceptionally.  A  little  ascites  may  develop  as  a 
terminal  phenomenon  shortly  before  death.  The  liver  is  enlarged, 
sometimes  to  an  extreme  degree.  The  surface  is  smooth  and  the 
12 


178  DISEASES    OF   THE    LIVER. 

fibrosis  of  a  mixed,  diffuse,  or  monolobular  type.     The  spleen  is 
enlarged,  sometimes  greatly. 
In  this  work  these  two  main  types  of  cirrhosis  will  be  adhered  to, 
but  short  sections  on  the  subvarieties  of  cirrhosis,  included  under  these 
two  main  types,  will  be  added. 
Portal  Cirrhosis. 

Variety:  Pigmentary  Cirrhosis. 
Biliary  Cirrhosis. 

(i)  Hypertrophic  Biliary  Cirrhosis, 
(ii)  Obstructive  Biliary  Cirrhosis. 
Comparison  of  the  Main  Forms  of  Cirrhosis  with  some  Forms  of 
Kidney  Disease. — Portal  cirrhosis  may  be  compared  to  a  granular  kidney. 
Hypertrophic  biliary  cirrhosis  may  be  likened  to  chronic  parenchymatous 
nephritis,  the  changes  being  due  to  poisons  reaching  the  organs  by  the 
arterial  blood-stream.  The  terminal  production  of  multilobular  cirrhosis 
in  long-standing  hypertrophic  biliary  cirrhosis  corresponds  to  the  evo- 
lution of  a  contracting  or  small  white  kidney,  due  to  the  addition  of  the 
changes  of  a  granular  or  arteriosclerotic  kidney  to  chronic  parenchyma- 
tous nephritis  (large  white  kidney).  Lastly,  obstructive  biliary  cirrhosis 
is  comparable  to  consecutive  nephritis. 


PORTAL  CIRRHOSIS. 

Synonyms:    Common,  Alcoholic,  or  Atrophic  Cirrhosis,     Multilobular,  Annular,  or 
Venous  Cirrhosis,  Laennec's  Cirrhosis,  Hobnailed,  Gin,   or  Whisky- 
drinker's   Liver,    Chronic    Interstitial    Hepatitis. 

The  term  atrophic  cirrhosis,  though  commonly  used  as  synonymous 
with  portal  cirrhosis,  is  unsuitable,  inasmuch  as  the  liver  is  often  larger 
than  natural.  The  adjectives  portal,  multilobular,  and  common  are  more 
accurate.  Old  names,  now  forgotten,  for  the  condition  are  granulated, 
tuberculated,  lobulated  liver. 

DEFINITION. 

The  disease  is  characterised  anatomically  by  fibrosis  spreading  from 
the  portal  spaces  and  enclosing  varying  numbers  of  lobules,  in  which  the 
cells  tend  to  show  degenerative  changes.  Clinically  dyspepsia,  hsemat- 
emesis,  splenic  enlargement,  terminal  ascites,  and  oedema  of  the  feet 
are  the  essential  features,  while  jaundice  is  either  absent  or  transient 
and  slight.  The  disease  is  commonest  about  the  age  of  fifty  and  is 
frequently  related  to  chronic  alcoholism. 

HISTORY. 

The  hardened  condition  of  the  liver  was  described  by  Vesalius  (1514- 
1564),  Harvey,  Morgagni,  and  others.  Dr.  Payne*  in  reviewing  the  his- 
tory of  cirrhosis  reproduces  the  drawing  of  a  cirrhotic  liver  described  in 
the  Philosophical  Transactions  of  1685  by  John  Browne,  surgeon  to 
St.  Thomas'  Hospital.  The  ascites  in  this  case,  as  in  others  before  this 
*  Payne,  J.  F. :  Trans.  Path.  Soc,  vol.  xl,  p.  310. 


CIRRHOSIS    OF   THE   LIVER.  179 

date,  was  thought  to  be  the  result  of  drinking  too  much  water,  a  ''fault 
which,"  according  to  Dr.  Payne,  "the  bold  spirits  of  the  time  were  much 
on  their  guard  against."  Matthew  Baillie  *  gave  a  good  naked-eye 
description  of  the  disease  under  the  name  of  "common  tubercle  of  the 
liver";  he  says  it  was  generally  known  as  a  "scirrhous  liver,"  but  he 
regarded  it  as  a  disease  peculiar  to  the  liver  and  more  apt  to  occur  in 
those  accustomed  to  drink  spirituous  liquors. 

The  term  "cirrhosis"  was  invented  in  1819  by  Laennec,t  who  re- 
garded the  bile-stained  "hobnails"  as  masses  of  yellow  (y.tppik)  new- 
growth,  invading  the  liver,  hence  cirrhosis.  Hanot  dutifully  proposed 
that  portal  cirrhosis  should  be  spoken  of  as  Laennec's  cirrhosis.  It  is 
curious  to  note  that  in  the  last  quarter  of  last  century  the  other  form  of 
cirrhosis,  i.  e.,  hypertrophic  biliary,  was  named  after  Hanot. 

CarswellJ  in  1838  was  the  first  to  point  out  the  presence  and  im- 
portance of  fibrosis  in  cirrhosis,  and  was  confirmed  by  Kierman's  histo- 
logical researches.  Clinically  Todd,  Murchison,  and  Hale  White's  ob- 
servations have  in  more  recent  times  advanced  our  knowledge  of  the 
subject.  For  further  details  as  to  the  history  of  cirrhosis  the  reader  is 
referred  to  Dr.  Wickham's  Legg's  §  essay  on  this  point. 

ETIOLOGY. 

Age. — Portal  cirrhosis  is  a  disease  of  late  middle  life  and  usually 
proves  fatal  about  fifty  years  of  age. 

In  165  adults  whose  livers  wei'e  cirrhotic  the  average  age  was  48.7  years ;  of 
those,  121  were  males  (average  age,  49.4  years")  and  44  females  (average  age,  47 
years).     In  Yeld's||  128  cases  the  average  age  was  47.-5  years. 

There  is  a  definite  group  of  cases  of  genuine  portal  cirrhosis  in  young 
children,  which  will  be  specially  referred  to  elsewhere.  (Vide  p.  332.) 
The  existence  of  an  infantile  type  of  portal  cirrhosis,  as  distinct  from 
biliary  cirrhosis  and  the  pericellular  cirrhosis  of  congenital  syphilis,  has 
been  well  established,  but  the  cases  are  far  from  common. 

Hilton  Fagge**  found  that  the  average  age  of  persons  in  whose  bodies 
cirrhosis  of  the  liver  was  discovered  without  any  marked  symptoms 
during  life  was  five  years  higher  than  that  of  persons  dying  of  the  disease. 
This  would  tend  to  show  that  the  compensatory  processes  had  been  very 
successful.  My  own  figures,  however,  show  ver}^  little  difference  be- 
tween these  two  classes. 

In  78  patients  dying  from  cirrhosis  the  average  age  was  48.3  years,  while  in  87 
patients  who  died  from  independent  causes  but  whose  livers  were  cirrhotic  the 
average  age  was  49.1  years. 

There  is  reason  to  think  that  cases  of  cirrhosis  with  a  very  distinct 
alcoholic  history  are  fatal  at  an  earlier  age  than  cases  of  cirrhosis  in  which 

*  Bailhe,  M. :  Morbid  Anatomy,  p.  141,  1793. 

t  Laonneo:  Traits  de  I'auscultation  Med.,  tome  i,  p.  368,  note,  1819. 
t  Carswell :  Illustrations  of  Elementary  Forms  of  Disease. 
§  W.  Legg:  St.  Bartholomew's  Hospital  Reports,  vol.  vii,  p.  74. 
II  Yeld :  St.  Bartliolomew's  Hospital  Reports,  vol.  xxxiv,  p.  215. 
**  Plilton  Fagge :  Guy's  Hosp.  Reports,  Series  iii,  vol.  xx,  p.  193. 


180  DISEASES   OF  THE   LIVER. 

alcoholic  excess  either  did  not  exist  or  is  not  a  prominent  recent  feature  in 
the  history.     This  is  especially  marked  in  the  case  of  women. 

In  1 14  cases  tabulated  by  Fenton  and  myself  the  average  age  of  all  the  alcoholic 
cases  of  cirrhosis  was  46.6  years,  as  against  49.9  years  for  the  non-alcoholic  cases. 
Taking  the  ages  of  the  sexes  separately,  the  figures  read  as  follows — alcoholic 
males,  47.8  years;  non-alcoholic  males,  49.3;  alcoholic  females,  42.8;  non-alcoholic 
females,  51.5. 

Sex. — Portal  cirrhosis  is  commoner  in  men  than  in  women;  probably 
in  the  proportion  of  about  5  to  2. 

In  560  cases  where  cirrhosis  of  the  liver  was  found  after  death,  obtained  by 
adding  together  the  statistics  of  Price,  Kelynack,  Yeld,  and  St.  George's,  there  were 
412,  or  73.6  per  cent.,  in  males,  and  148,  or  26.4  per  cent.,  in  females.  In  a  larger 
number  of  figures  obtained  from  the  bills  of  mortality  of  New  York  for  the  years 
1889-1899,  Crook  *  found  that  in  4737  deaths  from  cirrhosis  2980,  or  62.3  per  cent., 
were  males,  and  1757,  or  37.7  per  cent.,  females. 

From  statistics  of  St.  George's  Hospital  it  appears  that  cirrhosis  is 
more  often  latent  in  men  than  in  women.     {Vide  p.  226,  "Latency.") 

In  children  some  doubt  seems  to  exist  as  to  the  sex  incidence;  in 
Palmer  Howard's  f  63  cases  males  were  affected  twice  as  often  as  females, 
while  Birch-Hirschfeld's  statistics  were  exactly  the  reverse. 

Occupation,  etc. — Cirrhosis  is  more  frequent  in  those  who  are  brought 
in  contact  with  alcoholic  drinks,  especially  publicans,  commercial  trav- 
ellers, and  others  who  have  occasion  frequently  to  drink  over  business 
or  to  "treat." 

In  149  persons  connected  with  the  liquor  traffic,  Dickinson  J  found  that  post- 
mortem examination  showed  cirrhosis  to  occur  in  22,  while  in  149  other  persons 
not  brought  specially  into  contact  with  alcohol  it  was  present  only  in  8. 

Cirrhosis  is  more  often  seen  in  those  whose  life  is  sedentary  than  in 
persons  leading  an  active  outdoor  life.  Sir  D.  Duckworth  §  in  1876 
quoted  the  experience  of  Sir  W.  Gull  and  Sir  G.  Burrows  to  the  effect  that 
cirrhosis  was  rare  in  the  upper  and  well-to-do  classes. 

Geographical  Distribution. — It  is  an  interesting  fact  that  the  dis- 
tribution of  cirrhosis  does  not  run  hand  in  hand  with  that  of  alcoholism. 
The  abuse  of  alcoholic  drinks  is  very  widespread,  but  the  distribution  of 
cirrhosis  does  not  by  any  means  correspond.  Thus,  in  hot  countries  alco- 
holic excess  more  often  tends  to  produce  a  rapid  reaction  in  the  liver, 
such  as  hepatitis,  while  in  cold  climates  cirrhosis  is  a  more  frequent 
result.  But  in  temperate  climates  the  incidence  of  cirrhosis  varies  veiy 
considerably;  thus,  cirrhosis  is  common  in  London,  but  comparatively 
rare  in  Scotland.  There  are  also  curious  differences  as  to  the  distribu- 
tion of  cirrhosis  in  France  which  cannot  be  correlated  with  that  of  tem- 
perance and  intemperance.  It  is  an  interesting  question  whether 
the  incidence  of  cirrhosis  has  undergone  any  marked  change  in  the  course 
of  years.     In  1857  Budd  I|  wrote  that  "cirrhosis  is  more  common  in 

*  Crook :  Medical  News  (N.  Y.),  Feb.  8,  1902,  p.  246. 

t  Palmer  Howard:  Trans.  Assoc.  American  Physicians,  vol.  v,  p.  1. 

X  Dickinson,  W.  H. :  Trans.  Royal  Medico-chirurg.  Soc,  1873,  p.  34. 

§  Duckworth :  St.  Bartholomew's  Hosp.  Reports,  vol.  x,  1874. 

il  Budd:  Diseases  of  the  Liver,  p.  150,  3d  ed.,  1857. 


CIRRHOSIS    OF   THE   LIVER.  181 

England  and  Scotland  than  in  France,"  while  at  the  present  day  cirrhosis 
is  probably  quite  as  frequent  in  France  as  in  England,  and  much  more  so 
than  in  Scotland.  In  this  connexion  it  is  significant  that  alcoholism  has 
enormously  increased  in  France  of  late  years. 

Heredity. — Multilobular  cirrhosis  is  not  a  ''family"  disease  or  one  that 
tends  to  recur  in  members  of  the  same  family;  in  this  way  it  contrasts 
with  hypertrophic  biliary  cirrhosis,  which  often  attacks  several  members 
of  the  same  family.  In  a  few  instances  several  adults  may  die  of  alco- 
holic cirrhosis,  probably  from  a  family  failing  towards  alcoholism.  In 
children,  the  death  of  two  or  more  members  of  the  same  family  from 
multilobular  cirrhosis  is  more  often  met  with.  This  may  depend  on 
hereditary  influences,  syphihs  disposing  the  organ  to  the  incidence  of 
ordinary  cirrhosis — ^parasyphilitic  cirrhosis  {vide  p.  189).  An  important 
factor  in  the  development  of  cirrhosis  is  the  vitality  of  the  liver;  if  its 
resistance  is  congenitally  feeble,  factors  which  would  otherwise  be  harm- 
less, such  as  the  poisons  of  the  specific  fevers,  indiscretions  in  diet,  and 
so  forth,  may  lead  to  cirrhosis.  It  is  conceivable  that  alcoholism  in  the 
mother  may  so  influence  the  livers  of  her  offspring  that  cirrhosis  develops 
in  them  more  readily  than  it  otherwise  would.  Precocious  alcoholism 
or  peculiarly  unsuitable  food,  such  as  pickles  or  fish  soaked  in  vinegar, 
may  be  the  causes  of  two  or  more  cases  of  cirrhosis  in  the  same  family. 
Jollye  *  described  cirrhosis  in  a  brother  and  sister  who  had  been  accus- 
tomed to  take  vinegar.  The  following  cases  are  interesting  in  this  con- 
nexion : 

Two  sisters,  aged  nine  years  and  ten  years,  died  in  St.  George's  Hospital  in  1899 
and  1901  with  hobnailed  livers  weighing  20  and  12  ounces  respectively.  In  both 
of  them  laparotomy  was  performed ;  in  the  younger  because  tuberculous  peritonitis 
was  suspected ;  in  the  older,  who  had  a  temperature  of  104°  and  diarrhoea,  because 
perforation  of  a  typhoid  ulcer  appeared  probable.  The  mother  was  extremely 
alcoholic,  but  persisted  that  she  had  not  given  alcohol  to  the  children.  A  brother 
aged  sixteen  years  was  in  St.  Thomas'  Hospital  in  1901  and  had  laparotomy  per- 
formed for  supposed  tuberculous  peritonitis;  no  evidence  of  perihepatitis  or  peri- 
tonitis was  found,  but  there  was  a  hobnailed  liver.  All  three  cases  died  shortly 
after  laparotomy  was  performed  and  were  examined  after  death.  No  abdominal 
lesion  except  hepatic  cirrhosis  was  found  and  no  evidence  of  syphilis  was  forth- 
coming in  any  of  them. 

THE  PATHOGENY  OF  CIRRHOSIS. 

Cirrhosis  of  the  liver  is  the  result  of  some  poison,  or  possibly  of  poison- 
producing  bodies,  such  as  micro-organisms,  reaching  the  liver.  The 
factors  in  question  may  travel  to  the  liver  either  (1)  by  the  portal  vein, 
or  (2)  by  the  hepatic  artery;  in  other  words,  they  may  be  derived  from 
the  alimentary  canal  or  from  the  general  circulation.  When  the  active 
agent  arrives  by  the  portal  vein,  the  resulting  cirrhosis  is  usually  of  the 
ordinary,  venous  or  portal  type ;  when  the  liver  is  affected  secondary  to 
an  arterial  infection  or  toxaemia,  the  cirrhosis  is  often  of  a  more  mixed 
type,  and  may  then  resemble  that  of  biliary  cirrhosis.  It  is,  however, 
true  that  in  some  instances  where  the  poison  arrives  by  the  hepatic 
artery  the  cirrhosis  is  of  the  portal  type. 

*  Jollye:  Brit.  Med.  Joum.,  1892,  vol.  ii,  p.  858. 


182  DISEASES    OF   THE    LIVER. 

In  reviewing  the  etiology  of  cirrhosis  it  will  be  convenient,  first  of  all, 
to  consider  the  poisons  and  micro-organisms  which  reach  the  organ  by 
the  portal  vein,  and  then  those  conveyed  by  the  hepatic  artery. 

SYNOPSIS. 

I. — Poisons  Conveyed  to  the  Liver  by  the  Portal  Vein. 
(a)  Ingested  poisons :  (1)  alcohol;  (2)  other  poisons. 
(6)  Poisons  manufactured  in  the  ahmentary  canal.     Dyspeptic  cirrhosis. 

(c)  Umbihcal  vein  cirrhosis  and  congenital  syphilis. 

(d)  Poisons  manufactured  in  the  spleen. 

II. — Micro-organisms  Conveyed  to  the  Liver  by  the  Portal  Vein. 

III. — Poisons  Conveyed  to  the  Liver  by  the  Hepatic  Artery. 

IV. — Micro-organisms  Conveyed  to  the  Liver  by  the  Hepatic  Artery. 

Conclusion. 

I. 

The  Poisons  that  Reach  the  Liver  by  Means  of  the  Portal 
Vein  may  be  divided  into  the  f oUowing  categories : 

(a)  The  poisons  introduced  into  the  intestinal  tract  from  without: 
(1)  alcohol,  and  (2)  other  bodies. 

(6)  Those  manufactured  in  the  alimentary  canal  as  the  result  of  faulty 
digestion,  fermentation,  and  putrefaction. 

(c)  The  poison  of  congenital  syphilis,  conveyed  by  the  umbihcal 
vein. 

(d)  Poisons  manufactured  in  the  spleen. 
(a)  Ingested  Poisons. 

Of  these,  alcohol  requires  much  the  most  consideration  and  discus- 
sion. 

(1)  Alcohol  and  Alcoholic  Drinks. — With  regard  to  the  question 
whether  alcohol  is  the  cause  of  cirrhosis,  chnical  and  experimental  evi- 
dence are  hardly  in  accord.  In  practice  there  are  few  points  more 
certain  than  that  the  abuse  of  alcoholic  drinks  is  a  frequent  precursor 
of  hepatic  cirrhosis,  while  from  experiments  on  animals  the  bulk  of  the 
evidence  is  in  a  contrary  direction.  In  67  cases  of  cirrhosis  analysed  ' 
by  the  Collective  Investigation  Committee,*  60  per  cent,  were  described 
as  hard  drinkers,  30  per  cent,  as  free  drinkers,  and  only  the  remaining 
10  per  cent,  as  fairly  temperate. 

Among  drunkards,  however,  cirrhosis  is  not  so  frequent  as  is  usually 
assumed.  Thus  in  250  postmortems  on  confirmed  drunkards  who  died 
suddenly  from  the  effects  of  alcohol,  Formad  f  only  found  cirrhosis  in 
six.  The  reason  why  alcohohcs  frequently  escape  cirrhosis  is  probably 
either  that  they  have  considerable  resistance  or  that  some  other  and 
necessary  factor,  which  usuaUy  accompanies  alcoholism,  is  wanting. 
The  curious  contrast  between  the  frequency  with  which  alcohohsm 
appears  in  the  history  of  cases  of  cirrhosis  and  the  percentage  of  cirrhosis 
in  drunkards  may  perhaps  be  elucidated  by  supposing  that  when  the 
liver  is  susceptible  and  likely  to  suffer  from  the  effect  of  alcohol  it  becomes 
comparatively  quickly  affected,  and  that  thus  before  the  tyi^ical  signs 

*  Collective  Investigation  Committee's  Report  upon  the  Connexion  of  Disease 
with  Habits  of  Intemperance,  by  Isambard  Owen,  M.D.  Brit.  Med.  Journal,  ISSO, 
vol.  i.  t  Formad :  Trans.  Assoc.  American  Physicians,  vol.  i,  p.  225. 


CIRRHOSIS    OF   THE    LIVER.  183 

of  alcoholism  have  become  well  marked  the  case  assumes  the  aspect  of 
hepatic  cirrhosis. 

There  are,  of  course,  many  cases  of  ordinary  cirrhosis,  especially  in 
children,  where  alcoholism  can  be  excluded  as  an  antecedent  factor  in 
the  production  of  cirrhosis. 

Experimentally  the  introduction  of  alcohol  into  the  stomach  or 
portal  vein  of  animals  has  usually  given  rise  to  fatty  change  and  some- 
times to  some  necrosis  of  the  liver  cells  with  a  little  small-cell  infiltration 
around,  but  in  only  a  few  instances  has  cirrhosis  resulted. 

Numerous  observers,  Strassmann,*  Afanasieff,t  von  Kahlden,J  Sabourin,§ 
Lafitte,  ||  Pohl,**  Scagliosi,tt  have  perseveringly  administered  alcohol  in  consid- 
erable quantities  to  animals  over  a  fairly  prolonged  period,  and  have  entirely  failed 
to  detect  any  evidence  of  cirrhosis  in  the  liver. 

Straus  and  Blocq  Jf  introduced  a  tube  into  the  stomach  of  rabbits,  and  by  this 
means  gave  10  grammes  of  alcohol  daily;  after  three  or  four  months  a  small-cell 
proliferation  was  found  at  the  periphery  of  the  lobules.  This  is  hardly  comparable 
to  genuine  cirrhosis,  and,  moreover,  the  introduction  of  the  tube  into  the  stomach 
complicates  matters,  inasmuch  as  it  may  have  led  to  catarrh,  and  thus  to  the  manu- 
facture and  subsequent  absorption  of  other  irritating  bodies.  De  Rechter  §§  is  the 
only  other  observer  who  has  seen  cirrhosis  follow  the  continued  administration  of 
alcohol ;  he  observed  it  in  dogs  and  rabbits. 

Since  alcohol  alone  is  not  sufficient  to  account  for  cirrhosis  either  in 
man  or  animals,  the  undoubted  association  between  alcohohsm  and 
cirrhosis  must  be  explained  in  some  other  way.  Two  possibihties  may 
be  referred  to:  (i)  That  though  ordinary  ethylic  alcohol  itself  does  not 
produce  cirrhosis,  alcoholic  drinks  in  virtue  of  other  bodies  contained 
in  them  are  responsible  for  cirrhosis.  It  has  been  suggested  that  amy  lie 
alcohol  is  the  important  factor,  but  this  requires  definite  proof.  Lan- 
cereaux  ||  ||  believes  that  sulphate  of  potash,  with  which  wines  in  Paris 
were  formerly  largely  "plastered"  (4  to  6  grammes  per  litre),  is  the 
causal  factor  in  the  production  of  cirrhosis,  and  supports  his  contention 
by  production  of  cirrhosis  in  rabbits,  guinea-pigs,  and  dogs  fed  on  sul- 
phate of  potash.  The  amount  of  the  salt  given  to  these  animals  was 
veiy  large,  corresponding  for  an  adult  man,  according  to  Vallin,***  to  a 
quantity  of  60  to  350  grammes  per  diem.  Viola's  fit  observations  on 
cirrhosis  in  Venice  lent  support  to  the  theory  that  sulphate  of  potash 
was  an  important  factor  in  the  production  of  cirrhosis.  Lancereaux's 
theory,  however,  is  invalidated  by  the  facts  that  potassium  sulphate 
has  not  been  shown  to  be  present  in  alcoholic  drinks  in  other  countries 
where  cirrhosis  is  common,  and  that  in  1891  the  amount  of  sulphate  of 
potash  allowed  to  be  added  to  wine  in  Paris  was  reduced  by  the  loi  griffe 

*  Strassmann:  Vierteljahr.  f.  gericht.  Med.,  1888,  Bd.  xlix,  232. 

t  Afanasieff :  Ziegler's  Beitrage,  Bd.  viii,  S.  443. 

X  V.  Kahlden :  Ziegler's  Beitrage,  Bd.  ix,  S.  349. 

§  Sabourin :  La  Gland  Biliare  d'Homme,  1888.     ||  Lafitte :  These  de  Paris,  1892. 
**  Pohl:  Archiv  f.  experiment.  Path.  u.  Pharmak.,  Bd.  31,  1893. 
ttScagliosi:  Virchow's  Archiv,  September  17,  1896,  Bd.  cxlv,  S.  546 
XX  Straus  and  Blocq:  Archiv  de  Physiol.  Norm,  et  Pathol.,  1887,  p.  409. 
§§  De  Rechter:  Bull.  Acad.  M6d.  de  Belg.,  1892,  No.  6,  p.  425. 

II II  Lancereaux:  Bull,  de  I'Acad.  de  M&l.  Paris,  Sept.  7, 1897,  t.  xxxvii,  p.  202. 
***  Vallin:  Bull,  de  I'Acad.  de  Med.,  1897,  t.  38,  pp.  285,  343;  1899,  t.  39,  p.  257. 
ttt  Viola:  Archiv  G6n.  de  Med.,  Jan.,  Feb.,  March,  1898,  pp.  1,  164,  318. 


184  DISEASES    OF  THE   LIVER. 

to  2  grammes  per  litre;  so  that,  if  his  theor\"  is  correct,  cirrhosis  ought 
to  have  become  less  common  in  Paris,  which  is  certainly  not  the  case. 

(ii)  According  to  the  other  theory,  alcohol  and  alcoholic  drinks  act 
in  a  secondary  manner,  and  either  (a)  set  up  gastro-intestinal  catarrh 
and  thus  lead  to  the  production  of  poisonous  bodies  which  when  carried 
to  the  liver  cause  cirrhosis,  or  (&)  when  acting  on  the  liver  simultaneously 
with  bacterial  poisons  so  lower  its  resistance  that  cirrhosis  results  from 
the  effects  of  the  latter. 

(a)  With  regard  to  the  first  view,  Boix  has  described  ''dyspeptic 
cirrhosis,"  which  is  not  necessarily  alcoholic,  but  is  due  to  the  action  of 
fatty  acids,  such  as  butyric,  lactic,  acetic,  and  valerianic;  this  he  supports 
by  experimental  results.  Clinically  the  frequent  existence  of  long- 
continued  dyspepsia  is  quite  in  accord  with  this  hAqiothesis.  This  point 
will  be  referred  to  later  (p.  186). 

(6)  Scagliosi  concludes  that,  while  alcohol  or  bacterial  poisons  alone 
do  not  permanently  damage  the  liver,  alcohol  may  render  persistent  the 
lesions  induced  temporarily  in  the  liver  by  the  poisons  of  the  specific 
fevers  and  other  infections,  and  so  induce  cirrhosis.  Ramond  *  comes 
to  much  the  same  result.  He  managed  to  produce  cirrhosis  by  giving 
alternate  doses  of  bacterial  toxines  and  alcohol  by  the  mouth  to  animals. 
He  found,  by  examination  of  the  toxicity. of  the  faces  in  man,  that 
alcohol  does  not  necessarily  increase  the  poisonous  bodies  in  the  ali- 
mentary canal;  he  was  therefore  not  inclined  to  support  the  first  view. 
He  believes  that  alcohol  acts  as  a  ceUular  poison  on  the  liver  cells  and 
thus  inhibits  their  special  function  of  destroying  poisons  brought  to 
the  liver.     These  poisons  are  then  free  to  induce  cirrhosis. 

There  is  not  much  to  choose  between  these  two  view^s,  and  it  is  neither 
necessary  nor  possible  to  adopt  one  exclusively.  It  is,  indeed,  not  im- 
probable that  both  of  them  may  be  true. 

To  conclude:  mth  regard  to  the  role  of  alcohol  in  the  production  of 
cirrhosis,  it  may  safely  be  held  that  alcoholism  is  frequently  an  ante- 
cedent condition,  but  that  'per  se  alcohol  has  no  specific  action  on  the  liver 
except  fatty  degeneration.  It  gives  rise  to  cirrhosis  in  a  secondary 
manner,  either  by  leading  to  the  production  of  sclerogenic  poisons  or  by 
enabling  such  poisons  to  have  fuU  sway  on  the  liver.  The  importance  of 
alcoholism  has  been  made  rather  too  much  of,  and  it  is  not  sufficiently 
recognised  that  other  factors  may  lead  to  cirrhosis,  and  that  a  congenital 
or  acquired  want  of  resistance  on  the  part  of  the  liver  itself  is,  though 
hard  to  estimate,  probably  of  great  importance. 

(2)  Cirrhosis  due  to  Ingested  Poisons  other  than  Alcohol. — There  are 
numerous  cases  of  undoubtedly  non-alcoholic  cirrhosis,  especially  in 
children.  In  some  of  these  there  has  been  a  definite  history  of  high 
living  and  occasionally  two  or  even  more  members  of  a  fainily  have  early 
in  life  become  affected  with  hepatic  cirrhosis.  Cases  are  on  record  in 
which  fish  pickled  in  vinegar  had  been  largely  taken,  while  spices,  curries, 
and  highly  flavoured  food  have  long  been  thought  to  account  for  some 
cases  of  cirrhosis.  But  here  it  at  once  becomes  evident  that  it  is  difficult 
*  Ramond :  La  Presse  M^dicale,  April  21,  1897. 


CIRRHOSIS   OF  THE   LIVER.  185 

to  draw  a  hard-and-fast  line  between  poisons  which  are  ingested  and 
give  rise  to  cirrhosis  by  virtue  of  their  own  inherent  irritating  properties, 
and  those  factors  which  set  up  gastro-intestinal  catarrh  and  by  the  man- 
ufacture of  fermentation  products  inside  the  ahmentary  canal  lead  to  what 
has  been  termed  dyspeptic  cirrhosis.  Experimentally,  it  is  true,  Boix  * 
produced  some  cirrhosis  in  rabbits  by  feeding  them  on  acetic,  butyric, 
valerianic,  and  lactic  acids,  but  these  acids  are,  on  the  whole,  more  likely 
to  be  produced  by  fermentation  in  the  human  ahmentary  canal  than  to 
be  swallowed  as  such  in  food.  A  good  example  of  cirrhosis  due  to  poison- 
ous food  is  reported  by  Segers  f  among  the  Fuegians,  who  eat  large 
quantities  of  mussels — from  12  to  25  pounds  daily.  At  a  certain  stage  of 
their  development  the  mussels  are  toxic  from  the  presence  of  myrtilo- 
toxin.  As  a  result  of  this  poison  the  livers  of  the  Fuegians  become  en- 
larged and  subsequently  cirrhotic  and  small. 

In  rare  instances  cirrhosis  has  been  found  to  be  associated  with  the 
presence  in  the  liver,  or  possibly  to  be  due  to  the  irritation  set  up  by, 
particles  of  carbon  absorbed  from  the  alimentary  canal.  This  form  of 
cirrhosis — cirrhosis  anthracotica — has  been  seen  in  connexion  with  pul- 
monary anthracosis,  and  Adami  I  refers  to  an  analogous  form  asso- 
ciated with  stonemason's  lung — silicosis.  Lancereaux  §  says  it  occurs 
in  workers  in  copper  and  in  coal-miners,  and  that  the  intestinal  walls 
are  pigmented  from  the  presence  of  the  carbon,  this  showing  the  route 
taken  in  its  absorption.  The  lymphatic  glands  in  the  abdomen  are  also 
crowded  with  particles  of  carbon.  Welch  ||  has  also  described  a  case. 
The  records  of  such  cases  are  few  and  the  amount  of  cirrhosis  compara- 
tively slight;  the  chief  interest  is  pathological.     {Vide  p.  300.) 

Arsenic  appears  to  be  capable  of  setting  up  cirrhosis  of  the  liver.  In 
the  epidemic  of  arsenical  peripheral  neuritis  due  to  poisoned  beer  in  the 
north  of  England  in  1900-1901  quite  an  unusual  number  of  cases  of 
cirrhosis  of  the  liver  and  ascites  were  seen  (Reynolds,**  Sturrockft)- 
Hutchinson  Jl  and  Hamburger  §§  have  reported  ascites  in  patients  who 
had  long  been  addicted  to  the  medicinal  use  of  arsenic ;  but  in  both  these 
instances  recovery  followed  suspension  of  the  drug,  so  that  the  existence 
of  cirrhosis  was  not  proved.  It  has  even  been  tentatively  suggested 
that  Banti's  disease  or  the  terminal  cirrhosis  which  supervenes  in  some 
cases  of  chronic  splenic  aneemia  is  due  to  the  arsenic  given  medicinally 
(W.  Broadbentllll).  Experimentally  cirrhosis  has  been  produced  by 
chronic  arsenical  and  by  chronic  aluminium  poisoning,  but  cirrhosis  in 
man  has  not  been  traced  to  the  latter  metal. 

In  a  case  of  argyria,  in  which  nitrate  of  silver  had  been  taken  for 

*  Boix:  Archiv.  G^n^ral.  de  Med.,  Aug.  6,  1899,  p.  210. 

t  Segers:  LaSem.  Med.,  1891,  t.  xi,  p.  448. 

X  Adami:  Sajous'  Annual,  1898,  vol.  ii,  p.  313. 

I  Lancereaux:  Traite  des  Maladies  du  Foie  et  du  Pancreas,  p.  340,  1899. 

!|  Welch:  .Johns  Hopkins  Hospital  Bulletin,  1891,  vol.  ii,  p.  32. 
**  Reynolds,  E.  S. :   Medico-chirurg.  Trans.,  vol.  Ixxxiv,  p.  425. 
tt  Sturrock:  Brit.  Med.  Journ.,1900,  vol.  ii,p.  18ir>. 
XX  Hutchinson,  J. :  Archives  of  Surgery,  189.5,  vol.  vi,  .389. 
§§  Hamburger:  Johns  Hopkins  Hosp.  Bulletui,  April,  1900. 
i|j|  Broadbent,  W. :  Brit.  Med.  Journ.,  1903,  vol.  i,  p.  1140. 


186  DISEASES    OF   THE    LIVEK. 

four  months  for  epilepsy,  Frommann  *  found  early  hepatic  cirrhosis  with 
deposit  of  silver. 

Lead. — Experimentally  some  slight  degree  of  hepatic  fibrosis  has 
resulted  from  feeding  animals  with  lead  (Lafitte  f),  but  clinically  lead 
has  no  claim  to  be  considered  a  cause  of  cirrhosis;  Lavrand,^  indeed, 
states  that  the  liver  is  generaUy  unaffected  in  chronic  plumbism.  There 
is,  moreover,  some  doubt  as  to  the  mechanism  by  which  lead  would 
produce  cirrhosis;  perhaps  the  more  probable  view  is  that  it  leads  to 
arteriosclerosis  of  the  branches  of  the  hepatic  arter}^,  and  so  to  slight 
dj^strophic  fibrosis. 

Naphthol. — By  injecting  small  quantities  of  naphthol  into  the  portal 
vein  Bouchard  §  produced  some  fibrosis  in  the  liver. 

Bacterial  Toxines. — To  consider  now  the  effects  of  bacterial  toxines: 
experimentally  Charrin  ||  injected  boiled  cultures  of  the  BacUlus  pyo- 
cyaneus  into  the  portal  vein,  and  thus  produced  extensive  small-cell 
infiltration  in  the  portal  canals.  Krawkow**  obtained  cirrhosis  in  birds 
in  similar  experiments  when  prolonged,  but  Ramond  failed  to  induce 
cirrhosis  in  animals  hj  the  administration  of  toxines  by  the  mouth  alone, 
though  he  obtained  positive  results  where  alcohol  was  given  as  well. 

Krawkow,  by  introducing  cultures  of  Staphylococcus  pyogenes  aureus 
and  of  other  micro-organisms  into  the  ahmentar}^  canal  produced  ex- 
perimental cirrhosis.  The  micro-organisms  may  have  merely  manu- 
factured a  poison,  which  passed  into  the  portal  vein  and  so  to  the  liver, 
and  set  up  a  purely  toxic  cirrhosis,  but,  on  the  other  hand,  the  micro- 
organisms may  themselves  have  reached  the  liver  either  by  the  portal 
vein  or  by  ascending  the  bile-duct.  These  points  vill  be  referred  to 
later. 

(a)  Cirrhosis  due  to  the  Action  of  Poisons  Manufactured  in 
THE  Intestine. 

This  theor}^  has  already  been  referred  to  {vide  p.  184),  in  order  to 
explain  cirrhosis  super^'ening  in  alcohohc  subjects,  where  it  was  suggested 
that  alcohol  sets  up  gastro-enteritis,  and  thus  leads  to  the  formation  of 
poisons  which  are  the  direct  causes  of  cirrhosis.  Boixtt  and  Hanot  JJ 
have  described  non-alcohohc  cirrhosis  due  to  dyspepsia.  The  liver  is 
first  enlarged  and  tender,  and  later  cirrhosis  and  jaundice  may  develop. 
The  cirrhosis  ascribed  to  gout  may  be  of  this  nature,  while  the  non- 
alcohohc  cirrhosis  in  Mohammedans  and  the  natives  of  India  and  Egj'pt, 
a  form  long  ago  referred  by  Budd§§  to  the  action  of  spices,  curries,  and 
other  stimulating  articles  of  food,  such  as  ginger,  may  be  explained  as 
depending  on  the  irritating  effects  of  acetic,  butyric,  lactic,  or  other 

*  Frommann:  Archiv  f.  path.  Anat.  u.  Phvsiol.,  Berlin,  Bd.  xvii. 

t  Lafitte:  These  de  Paris,  1892. 

%  Lavrand:  Le  Nephrite  des  Satumines,  p.  12,  1899. 

§  Bouchard:  Therapeutics  des  Maladies  Infectieuses,  p.  313,  1889. 

ll  Charrin:  Archiv  de  Physiol.  Norm,  et  Path.,  1893,  p.  554. 
**  Krawkow:  Archiv.  de  Med.  experiment,  et  d'Anat.  Path.,  vol.  viii,  p.  268. 
tt  BoLx:  La  foie  des  dyspeptics,  These  de  Paris,  1894.  Archiv.  General,  de  Med., 
Aug.,  1899,  p.  210.  tt  Hanot  and  BoLx:  Congres  de  Rome,  1894. 

§§  Budd:  Diseases  of  the  Liver,  p.  151,  1857. 


CIRRHOSIS    OF  THE   LIVER.  187 

acids  manufactured  as  the  result  of  intestinal  fermentation.  Cirrhosis 
of  this  kind  is  sometimes  described  as  due  to  auto-intoxication  or  as 
autochthonous^  and  in  a  posthumous  article  by  Hanot  *  was  called 
"Budd's  cirrhosis."  In  order  to  meet  the  obvious  objection  that  dys- 
l^epsia  is  comparatively  seldom  followed  by  cirrhosis,  Boix  argues  that 
the  resistance  of  the  liver  is  an  important  factor,  and  that  where  this 
is  congenitally  feeble  continued  dyspepsia  will  lead  to  cirrhosis.  This 
idiosyncrasy  or  predisposition  is  included  under  the  French  term 
"arthritism." 

In  cases  of  long-standing  mitral  disease  hepatic  fibrosis  may  be  due 
to  several  causes.  A  certain  degree  of  fibrous  replacement  as  a  result 
of  atrophy  of  the  liver  ceUs  may  occur.  An  explanation  of  this  "cardiac 
cirrhosis,"  which  may  be  appropriately  mentioned  here,  is  gastro-intes- 
tinal  catarrh;  this  gives  rise  to  the  formation  of  irritating  bodies  which, 
when  absorbed,  find  the  liver  in  a  condition  of  diminished  resistance 
and  are  thus  able  to  set  up  inflammatory  changes.  It  may  be  noted, 
however,  that  the  fibrosis  secondary  to  chronic  venous  engorgement, 
however  produced,  is  slight  and  of  no  real  clinical  importance.  (Vide 
"Chronic  Venous  Engorgement.")  The  ascites  often  accompanying 
backward  pressure  is  nearly  always  the  result  of  concoirdtant  chronic 
■  peritonitis. 

Among  the  children  of  Brahmins  around  Calcutta,  and  probably 
elsewhere  in  India,  a  peculiar  form  of  cirrhosis  described  as  intercellular 
and  perilobular,  or  "biliary,"  has  been  described. f  It  occurs  usually 
when  the  infants  are  about  eight  months  old,  and  about  95  per  cent, 
of  those  who  suffer  from  it  die  before  the  end  of  the  second  year.  It 
is  very  apt  to  occur  in  the  same  fairdly;  thus,  no  less  than  fourteen 
children  of  the  same  parents  have,  died  of  it  one  after  the  other.  There 
is  no  evidence  that  it  is  syphilitic;  it  is  ascribed  to  bad  milk,  faulty 
digestion,  and  to  poisonous  products  generated  in  the  intestines.  The 
mothers'  milk  is  not  improbably  the  causal  factor,  as  they  restrict  them- 
selves to  a  dry  diet  and  take  a  decoction  of  black  pepper.  Whether 
the  poisons  are  introduced  in  the  food  or  formed  in  the  infant's  intes- 
tines it  is  impossible  to  say;  perhaps  both  methods  obtain,  but  the  latter 
is  the  more  probable  of  the  two. 

Among  Brahmins  and  other  high-class  Hindus  who,  as  a  rule,  lead 
abstemious  lives  and  never  touch  alcohol,  cirrhosis  of  the  liver  is  of  fre- 
cjuent  occurrence  (Young  J).  Ginger-eating  is  a  prevalent  practice  with 
them  and  they  are  addicted  to  cardamoms,  red  pepper,  and  other  hot 
spices.  The  cirrhosis  may  well  be  secondary  to  dyspeptic  changes  thus 
induced  in  the  alimentary  canal.  In  Egypt  cirrhosis  is  found  among 
Mahommedans,  who  take  no  alcohol,  and  may  possibly  be  due  to  anchylos- 
tomiasis  and  the  production  of  toxines  inside  the  intestine,  since  slight 

*  Hanot :  La  Cirrhose  de  Budd,  Archiv.  G^iK^ral.  de  Med.,  1899,  p.  3. 

t  J.  B.  Gibbons :  "  Scientific  Memoirs  by  Medical  Ojfficers  of  tlie  Arm}"-  of  India, ' ' 
Part  vi,  1891,  The  Indian  Lancet,  May,  1896,  p.  426.  Togendro  Nath  Ghose :  Lancet, 
1895,  vol.  i.  E.  Mackenzie:  Lancet,  1895,  vol.  i.  Nil  Ratan  Sircar:  The  Indian 
Lancet,  July  1 ,  1896. 

t  Young,  L.  T. :  Carlsbad  Treatment,  p.  129,  2d  cd.,  1899  ("  Ginger  Liver  "). 


188 


DISEASES   OF  THE   LIVEE. 


cirrhosis  has  been  found  in  the  -bodies  of  persons  affected  by  anchylos- 
tomiasis  and  bilharzia. 

In  typhoid  fever  *  necrotic  areas  of  small  size,  focal  necroses,  "lym- 
phomata,"  or  "lymphoid  nodules,"  as  they  have  been  variously  called, 
are  often  met  ^dth.  The  liver  cells  first  degenerate  and  subsequently  a 
certain  amount  of  small-round-cell  infiltration  surrounds  the  necrotic 
areas.  It  is  conceivable,  therefore,  that  under  favourable  conditions  a 
sporadic  multiple  fibrosis  may  result  throughout  the  liver;  usually  these 
lesions  are  recovered  from.  Some  observers  have  regarded  typhoid 
fever  as  a  starting-point  for  cirrhosis.  It  is  possible  that  if  alcohol  is 
taken  and  the  resistance  of  the  liver  thus  further  diminished,  this  change 
may  be  rendered  permanent.     If  this  be  so,  it  is  desirable  that  some 

caution  should  be 
maintained  in  giving 
stimulants  during 
convalescence.  From 
Reed's  careful  obser- 
vations it  appears 
probable  that  these 
focal  necroses  are  due 
to  toxalbumins  con- 
veyed to  the  liver  and 
that  these  areas  do 
not  contain  typhoid 
bacilli.  Hanot  has 
found  similar  nodules 
in  the  liver  in  cases 
of  tuberculous  enter- 
itis. According  to 
Mallory,t  two  distinct 
lesions  have  been  de- 
scribed under  the  term 
lymphoid  nodules:  (1) 
a  focus  of  lymphoid 
and  plasma  cells  con- 
fined to  the  connective  tissue  around  the  portal  vessels  and  independent 
of  the  liver  cells;  (2)  focal  necrosis  of  cells  in  hepatic  lobules  due  to 
blocking  of  capillaries  by  proliferated  and  phagocytic  cells. 

Cirrhosis  has  been  regarded  as  a  late  result  of  cholera,  and  it  seems 
reasonable  to  beheve  that  the  slightly  increased  fibrosis  around  the  portal 
spaces  sometimes  seen  in  rickets  is  due  to  gastro-intestinal  catarrh  giving 
rise  to  the  manufacture  and  absorption  of  poisonous  bodies  which  pass 
up  to  the  liver  by  the  portal  vein.  The  question  also  arises  as  to  what 
part  prolonged  diarrhoea  and  gastro-enteritis  in  children  may  play  in 

*  Friedreich:  Virchow's  Archiv,  Bd.  xii,  S.  53.  Reed:  Johns  Hopkins  Hospital 
Reports,  V,  p.  379.  Handford:  Trans.  Path.  Soc,  vol.  xl,  p.  129.  Hanot:  C.  R. 
Soc.  de  Biolog.,  p.  8.56,  1893.  Siredey :  Rev.  de  Med.,  t.  vi,  1886.  Legrey :  These  de 
Pans,  1892.     Amyot:  Canadian  Practitioner,  January,  1898. 

t  Mallory:  Journ.  Experim.  Med.,  vol.  iii,  p.  622. 


Fig.  25. — Focal   Necrosis  in  Typhoid    Fever. 

The  liver  cells  around  the  area  of  necrosis  show  pigmentation. 

X  110. 


CIRRHOSIS   OF  THE   LIVER.  189 

the  development  of  cirrhosis.  It  is  conceivable  that  toxines  absorbed 
in  the  course  of  appendicitis  *  may  imitate  cirrhotic  changes  in  the 
liver.  In  pernicious  anaemia  where  a  poison  is  probably  absorbed 
from  the  intestinal  tract  and  carried  to  the  liver  no  cirrhosis  results. 
Possibly  the  organ  is  in  such  a  poor  state  of  nutrition  that  it  is 
incapable  of  any  inflammatory  reaction.  The  same  explanation  has  been 
invoked  to  account  for  the  absence  of  fibrosis  in  lardaceous  disease 
of  the  liver.     (Kanthack.f) 

By  intraperitoneal  injection  of  a  micro-organism  allied  to  the  colon  group 
Weaver  :j:  obtained  cirrhosis  in  guinea-pigs,  but  the  micro-organism  was  not  found  in 
the  liver,  hence  the  change  in  the  liver  may  be  regarded  as  due  to  the  toxmes  ab- 
sorbed into  the  portal  vein. 

(c)  Umbilical  Vein  Cirrhosis. 

In  congenital  syphilis  the  blood,  presumably  containing  the  toxine, 
arrives  by  the  umbilical  vein  and  thus  passes  into  the  branches  of  the 
portal  vein  in  the  liver.  Here  the  poison  reaches  the  liver  by  the  portal 
vein,  being  derived  from  the  placenta  which,  in  the  foetus,  functionally  rep- 
resents the  intestine.  The  resulting  lesion  is  a  diffuse  pericellular  cirrhosis. 
In  exceptional  instances  a  similar  change  is  found  in  acquired  syphilis; 
but  with  these  exceptions  syphilis  does  not  directly  produce  hepatic 
cirrhosis,  though  it  may  lead  to  local  fibroses,  gummata,  and  cicatrices. 
Though  this  is  undoubtedly  true,  it  appears  that  pericellular  cirrhosis, 
which  is  a  secondary  lesion  of  syphihs  and  thus  curable,  often  leaves 
behind  it  a  deficient  resistance  on  the  part  of  the  fiver  and  thus  disposes 
it  to  become  cirrhotic  in  the  ordinary 'way.  I  have  seen  several  cases 
of  well-marked  cirrhosis  of  the  common  type  in  the  subjects  of  congenital 
syphilis,  and  therefore  believe  that  indirectly  sj^Dhilis  plays  a  part  in  the 
incidence  of  cirrhosis.  In  other  words,  congenital  syphilis  so  prepares 
the  soil  that  cirrhosis  of  the  ordinary  type  may  supervene.  Under  these 
conditions  the  cirrhosis  may  be  regarded  as  a  parasj^^hifitic  lesion. 

Other  poisons,  besides  that  of  syphihs,  may  travel  from  the  mother 
to  the  foetus  by  the  umbilical  vein  and  give  rise  to  changes  in  the  fiver. 
Our  knowledge  of  umbilical  vein  cirrhosis  is  extremely  meagre,  but  it 
is  reasonable  to  believe  that  the  disease  known  as  congenital  obliteration 
of  the  bile-ducts  may  start  in  the  liver  and  be  due  to  toxines  conveyed 
there  by  the  umbilical  vein,  and  that  the  subsequent  obliteration  of 
the  ducts  is  a  later  and  secondary  change  due  to  a  descending  cholan- 
gitis. 

(d)  Poisons  Manufactured  in  the  Spleen. 

In  hsemic  infections  micro-organisms  tend  to  accumulate  in  the  spleen, 
and,  if  not  rapidly  destroyed,  produce  toxines  which  travel  to  the  fiver 
and  may  there  produce  changes  analogous  to  cirrhosis.  Chauffard  §  has 
argued  in  favour  of  cirrhosis  being  in  some  cases  secondar}^  to  morbid 

*  Tuflier  et  MauU:  La  Presse  M6d.,  p.  408,  June  29,  1904. 

t  Kanthack,  A.  A. :  St.  Bartholomew's  Hosp.  Journ.,  Nov.,  1896,  vol.  iv,  p.  22. 

t  Weaver :  Philadelphia  Med.  Journal,  Feb.  4,  1899,  p.  283. 

§  Chauffard :  Scm.  Med.,  p.  177, 1899. 


190  DISEASES   OF  THE   LIVER. 

processes  originating,  or  at  any  rate  most  marked,  in  the  spleen.  Thus, 
in  malaria  the  spleen  is  greatly  enlarged  and  cirrhosis  of  the  liver  in 
malarial  subjects  may  in  part  be  due  to  poisons  manufactured  in  the 
spleen.  In  chronic  splenic  anaemia  it  may  sometimes  happen  that  a 
terminal  cirrhosis  of  the  liver  with  jaundice  occurs;  this  has  been  termed 
Banti's  disease,  and  is  regarded  by  Chauffard  as  a  good  example  of  cir- 
rhosis of  splenic  origin.  The  difficulty  is  to  be  sure  the  cirrhosis  has  not 
existed  throughout. 

As  will  be  seen  in  the  description  of  h3^pertrophic  bihary  cirrhosis, 
the  typical  monolobular  cirrhosis  is  very  frequently  obscured  by  the 
addition  of  multilobular  cirrhosis.  This  latter  change  may  be  explained 
as  due  to  the  infective  agent,  which  primarily  reached  the  liver  by  the 
hepatic  artery  and  sets  up  monolobular  cirrhosis,  settling  down  in  the 
spleen  and  producing  toxines  which,  when  conveyed  by  the  splenic  vein 
to  the  liver,  induce  multilobular  cirrhosis.  In  support  of  the  theory 
that  poisons  are  manufactured  in  the  spleen  and  conveyed  to  the  liver 
is  the  fact  that  endophlebitis  of  the  splenic  vein  has  been  described  in 
malaria  by  Kelsch  and  Kiener,*  in  enteric  fever  by  Bezangon,t  and  in 
splenic  anaemia. 

The  portal  vein  may  indeed  be  regarded  as  having  two  main  sources 
in  adult  life — (a)  the  gastro-intestinal  veins,  by  which  poisons  commonly 
travel  to  the  liver,  and  (6)  the  splenic  vein.  In  foetal  life  the  umbilical 
vein  is  a  third  distinct  tributary  and  may  also  convey  poisons  to  the  liver. 

A  point  of  speculative  interest  in  connexion  with  cirrhosis  of  the  liver  due  to 
poisons  manufactured  in  the  spleen  arises  from  S6rege's  J  view,  based  on  injection 
experiments  with  methylene-blue,  that  the  blood  from  the  spleen  goes  exclusively 
to  the  left  lobe  of  the  liver.  If  this  is  true,  cirrhosis  due  to  poisons  produced  in  the 
spleen  should  be  confined  to,  or  chiefly  in  evidence  in,  the  left  lobe  of  the  liver.  I  am 
not  aware  that  there  is  anything  in  support  of  this  to  be  found  in  literature. 

At  present  the  existence  of  hepatic  cirrhosis  as  a  sole  result  of  poisons 
manufactured  in  the  spleen  requires  further  investigation,  but  it  is  an 
attractive  idea  and  is  compatible  with  the  fact  that  in  one  variety  of 
hypertrophic  biliary  cirrhosis,  the  so-called  metasplenomegalic,  the  spleen 
is  enlarged  before  there  is  any  manifest  change  in  the  liver. 


II. 

Mi  CEO-ORGANISMS    ABSORBED    FROM    THE    ALIMENTARY    CaNAL. 

Cirrhosis  thus  produced  would  be  described  as  septic  or  infectious 
in  contradistinction  to  toxic  cirrhosis,  which  is  due  to  the  action  of 
poisons  without  the  presence  of  microbes  in  the  liver.  Such  a  suggestion 
is  highly  probable,  but  cannot  be  accepted  at  present.  Adami,§  while 
investigating  the  Pictou  cattle  disease,  found  intercellular  or  pericellular 
cirrhosis  accompanied  by  swelling  of  the  peri-portal  and  retro-peritoneal 

*  Kelsch  and  Kiener:  Traits  des  Maladies  des  Pays  chaudes,  p.  405,  18S9. 
t  BezanQon,  F. :  Th^se  de  Paris,  1895. 

t  S^rege,  H. :  Journ.  de  Med.  de  Bordeaux,  Mav  25,  June  1,  S,  1902. 
§  Adami:  Brit.  Med.  Journ.,  1898,  vol.  ii,  p.  1215. 


CIRRHOSIS    OF  THE   LIVER.  191 

lymphatic  glands,  and  cedema  of  parts  of  the  intestine.  These  lesions 
were  associated  ^dth  a  minute  bacillus  belonging  to  the  colon  group. 
Adami  has  found  the  colon  bacillus  almost  constantly  in  human  livers. 
When  the  livers  are  healthy,  the  bacilli  appear  to  have  been  killed  by 
the  bactericidal  action  of  the  liver  cells.  In  progressive  cirrhosis  there 
are,  in  addition  to  dead  baciUi,  some  areas  where  they  appear  active. 
This  suggests  the  possibility  that  virulent  colon  bacilli  may  under  con- 
ditions of  diminished  resistance  of  the  liver  cells,  such  as  may  be  induced 
by  alcohol,  lead  to  cirrhosis.  Adami  *  considered  that  a  primary  in- 
flammation of  the  alimentary  canal  favoured  invasion  of  the  liver  by 
the  bacilli  which  set  up  cirrhotic  changes  in  that  organ. 

It  is,  a  priori,  extremely  probable  that  an  acute  hepatitis  due  to  the 
brunt  of  a  hsemic  infection  falling  on  the  liver  would,  if  not  fatal,  leave 
behind  it  hepatic  cirrhosis.  Cases  in  human  beings  occur  where  a  febrile 
condition,  accompanied  by  enlargement  and  tenderness  of  the  spleen 
and  liver,  ushers  in  and  precedes  an  illness  which  eventually  is  seen  to 
have  for  its  chief  anatomical  lesion  a  cirrhotic  liver.  At  present  the 
sequence  of  microbic  hepatitis  resulting  in  ordinary  cirrhosis,  though 
highly  probable,  cannot  be  regarded  as  resting  on  a  sufficient  basis  of 
fact.     Some  fibrosis  is  seen  in  prolonged  cases  of  acute  yellow  atrophy. 

In  a  boy,  aged  sixteen  years,  death  occurred  fourteen  days  after  the  onset  of 
measles.  Roger  and  Conte  f  found  that  an  acute  localized  enteritis  in  the  ileum  had 
given  rise  to  hepatitis,  inflammation  between  the  liver  and  diaphragm,  an  acute  rapid 
putrid  effusion  into  the  right  pleura,  and,  finally,  gangrene  of  the  lung.  _  The  bacillus 
foimd  resembled  the  B.  coli.  The  liver  showed  masses  of  round-ceUed  infiltration  in 
the  portal  spaces,  degeneration  of  the  liver  cells,  cholangitis,  and  endarteritis.  The 
process  was  very  acute,  but  it  makes  it  easy  to  imderstand  that  a  slighter  degree  of 
the  same  process,  if  recovered  from,  might  be  the  starting-point  of  cirrhosis. 

By  intraperitoneal  injections  of  cultures  of  a  bacillus  belonging  to 
the  pseudo-diphtheria  group  Hektoen  J  produced  cirrhosis  of  the  liver 
in  animals.     The  bacilli  were  found  in  the  capillaries  of  the  liver. 

Experimentally  by  introducing  cultures  of  micro-organisms  into  the  intestines 
of  birds  Krawkow  sometimes  found  that  cirrhosis  developed,  but  the  result  may  have 
been  merely  due  to  their  toxines  being  carried  to  the  liver,  and  there  is  no  evidence 
that  in  his  experiments  the  micro-organisms  themselves  travelled  to  the  liver. 

It  is  possible  that  in  some  exceptional  instances  tubercle  bacilli 
carried  from  the  intestines  to  the  liver  may  set  up  some  degree  of  cir- 
rhosis. Hanot  and  Gilbert's  §  experiments  show  that  avian  tubercle 
bacilli  may  induce  cirrhosis  in  guinea-pigs,  and  they  believe  that  this 
sclerogenic  result  depends  either  on  relatively  high  resistance  on  the 
part  of  the  liver  or  on  a  slight  degree  of  virulence  on  the  part  of  the 
bacilli.  As  a  rule,  of  course,  tubercle  bacilli  either  give  rise  to  tuberclic 
or  to  degenerative  changes  in  the  liver  cells.  As  a  curiosity  reference 
may  be  made  to  bilharzia  passing  up  the  portal  vein  and  giving  rise  to 

*  Adami:  Report  of  Minister  of  Agriculture  for  the  Dominion  of  Canada  for 
year  1901,  p.  135. 

t  Roger  and  Conte:  La  Presse  M^dicale,  Sept.  29,  1897. 
X  Hektoen:  .Journ.  Path,  and  Racteriol.,  vol.  vii,  p.  214. 
§  Hanot  and  Gilbert:  Soc.  de  biolog.,  Jan.  30,  1892. 


192  DISEASES   OF  THE   LIVER. 

cirrhosis.*     According  to  Kartulis,t  the  liver  is  usually  enlarged  in  size 
and  there  are  no  symptoms  of  cirrhosis. 


III. 

Cirrhosis  due  to  Poisons  in  the  General  Circulation  which 
Reach  the  Liver  by  the  Hepatic  Artery. 

This  cirrhosis  may  be  spoken  of  as  toxic  and  due  to  the  action  of 
poisons  on  the  liver.  It  has  been  suggested  that  cirrhosis  may  be  set 
up  by  the  specific  fevers,  typhoid  fever,  scarlet  fever,  measles,  and 
variola,  and  pneumonia.  Theoretically,  the  toxines  of  these  diseases  maj'", 
when  absorbed  into  the  general  circulation,  set  up  focal  necrosis  of 
the  liver  cells,  and  under  certain  conditions  fibrosis  might  develop  around 
these  areas  of  necrosis. 

Focal  necrosis  may  occur  in  tyi^hoid,  scarlet  fever,  measles,  variola, 
and  diphtheria.  In  cases  of  typhoid  fever  the  poison  might  reach  the 
liver  by  the  hepatic  artery  and  give  rise  to  focal  necrosis.  Klein  J  and 
Crooke  §  described  acute  interstitial  hepatitis  in  scarlet  fever,  and  more 
recently  Pearce  ||  has  met  with  focal  necroses  of  the  liver  cells;  this  is 
analogous  to  scarlatinal  nephritis,  but  it  probably  is  a  transient  condi- 
tion and  clinically  there  is  little  relation  between  scarlet  fever  and  hepatic 
cirrhosis.  Focal  necroses  in  measles  have  been  described  and  figured  by 
Freeman.**  Small-cell  accumulations,  like  those  produced  in  typhoid 
fever,  have  been  described  in  the  liver  in  variola  by  Roger  and  WeiLft 
Arnaud,  JJ  who  describes  in  addition  small-cell  infiltration  near  the  portal 
spaces,  suggests  that  cirrhosis  may  subsequently  follow. 

In  diphtheria  focal  necroses  occur  and  are  described  by  Councilman, 
Mallory,  and  Pearce  §  §  as  being  situated  round  the  intralobular  vein. 
There  are  degeneration  of  the  liver  cells  and  some  proliferation  of  the 
endothelium.  These  changes  are  due  to  the  action  of  poisons  and  not 
to  the  presence  of  diphtheria  bacilli  in  the  liver.  Weaver  1|  ||  injected  a 
micro-organism  allied  to  the  colon  group  into  the  abdominal  wall  of 
guinea-pigs  and  produced  local  abscesses  in  which  the  bacilli  were  found, 
none  being  present  in  the  liver,  which  showed  focal  necroses  and  cirrhosis. 
It  is  reasonable  to  believe  that  as  the  result  of  other  local  infections 
focal  necroses  in  the  liver  may  be  produced,  and  that  under  favourable 
conditions  some  sporadic  fibrosis  might  develop  around  these  foci.  The 
question  whether  absorption  from  tuberculous  pulmonary  vomicae  which 
are  secondarily  infected  with  streptococci  can  induce  cirrhosis  is  referred 
to  elsewhere. 

*  Symmers    Jour.  Path,  and  Bacteriol.,  vol.  ix,  p.  237. 
t  Kartulis:  Sem.  M^d.,  1894,  p.  415. 
X  Klein:  Trans.  Path.  Soc,  vol. xxviii, p. 439. 
§  Crooke :  Birmingham  Med.  Roview,  vols,  xx,  xxi. 
II  Pearce:  Boston  (U.  S.  A. )  City  Hosp.  Reports,  1899,  p.  74. 
**  Freeman :  Medical  Record,  July  28,  1898.     Pediatrics,  Feb.,  1900. 
tt  Roger  and  Weil :  Soc.  de  biolog.,  Nov.  2,  1900. 
jj  Arnaud:  Marseille  MMical,  1899,  p.  39. 

§§  Councilman,  Mallory,  Pearce:  Diphtheria,  a  study  of  220  fatal  cases,  Boston, 
U.  S.  A.,  1901.  II II  Weaver :     Philadelphia  Med.  Journ.,  Feb.  4,  1899. 


CIRRHOSIS    OF  THE   LIVER.  193 

The  conditions  favouring  the  development  of  permanent  cirrhosis 
after  infections  are  congenital  susceptibility  or  want  of  resistance  on 
the  part  of  the  liver,  and  the  presence  of  other  factors,  such  as  alco- 
holism. In  the  rare  condition  of  hsemochroniatosis,  in  which  there  is 
widespread  pigmentation  of  the  body,  the  liver  becomes  first  infiltrated 
with  pigment  and  then  cirrhotic;  the  liver  cells  degenerate  and  become 
pigmented.  The  pancreas  is  similarly  affected,  and  when  a  certain  degree 
of  intensity  is  reached,  diabetes  results.  This  constitutes  bronzed  dia- 
betes. Of  30  cases  of  hsemochromatosis  5  only,  have  not  shown  dia- 
betes. It  is  noteworthy  that  in  the  cirrhotic  livers  of  hsemochromatosis 
there  is  endarteritis  of  the  hepatic  artery;  this  suggests  that  there  is 
some  additional  factor  associated  with  the  process  of  hemolysis  which 
causes  the  change  in  the  liver  cells  and  the  cirrhosis.  Thus  the  cirrhosis 
seen  in  hsemochromatosis  may  possibly  be  due  to  a  poison  reaching  the 
liver  by  the  hepatic  artery,  which,  as  Adami  points  out,  is  probably 
of  bacterial  origin. 

Experimentally,  a  certain  amount  of  hepatic  fibrosis  has  followed 
prolonged  poisoning  with  vegetable,  mineral,  and  bacterial  poisons. 
The  intoxication  must  be  induced  gradually  and  continued  for  a  con- 
siderable period.  If  the  poison  is  employed  in  too  large  amounts,  the 
results  are  those  of  acute  poisoning,  viz.,  degeneration  and  necrosis  of 
the  liver  cells,  focal  or  diffused,  as  in  phosphorus  poisoning.  In  the 
same  way,  the  injection  of  bacterial  poisons  into  the  circulation,  when 
carried  on  rapdily,  gives  rise  to  necrotic  changes  in  the  liver  cells  around 
the  intralobular  veins;  when  the  process  is  less  intense  and  more  pro- 
longed, a  certain  amount  of  cirrhosis  results.  Krawkow  *  obtained 
positive  results  with  sterilised  cultures  of  Bacillus  pyocyaneus,  and 
Claude  t  with  diphtheritic  toxine.  But  it  is  probable  that  these  effects 
are  transitory,  and  do  not,  when  uncomplicated  (vide  p.  184)  by  alco- 
holism, give  rise  to  cirrhosis  in  man.  Flexner,J  in  a  careful  study  of 
chronic  intoxication  by  ricin  and  abrin, — ^vegetable  alkaloids  or  phytalbu- 
moses, — produced  a  form  of  cirrhosis.  As  a  result  of  injection  of  phos- 
phorated oil  into  the  subcutaneous  tissues  of  rabbits,  Aufrecht  §  found 
that  the  liver  cells  showed  degenerative  changes  and  that  later  some 
small-cell  infiltration  took  place  around  the  lobules.  Other  poisons, 
when  injected  into  the  circulation,  such  as  carbonate  of  ammonia,  indol, 
skatol,  phenol,  sulphonal,  have  also  led  to  a  slight  degree  of  microscopic 
fibrosis. 

IV. 

Cirrhosis  due  to   Micro-organisms  in  the    General  Circulation 

Reaching  the  Liver  and  there  Producing   Poisons  that 

SET  UP  Cirrhosis. 

In  hsemic  infection  the  liver  changes  are  often  extremely  acute  and 

give  rise  either  to  suppuration  or  to  widespread  degenerative  changes 

*  Krawkow:  Archiv  de  M^d.  experiment  et  d'  anat.  path.,  vol.  viii,  p.  269,  1896. 
t  Claude:  Th^se  Paris,  1897. 

X  Flcxner:  Journ.  Experiment.  Med.,  vol.  ii,  p.  19,  1897. 
§  Aufrecht:  Deutsch.  Archiv.  f.  Idin.  Med.,  1897. 
13 


194  DISEASES    OF  THE   LIVER. 

allied  to  acute  yellow  atroiDhy.  In  less  acute  hsemic  infections  the  sup- 
porting fibrous  tissues  show  proliferation  and  accumulation  of  leucocytes 
in  the  portal  canals  and  in  the  peripheral  parts  of  the  lobules  of  the  liver. 
These  changes  are  the  same  as  those  seen  in  the  acute  specific  fevers, 
such  as  variola,  scarlet  fever,  etc.  (Vide  p.  192.)  Occasionally  in 
pygemia  and  septicsemia,  due  to  streptococci,  staphylococci,  etc.,  as  in 
acute  necrosis,  infective  endocarditis,  puei-peral  septicsemia,  and  er}^- 
sipelas,*  considerable  small-cell  infiltration  of  the  liver  is  met  with. 

In  the  hepatitis  due  to  repeated  attacks  of  malaria  there  is  considerable 
damage  done  to  the  liver  ceUs,  as  shoT\Ti  by  focal  necroses  (Barker!), 
and  fibrous  h^-perplasia  is  sometimes  seen.  The  actual  importance  of 
malaria  as  a  cause  of  cirrhosis  appears  to  be  sur^Drisingly  small.  {Vide 
p.  305.) 

Typhoid  fever  has  already  been  referred  to  as  leading  to  small  necrotic 
areas  in  the  liver  (p.  188).  In  ordinary-  tj^Dhoid  fever  these  nodules 
appear  to  be  due  to  the  action  of  toxines  conveyed  from  the  alimentary 
canal,  and  not  to  baciUi.  But  in  cases  of  general  t}'phoid  septicsemia, 
where  there  may  be  no  intestinal  lesions,  infection  of  the  liver  by  the 
hepatic  artery  is  possible.  In  fifteen  cases  of  this  kind  collected  by 
Bryant,J  typhoid  baciUi  were  recovered  from  the  liver  in  four  cases. 
The  changes  in  the  hver  due  to  general  hsemic  infections  are  probably 
usually  recovered  from  if  the  patient  lives,  but  should  conditions  arise 
which  depress  the  resistance  of  the  liver,  such  as  alcoholism,  cirrhosis 
might  conceivably  result. 

Experimentally  there  is  some  evidence  that  hsemic  infections  may 
induce  hepatic  cirrhosis.  Krawkow  §  injected  cultures  of  various  micro- 
organisms into  the  muscles  of  fowls  and  pigeons,  and  found  that  after  a 
considerable  interi^al  hepatic  cirrhosis  developed.  This  was  especially 
well  marked  when  the  Bacillus  pyocyaneus  and  the  Staphylococcus 
pyogenes  aureus  were  employed.  Bj^  subcutaneous  injection  of  cultures 
of  a  baciUus  belonging  to  the  pseudo-diphtheria  group,  Hektoen  |1  ob- 
tained well-marked  portal  cirrhosis  in  animals. 

It  must,  however,  be  remembered  that  in  chronic  hsemic  infections 
the  spleen  becomes  crowded  with  micro-organisms,  and  that  if  they 
multiply  there,  toxines  may  be  manufactured  in  considerable  quantities 
and  carried  by  the  splenic  and  portal  veins  to  the  fiver,  and  there  set  up 
a  cirrhosis  of  splenic  origin.     {Vide  p.  189.) 

COXCLUSION. 

Experiment  shows  that  a  large  number  of  poisons  are  capable  of 
giving  rise  to  changes  in  the  hver  comparable  to  those  of  cirrhosis.  Often, 
it  is  true,  these  lesions  are  early,  or,  at  the  best,  not  well  marked.  But 
the  facts  are  of  value  as  indicating  that  cirrhosis  in  man  may  reasonably 

*  Roger  and  Gamier:  Rev.  deMed.,  March,  1901. 

t  Barker :  Johns  Hopkins  Hosp.  Reports,  vol.  v. 

t  Brj^ant,  J.  H. :  Brit.  Med.  Journ.,  1899,  vol.  i,  p.  778. 

§  Krawkow:  Archiv  de  Med.  experim.  et  d'  anat.  path.,  tome  viii,  p.  268. 

li  Hektoen:  Journ.  Path,  and  Bact.,  vol.  vii,  p.  214. 


CIRRHOSIS    OF   THE   LIVER.  195 

be  considered  as  the  result  of  a  toxic  process.  These  poisons  may  be 
absorbed  either  from  the  alimentary  canal,  and  then  reach  the  liver  in 
a  comparatively  concentrated  form,  or  they  may  travel  to  the  liver  by 
the  hepatic  artery;  the  dose  is  then  comparatively  dilute  as  compared 
with  the  former  class.  Ordinarv^  cirrhosis  in  man  is  generally  due  to 
poisons  travelhng  by  the  portal  vein.  Alcoholism  is  rather  an  antecedent 
condition  than  a  causa  vera,  and  acts  indirectly  or  in  an  accessory  manner; 
though  in  ordinary  practice  the  association  between  cirrhosis  and  ante- 
cedent alcoholism  is  of  fundamental  importance.  The  possibility  of 
cirrhosis  being  definitely  due  to  micro-organisms  is  one  that  must  be 
faced;  from  analogy  it  is  most  probable,  but  at  present,  as  in  the  case 
of  s}^hilis,  it  has  not  been  certainly  established.  It  is  also  highly  prob- 
able that  poisons,  or  perhaps  micro-organism,  reaching  the  liver  by 
the  hepatic  artery  may  give  rise  to  changes  of  a  cirrhotic  nature.  The 
mechanism  of  this  change  will  be  further  referred  to  in  the  section  on 
"Hypertrophic  Biliary  Cirrhosis." 

NATURE    OF   THE   FIBROSIS  OF  CIRRHOSIS. 

It  is  perhaps  most  widely  held  that  cirrhosis  is  primarily  and  essen- 
tially a  chronic  inflammation  or  h3rperplasia  of  the  connective  tissue  in 
the  portal  areas,  and  that  the  atrophic  and  degenerative  changes  in  the 
liver  cells  are  either  (i)  entirely  secondary  and  due  to  pressure  exerted 
by  the  contracting  fibrous  tissue,  or  to  impaired  nutrition  from  curtailed 
blood  supply,  or  (ii)  unimportant  and  almost  accidental  concomitant 
phenomena. 

Powell  White*  has  gone  to  the  opposite  extreme  and  suggested  that  large  smooth 
cirrhotic  livers  are  not  due  to  inflammatory  processes,  since  they  show  none  of  the 
contraction  which  is  so  characteristic  of  inflammatory  hyperplasia  and  to  a  lesser 
extent  of  replacement  fibrosis.  His  view  is  that  there  is  a  diffuse  fibroma  of  the 
liver. 

The  alternative  view  is  that  cirrhosis  is  essentially  a  replacement 
fibrosis  and  is  secondary  to  a  primary  degeneration  and  atrophy  of  the 
liver  cells.  Payne f  and  Lionel  Beale  regarded  cirrhosis  as  essentially 
an  atrophic  change.  On  the  theory  that  it  is  a  replacement  fibrosis  the 
changes  in  cirrhosis  of  the  liver  would  be  regarded  as  analogous  to  those 
in  systemic  sclerosis  of  the  spinal  cord  or  to  those  in  an  arteriosclerotic 
kidney. 

Against  this  it  may  be  urged — 

1.  That  extensive  atrophy  or  degeneration  may  occur  without  any 
fibrosis  resulting.  Thus,  in  old  age  there  may,  as  I  have  seen,  be  marked 
atrophy  of  the  cells  in  the  peripheral  zone  of  the  hepatic  lobule,  with 
little  or  no  fibrosis.  In  lardaceous  disease,  and  in  universal  fatty 
change,  there  may  be  complete  freedom  from  fibrosis.  In  reply,  it  may 
be  said  that  in  such  cases  there  is  a  general  debility  of  the  whole  organ, 
and  that  the  fibrous  tissues  share  in  it,  and  are  therefore  unable  to  undergo 
proliferative  changes.     (Kanthack.|) 

*  Powell  White:  Brit.  Med.  Joum.,  1900,  vol.  ii,  p.  1057. 

t  Payne,  J.  F. :  Trans.  Path.  Soc.  London,  vol.  xl,  p.  321, 1889. 

I  St.  Barth.  Hosp.Journ.,  London,  Nov.,  1896. 


196  DISEASES    OF   THE    LIVER. 

2.  That,  microscopically,  the  proliferation  of  the  comiective  tissues 
is  so  exuberant,  so  exactly  like  those  of  active  infianimation  elsewhere, 
and  the  degenerative  changes  in  the  ceUs  so  shght  in  comparison,  that 
it  is  difficult  to  beheve  that  the  latter  changes  can  be  primar}^  In  such 
cases  there  may  well  be  two  factors  at  work,  namely,  prohferation  of 
the  connective  tissues  and  degenerative  changes  in  the  liver  cells,  and- 
both  may  be  due  to  the  simultaneous  action  of  the  toxine.  But,  while 
bearing  this  explanation  in  mind,  it  must  be  remembered  that  a  replace- 
ment fibrosis  shows  itself,  not  only  as  a  passive  overgroT\~th,  but  as  a 
proliferation,  for,  both  in  degenerative  "neuritis"  and  in  granular  kidney 
(arteriosclerotic  in  origin),  much  small-ceU  proliferation  maj'  sometimes 
be  seen. 

3.  That  inasmuch  as  cirrhosis  is,  in  ordinary^  conditions,  due  to  the 
action  of  a  poison,  it  is  reasonable  to  beheve  that  the  effects  T\iU  be  no 
more  limited  to  the  hepatic  cells  than  to  the  fibrous  tissues,  as  was  for- 
merly supposed  to  be  the  case.  In  other  words,  that  the  parenchymatous 
and  interstitial  changes  are  both,  in  the  first  instance,  due  to  the  same 
pause,  and  therefore  vary  directly  in  intensity.  If  this  be  so,  it  is  easy 
to  understand  that  the  hepatic  cells,  being  more  sensitive,  "^^dU  react 
before  the  more  resistant  connective  tissue,  and  that  degenerative  changes 
in  them  wih  usually,  for  this  is  their  usual  method  of  reacting,  precede 
hyperplasia  of  the  connective  tissues.  There  are  further  grounds  sup- 
porting the  view  of  a  simultaneous  reaction  on  the  part  of  the  hver 
cells  and  framework  as  the  starting-point,  or  first  stage  at  any  rate,  in 
some  cases  of  cirrhosis.  In  multiple  adenoma  or  nodular  cirrhosis  the 
liver  cells  may  actively  prohferate,  and  so  give  rise  to  the  so-called 
adenomata,  while  at  the  same  time  there  is  fibrosis.  This  process  might 
perhaps  be  regarded  as  a  general  h^-perplasia,  and  manj^  cirrhoses,  such 
as  the  nodular  cirrhosis  sometimes  met  with  in  the  subjects  of  malaria 
or  tuberculosis,  might  be  spoken  of  as  hj'pertrophies  that  failed. 

The  so-caUed  new  bile-ducts,  or  pseudobile  canahcuH,  met  with  in 
Hanot's  hypertrophic  cirrhosis  with  chronic  jaundice,  in  ordinar}^  cir- 
rhosis, around  hepatic  gummata,  etc.,  are,  as  Dreschfeld  *  pointed  out 
years  ago,  due  to  active  proliferation  of  the  liver  cells,  and  may  be  re- 
garded as  an  attempt,  not,  it  is  true,  entirely  successful,  at  compensatorv' 
hyperplasia  of  the  liver  cells. f  But  it  is  important  to  bear  in  mind 
that  there  are  possibly,  if  not  probably,  different  ways  in  which  the 
fibrosis  of  cirrhosis  is  brought  about,  and  that  the  causative  factors 
may  varj^  during  the  course  of  an  individual  case.  Thus,  while  the 
changes  may  at  the  outset  both  be  the  result  of  the  toxine,  irritative 
hyperjDlasia  in  one  case,  degeneration  in  the  other,  subsequently  one  of 
these  changes  maj^  react  on  the  other  process.  Thus,  the  products  of 
the  degenerating  liver  cells  may  act  as  a  further  irritant  and  stimulus  to 
the  fibrosis,  and,  conversely,  the  presence  of  fibrosis  may  hamper  the 
nutrition  of  the  liver  ceUs.     As  Adami  %  has  pointed  out  in  discussing 

*  Dreschfeld :  Journ.  Anat.  and  PhvsioL,  London,  vol.  xir,  p.  6fl 
tHanot:  Gaz.  d.  hop.,  Paris,  .Julv'lO,  1896. 
t  Montreal  Med.  Jour.,  Dec.  1896. 


CIRRHOSIS   OF  THE    LIVER.  197 

the  etiology  of  cirrhosis,  there  is  a  tendency  for  secondary  changes  to 
occur  in  the  course  of  cirrhosis,  so  that  a  pure  venous  cirrhosis  starting 
from  the  portal  vein  readily  spreads  to  the  bile-ducts,  and  sets  up  changes 
in  them,  and  a  mixed  form  of  cirrhosis  results. 

In  conclusion,  it  is,  in  the  present  state  of  our  knowledge,  safest 
not  to  regard  the  cirrhotic  process  as  exclusively  due  either  to  irritative 
hjToerplasia  of  the  connective  tissues,  the  hepatic  cells  being  quite  pas- 
sive, on  the  one  hand,  or  to  primarv'-  degenerative  or  atrophic  changes  in 
the  hepatic  cells  with  a  resulting  replacement  fibrosis  on  the  other,  but 
to  steer  a  middle  course,  and  to  remain  content  T\dth  the  view  that  the 
irritating  poisons  leading  to  cirrhosis  affect  both  elements  in  different 
ways,  and  that  the  resulting  changes  in  one  tissue  may  further  initiate 
fresh  changes  in  the  other  tissue,  or  modify  those  already  existing. 

MORBID  ANATOMY. 

Size  and  Weight. — The  size  of  the  liver  in  ordinary  cirrhosis  may 
vary  very  greatly;  it  may  be  smaller  than  natural,  and  is  then  often 
spoken  of  as  "atrophic,"  and  in  extreme  instances  may  not  weigh  more 
than  30  ounces;  or,  on  the  other  hand,  it  may  be  extremely  large  and 
weigh  as  much  as  150  or  200  ounces.  It  is  noteworthy  that  a  cirrhotic 
liver  which  is  actually  smaller  than  natural  often  weighs  as  much  as  a 
healthy  liver  or  even  more,  its  specific  gravity  being  much  increased. 
There  are  transitions  between  a  small  and  a  large  multilobular  cirrhotic 
liver,  but  they  all  belong  to  the  same  category  of  disease.  It  is  unde- 
sirable to  speak  of  the  small  ones  as  ''atrophic"  and  the  large  ones  as 
"hypertrophic"  cirrhosis,  since  the  practice  of  calling  a  large  multilobular 
cirrhotic  hver  "hypertrophic"  has  been  the  cause  of  much  confusion  with 
h^T^ertrophic  biliarj^  cirrhosis. 

The  large  size  of  some  cirrhotic  livers  may  be  due  to  considerable 
fatty  change  in  the  liver  cells.  It  has  been  assumed,  I  believe  quite 
incorrectly,  that  increased  size  and  fatty  change  in  cirrhosis  are  especially 
connected  with  over-indulgence  in  malt  liquors  rather  than  in  spirits. 

Some  years  ago  these  points  were  considered  in  the  course  of  an  anal3^sis  of 
114  cases  of  cirrhosis  undertaken  by  Fenton  and  myself.*  Taking  an  equal  number  of 
alcoholic  cirrhotic  livers  from  cases  in  which  malt  liquors  on  tlie  one  hand  and  spirits 
on  the  other  had  been  chiefly  drunk,  there  was  found  to  be  very  little  difference 
between  the  average  weights  of  the  livers  in  the  two  series.  The  number  of  cases 
available  was  very  small,  since  in  most  of  the  114  cases  where  the  form  of  stimulant 
taken  is  mentioned,  both  beer  and  spirits  were  taken.  In  10  beer  livers  the  average 
was  69  ounces,  and  in  10  spirit  livers  67  ounces.  The  spirit  livers  appeared  to  be 
more  frequently  fatty.  The  number  of  cases  is  so  small  that  no  stress  can  be  laid 
on  these  figures;  they  are  mentioned,  however,  because  an  analysis  of  Foxwell's 
cases  does  not  support,  in  fact  militates  against,  the  commonly  received  opinion 
that  a  beer  drinker's  liver  is,  as  a  rule,  large,  and  a  spirit  drinker's  liver  small. t 
In  a  series  of  microscopic  examinations  it  was  found  rather  luiexpectedly  that  fatty 
change  occurred  in  an  equal  proportion  in  large  and  in  small  cirrhotic  livers,  and 
that  half  the  large  livers  examined  did  not  show  fatty  change. 

In  cirrhosis  complicating  pulmonary  tuberculosis  the  liver  is  usually 
somewhat  enlarged  from  fatty  change.     As  will  be  shown  later  (p.  199), 

*  RoUeston  and  Fenton,  W.  J. :  Birmingham  Med.  Review,  Oct.,  1896,  p.  ^'^><. 
t  Foxwell,  \. :  Birmingham  Med.  Rev.,  April,  1896,  p.  221. 


198  DISEASES    OF   THE    LIVER. 

the  liver  is  larger  in  cases  of  cirrhosis  where  the  disease  is  latent 
and  death  occurs  from  some  independent  cause  than  in  those  cases  that 
die  directly  from  cirrhosis.  The  enlargement  is  chiefly  due  to  compensa- 
tory hyperplasia  of  the  liver  cells,  but  there  may  be  considerable  fatty 
change  in  the  hepatic  cells;  this  form  had  been  specially  described  by 
Hanot  and  Gilbert  *  as  "hy[3ertrophic  alcoholic  cirrhosis."  In  other 
instances  the  large  size  of  the  liver  is  due  to  the  fibrosis  having  a 
smaller  mesh  and  approaching  a  monolobular  type  or  showing  that  ar- 
rangement in  parts.  Enlargement  of  a  cirrhotic  liver  is  often  temporary 
and  due  to  congestion,  either  active,  when  the  cirrhotic  process  is  pro- 
gressing, or  passive,  and  due  to  backward  pressure  from  dilatation  of  the 
heart. 

In  cases  dying  from  the  effects  of  cirrhosis  the  liver  is  larger  in  younger 
subjects  than  in  those  of  more  advanced  years.  There  are  grounds  for 
thinking  that  in  patients  dying  from  cirrhosis  in  whom  no  alcoholic 
history  is  forthcoming,  the  liver  is  smaller  than  in  the  more  fainiliar  type 
of  alcoholic  patients  dying  from  cirrhosis. 

In  6  cases  in  which  cirrhosis  was  fatal  and  in  which  there  was  no  evidence  of 
alcohohc  excess  the  average  weight  of  the  liver  was  41  ounces,  whereas  in  36 
fata]  cases  of  alcoliolic  cirrhosis,  the  average  weight  was  67.7  ounces. 

In  cases  of  latent  cirrhosis  the  liver  is  a  little  larger  in  patients  addicted 
to  alcoholic  excess  than  in  the  non-alcoholic,  but  the  difference  is  very 
small  as  compared  with  that  mentioned  above  in  patients  dying  from 
the  effects  of  cirrhosis. 

In  29  cases  wliere  death  was  due  to  some  other  cause  and  the  evidence  of  alco- 
holic excess  was  forthcoming,  the  average  weight  of  the  cirrliotic  liver  was  62.2 
oimces,  while  in  26  cases  where  alcoholic  cirrhosis  was  latent  the  average  weight  of 
the  liver  was  67.9  ounces. 

Sex  does  not  seem  to  exert  any  very  special  influence  on  the  size  and 
weight  of  the  cirrhotic  liver. 

In  116  men  the  average  weight  of  the  cirrhotic  liver  was  61.5  ounces,  or  8J  ounces 
in  excess  of  53  ounces,  the  normal  weight,  while  in  41  females  the  average  weight  was 
55.5  ounces,  or  10  ounces  in  excess  of  the  normal  weight,  45  ounces.  Hale  White  t 
examined  50  cases  to  see  whether  large  or  small  cirrhotic  livers  were  commoner  in 
women,  and  found  that  large  cirrhotic  livers  were  rather  more  frequent  in  women. 

The  large  cirrhotic  livers  are  less  knobby  than  the  smaller  examples 
which  especially  merit  the  title  hobnailed. 

When  both  the  liver  and  the  spleen  are  inuch  enlarged,  the  left  lobe 
of  the  liver  may  touch  or  overlap  the  spleen.  This  is  much  more  likely 
to  occur  in  hypertrophic  biliary  cirrhosis,  but  I  have  seen  it  in  undoubted 
multilobular  cirrhosis. 

The  weight  of  the  liver  in  portal  cirrhosis  may  be  diminished,  normal, 
or  increased,  but  it  is  less  often  below  than  above  or  of  the  normal  weight. 

In  142  cases  tabulated  by  Price  J  the  liver  was  less  than  the  normal  weight  in 
27  per  cent. 

*  Hanot  and  Gilbert :  Soc.  Med.  des  Hop.  Paris,  May  23, 1890. 

t  Hale  White:  Guy's  Hosp.  Gaz.,  May  27,  1898. 

X  Price :  Guy's  Hosp.  Reports,  series  iii,  vol.  xxvii,  p.  295. 


CIRRHOSIS    OF   THE    LIVER.  199 

My  own  statistics  show  a  ver^'  considerable  increase  in  the  weight  of 
the  cirrhotic  hver,  but  in  100  cases  collected  by  Hawkins  *  the  average 
weight  was  52  ounces,  and  in  93  tabulated  by  Kelynack  f  53  ounces, 
which  is  very  close  to  Reid's  average  weight  for  the  normal  liver  (53 
ounces  for  males,  45  ounces  for  females).  The  average  weight  of  the 
liver  in  cases  d}dng  from  the  effects  of  cirrhosis  appears  to  be  less  than 
that  of  patients  with  latent  cirrhosis  who  die  from  independent  causes. 

In  155  consecutive  postmortem  examinations  on  patients  with  cirrhotic  livers 
at  St.  George's  Hospital  the  average  weight  was  63.6  ounces.  Of  these,  75  died 
from  the  effects  of  cirrhosis,  the  average  weight  of  the  liver  being  60  ounces,  while 
the  average  weight  of  the  hver  in  the  remaining  SO  patients  who  had  cirrhotic 
livers  but  died  froiu  other  causes  was  67  ounces.  In  11  of  the  142  cases  tabulated 
by  Price  death  was  due  to  accident,  and  the  average  weight  of  these  cirrhotic  hvers 
was  76  ounces. 

In  latent  cirrhosis  the  weight  of  the  liver  diminishes  as  age  advances; 
this  is  probably  a  senile  atrophic  change.  In  this  connexion  it  is  inter- 
esting to  note  that  in  cases  of  latent  cirrhosis  in  fatal  granular  kidney, 
which  is  perhaps  a  premature  senile  change,  the  weight  of  the  liver  is 
not  increased. 

Thus,  in  8  cases  of  combined  hepatic  and  renal  cirrhosis  examined  at  St.  George's 
Hospital  the  average  weight  of  the  liver  was  56.5  ounces,  the  average  age  of  the 
patients  being  52.25  years,  or  3.5  years  above  the  average  age  at  death  in  cirrhosis. 
Pitt's  t  figures  pointed  to  the  same  conclusion,  but  Price's  figures,  also  from  Guy's, 
tended  to  show  that  granular  kidney  was  associated  more  often  with  a  large  than 
with  a  small  cirrhotic  liver. 

In  cases  djdng  from  cirrhosis  the  weight  of  the  liver  becomes  less  as 
age  advances;  this,  again,  may  be  partly  due  to  the  advance  of  years. 

Morbid  Appearances  in  the  Liver. — The  peritoneal  surface  of  the 
liver  is  opaque;  this  ma}^  be  clue  to  chronic  peritonitis,  which  is  some- 
times (vide  p.  222)  associated  with  cirrhosis.  Not  uncommonly  there 
is  more  thickening  of  the  peritoneum  over  the  liver  than  elsewhere. 
The  opacity  of  the  capsule  is,  however,  largely  due  to  subcapsular  fibrosis 
and  atrophy  of  the  liver  cells,  which,  though  it  gives  somewhat  the  same 
naked-eye  appearance,  is  essentially  quite  different  from  genuine  peri- 
hepatitis. It  is  probable  that  chronic  perihepatitis  is  often  described 
when  subcapsular  fibrosis  is  the  actual  condition  present.  This  opacity 
is  not  uniform;  it  is  more  marked  between  the  projections  or  hobnails, 
where  there  is  underlying  fibrous  tissue. 

General  perihepatitis  occurred  in  15  out  of  53  cases  of  cirrhosis  recorded  by 
Cheadle,§  or  28  per  cent.,  and  in  13  out  of  78  autopsies  tabulated  by  Sears  and 
Lord,  II  or  16.6  per  cent. 

There  may  be  adhesions  between  the  liver  and  adjacent  parts,  espe- 
cially between  its  convexity  and  the  diaphragm.  These  adhesions  may 
be  dense,  but  are  often  comparatively  delicate.  They  maj'  be  remark- 
ably vascular.     The  surface  of  the  organ  is  irregular;    the  projections 

*  Hawkins :  Allbutt's  System,  vol.  iv,  p.  174. 

t  Kelynack:  Birmingham  Med.  Review,  Feb.,  1897. 

tPitt,  G.  X.:    Trans.  Path.  Soc,  vol.  xl,  p.  348. 

§  Cheadle,  W.  B.:    Lancet,  1900,  vol.  1. 

II  Sears  and  Lord:   Boston  Medical  and  Surg.  Journ.,.vol.  cxlvii,  p.  285. 


200 


DISEASES    OF   THE    LIVER. 


A'ary  in  size  from  a  pea  to  that  of  a  pigeon's  egg.  When  they  are  small, 
the  surface  of  the  organ  somewhat  resembles  that  of  a  granular  kidney, 
and  the  term  "granular  liver"  is  applicable.  "VNTien,  as  more  rarely 
occurs,  the  hobnails  are  large,  the  organ  may  look  as  if  it  was  occupied 
by  numerous  secondar}*  growths,  especially  when  the  projections  show 
marked  fatty  change  and  appear  white,  though  it  is  worthy  of  note  that 
the  hobnails  never  show  the  umbilication  usually  present  in  secondary 
carcinoma.  "V\'Tien  the  projections  are  exceptionally  large,  the  condition 
is  sometimes  spoken  of  as  nodular  cirrhosis  or  cirrhosis  with  multiple 
adenoma. 

Occasionally  in  an  otherwise  uniformly  cirrhotic  liver  there  is  one  large  prom- 
inent hobnail;  this  has  been  described,  rather  unnecessarily,  as  sohtary  adenoma 
with  cirrhosis.  It  is  probable  that  this  condition  is  of  the  same  nature  as  multiple 
adenomata  in  cirrhosis,  but  differs  in  there  being  only  one  area  of  marked  hyper- 
plasia.    Caminiti  *  has  described  two  examples  of  solitary  adenoma  with  cirrhosis. 

The  hobnails  are  of  a  tawny  yellow  or  brown  colour,  being  often  stained 
by  bile;    the  peritoneum  over  them  sometimes  shows  dilated  vessels. 

During  life  the  liver 
looked  uniformly  red 
in  the  laparotomies 
on  cases  of  cirrhosis  I 
have  seen.  The  cap- 
sule, which  is  not 
much  thickened  as  a 
rule,  is  more  opaque 
in  the  depressions  be- 
tween the  nodules. 
Usually  the  liver  is 
uniformly  affected, 
especially  when  it  is 
enlarged  and  the 
nodules  are  small,  but 
the  change  may  be 
irregular  and  the  left 
lobe  is  often  in  a  more 
advanced  condition  and  may  be  very  small.  It  is  possible  that  the 
resistance  of  the  left  lobe  is  less  than  that  of  the  right,  for  it  is  not 
infrequently  more  affected  in  acute  yellow  atrophy  (g.  v.)  than  the 
right.  Sometimes,  on  the  other  hand,  one  of  the  smaller  lobes,  such  as 
the  spigelian  or  caudate,  may  be  enlarged  out  of  proportion  to  the  others, 
even  when  the  organ  as  a  whole  is  Httle,  if  at  all,  bigger  than  normal. 

On  section  the  liver  is  tough  and  like  a  section  of  conglomerate  stone 
being  divided  up  into  areas  of  irregular  size  by  grey,  slightly  gelatinous- 
looking,  fibrous  tissue.  The  interlobular  tissue  in  cases  of  very  marked 
cirrhosis  may  have  a  red,  somewhat  spongy  appearance  and  be  rather 
depressed,  as  compared  vnth.  the  masses  of  liver  tissue  that  are  embedded 
in  it  and  stand  up  on  section  on  a  higher  level.     This  fibrous  tissue  is 

*  Caminiti:    Archiv  f.  klin.  Chirurg.,  1903,  S.  630. 


Fig.  26. — Under  Surface  of  Liver  Showing  Hobnailed 

Appearance. 

The  portal  vein  is  thrombosed.    (Drawn  by  Dr.  E.  A.  Wilson.) 


Plate  2. 


Portion  of  a  Finki.y  G];axui,au  Cirhuotic  Liver  Showing  the  Surface  and  the  Section. 

Dr.  K.  A.  Wilson. 


CIRRHOSIS    OF   THE   LIVER.  201 

continuous  with  the  depressed,  more  opaque  areas  on  the  capsule,  and 
by  its  contraction  has  squeezed  into  prominence  the  more  healthy  parts 
of  the  liver,  which  thus  form  the  nodules  or  hobnails. 

This  fibrosis  spreads  out  from  the  medium-sized  portal  canals  and 
exerts  its  constricting  influence  on  the  branches  of  the  portal  vein.  This 
is  shown  by  the  difficulty  of  injecting  the  hepatic  capillaries  from  the 
portal  vein.  The  areas  of  liver  substance  thus  enclosed  vary  in  size, 
being  usually  from  ^  to  ^  inch  in  diameter,  and  contain  six  to  ten  lobules, 
each  of  which  normally  measures  ^V  "to  tf  ^^^^  ^^^  diameter.  The  liver 
substance  is  much  paler  than  in  health  and  has  a  yellowish  brown  colour 
either  from  staining  with  bile  or  from  fatty  change.  In  the  same  liver 
the  colour  of  different  hobnails  often  varies,  some  being  yellow,  others 
of  a  brownish-red  colour.  This  may  be  due  to  irregularity  in  the  amount 
of  fatty  change. 


Jn^-'.:  ^r    '  '  t         > 


K 


K 


4 


Fig.  27. — Section  of  Multilobular  Cibrhotic  Liver  Showing  Irregularity  in  the  Mesh 
OF  the  Fibrous  Trabecule.     (Drawn  by  Dr.  E.  A.  Wilson.) 

Occasionally  haemorrhages  are  found  in  the  interstitial  tissue,  in  the 
hobnails,  or  in  both.  The  liver  cells  may  be  compressed  by  the  extrava- 
sated  blood  and  sometimes  show  necrosis.  When  the  hasmorrhage  is 
widespread  in  the  interlobular  tissue  and  the  hobnails  have  undergone 
fatty  change,  an  appearance  exactly  like  new-gro^vth  may  be  produced. 
The  haemorrhages  may  possibly  be  clue  to  the  toxic  condition  of  the  blood, 
but  this  is  unlikely,  since  hepatic  haemorrhages  are  rare  in  fatal  cases  of 
cirrhosis,  where  death  is  usually  due  to  toxaemia.  In  some  instances  it 
is  due  to  fatty  change  in  the  cells  in  the  hobnails  removing  the  support 
of  the  contained  vessels;  while  Bonone  *  has  suggested  that  endarteritis 
of  the  hepatic  artery  may  produce  necrosis  of  the  liver  cells  and  hemor- 
rhages. As  a  coincidence  I  have  seen  numerous  haemorrhages  into  the  cir- 
rhotic liver  of  a  man  who  died  from  haematemcsis.  Occasionally  small  throm- 
bosed veins  may  be  seen  in  the  liver  without  any  similar  change  in  the 
*  Bonone:    Quoted  Rev.  Gencr.  de  Path.  Intern.,  1900,  p.  70. 


202 


DISEASES    OF   THE    LIVER. 


portal  vein  or  its  larger  branches.  It  has  been  suggested  that  thrombosis 
of  the  terminal  branches  of  the  portal  vein  may  determine  ascites,  but 
there  is  no  proof  that  there  is  any  relationship  between  the  two  events; 
as  a  matter  of  fact,  thrombosis  of  the  smaller  veins  is  seldom  observed. 

Histology. — In  the  early  or  more  progressive  stages  there  is  small- 
cell  infiltration  in  and  around  the  portal  spaces;  these  cells  are  due  to 
hyperplasia  of  the  existing  connective  tissues  of  Glisson's  capsule  and 
to  some  leucocytic  invasion.  In  a  well-marked  case  there  is  an  irregular 
meshwork  of  connective  tissue  extending  throughout  the  liver  and 
dividing  it  up  into  variously  sized  islands  of  liver  tissue.  Inasmuch  as 
a  number  of  lobules  are  enclosed  within  the  same  fence  of  connective 


Fig.  28. — Multilobular  Cirrhosis 
Well-formed  fibrous  tissue  separating  off  masses  of  liver  cells  of  various  sizes^ 
arrangement  of  the  liver  cells  is  lost 
ducts." 


_^  __  _  The  normal 

In  the  fibrous  tissue  there  are  a  few  "  newly  formed  bile- 


tissue,  the  term  multilobular  cirrhosis  is  applied.  The  number  of  lobules 
enclosed  in  different  compartments  differs;  in  some  parts  there  are  many, 
in  other  areas  a  single  lobule  or  half  a  lobule  is  separated  off  from  the 
rest. 

The  French  school  considers  that  the  fibrosis  is  not  only  portal,  but 
also  around  the  sublobular  veins  or  bivenous.  (Sabourin.*)  It  is  true 
that  the  pressure  of  the  surrounding  trabeculse  may  obliterate  the  intra- 
lobular veins,  and  by  condensation  and  contraction  so  alter  the  appear- 
ance of  the  enclosed  lobules  that  it  is  difficult  to  count  the  number 
enclosed  in  the  alveoli  of  the  connective  tissue,  but  it  does  not  appear, 
*  Sabourin:  Revue  de  Med.,  1882,  p.  465. 


CIRRHOSIS    OF  THE   LIVER. 


203 


at  any  rate  to  me,  that  there  is  fibrosis  around  the  intralol3ular  veins. 
At  the  margin  of  the  lobules  the  fibrous  tissue  can  be  seen  to  surround 
bits  of  the  lobule  and  thus  to  shave  off  groups  of  cells  from  the  edge  of  the 
lobule.  In  some  large  cirrhotic  livers,  where  the  meshwork  is  still  multi- 
lobular as  a  whole,  there  are  parts  where  it  is  more  diffuse  and  approaches 
the  monolobular  type;  this  condition  of  mixed  cirrhosis  is,  from  an  ana- 
tomical point  of  view,  a  transitional  stage  to  hypertrophic  biliary  cir- 
rhosis; but  it  is  cjuite  commonly  seen  in  ordinary  portal  cirrhosis  when 
the  disease  is  rapidly  advancing. 

When  the  morbid  process  is  progressing  rapidly  the  lobules  are  often 
actuall}^  invaded,  so  that  a  certain  amount  of  intercellular  fibrosis  is 


Fig.  29. — Multilobular  Cirrhosis. 
Shows  invasion  of  a  lobule  by  young  connective  tissue,  so  that  there  is  local  intercellular 
cirrhosis.     Some  of  the  liver  cells  thus  isolated  show  hypertrophy  and  are  beginning  to  divide 
and  form  columns  of  small  cells — "  the  so-called  new  bile-ducts."     The  older  connective  tissue 
has  some  so-called  new  bile-ducts  in  its  meshes.     /,  140. 


superadded.  It  thus  often  happens  that  the  liver  of  portal  cirrhosis 
shows  a  very  mixed  cirrhosis,  there  being  areas  of  monolobular  and  inter- 
cellular cirrhosis  in  addition  to  the  prevailing  multilobular  type.  It  is 
not  justifiable  or  necessary,  however,  to  attempt  to  construct  a  special 
clinical  type  of  mixed  cirrhosis  to  correspond  to  these  microscopic  appear- 
ances. The  nature  of  the  fibrous  tissue  varies  according  to  its  age,  and 
whether  the  process  is  progressing  or  stationary.  There  is  nearly  always 
some  weU-formed  fibrous  tissue  containing  small  round  and  spindle 
cells.  In  cases  running  a  rapid  course  the  amount  of  small  round  cells 
is  increased,  while  in  latent  or  stationary  cases  there  ma>-  only  be  old 
fibrous  tissue.     The  interstitial  tissue  contains  numerous  newly  formed 


204 


DISEASES    OF   THE    LIVER. 


vessels   derived  from  the  hepatic   artery,  which  are  sometimes  much 
dilated. 

The  increase  in  connective  tissue  was  formerly  assumed  to  consist 
solely  of  white  fibrous  tissue  derived  from  proliferation  of  the  preexisting 
tissue  in  the  portal  canals.  Recent  histological  methods  show  that  there 
is  an  increase  in  the  amount  of  elastic  tissue. 

Hohenemser,*  in  1895,  using  Unna's  acid  orcein  stain  for  elastic  tissue,  showed 
the  presence  of  elastic  fibres  in  the  connective  tissue  of  portal  cirrhosis;  this 
has  been  confirmed  by  Melnikow-Rasnednekow  f  and  Flexner.J  The  elastic  tissue 
spreads  out  from  the  sheaths  of  the  hepatic  artery,  portal  vein,  and  bile-duct,  and 
is  also  found  in  the  capsule.  More  elastic  tissue  is  found  in  cases  of  portal  cirrhosis 
than  in  biliarv  and  mixed  forms  of  cirrhosis. 


Fig.  30. — Cirrhosis  in  H.emochromatosis. 
Section  at  margin  of  lobule.     Shows   hsemosiderin  as   dark  granules  in  the  liver   cells  and 
also  in  the  fibrous  tissue  surrounding  the  lobules.     Prepared  from  Dr.  Maude  Abbott's  case. 
(Fide  Trans.  Path.  Soc,  vol.  li,  p.  .56.)     X  220. 


In  pigmentary  cirrhosis  {vide  p.  299),  which  may  be  due  to  more 
than  one  cause,  the  fibrous  tissue  may  become  occupied  by  opaque  masses 
of  pigment.  In  hsemochromatosis,  where  there  is  a  liberation  of  hsemo- 
globin  from  the  red  blood-corpuscles  in  the  general  circulation  with  a 
deposit  of  blood-pigment  in  the  cells  of  the  liver,  pancreas,  and  other 
glands,  and  an  accompanying  fibrosis,  the  pigment  is  eventually  liberated 
from  the  liver  cells  and  passes  into  the  connective  tissues. 

Pigmentation  of  the  fibrous  tissue  in  cirrhosis  is  also  seen  in  malaria  and 
in  the  extremely  rare  condition  of  cirrhosis  anthracotica.     {Vide  p.  185.) 

*  Hohenemser:    Virchow's  Archiv,  Bd.  cxl,  S.  192,  April  2,  1895. 

t  Melnikow-Rasnednekow:    Ziegler's  Beitriige,  Bd.  xxvi,  S.  526. 

X  Flexner:  University  Medical  Magazine,  Philadelphia,  Nov.,  1900,  p.  613. 


CIRRHOSIS    OF   THE    LIVER. 


205 


Neioly    Formed    Bile-ducts— Pseudohile    Canalicidi. ^Tl\e   interstitial 
tissue  shows  as  a  prominent  feature  columns  of  small  cells  which  stain 


*•,* 


Fig.  31. — Photomicrogkaph   Showing  Deeply  Stained  Pseudobile  Canaliculi  Bka.mching 
AND  Twisting  in  the  Fibrous  Tissue. 
The  margin  of  a  lobule  is  also  shown.     From  a  ca.se  of  multilobular  cirrho.si.s.     (Dr.  H.  R. 
Spitta.) 

deeply,  show  karyokinesis,  and  arc  therefore  in  a  state  of  active  growth. 
The  cells  are  small  and  may  be  cubical,  but  are  often  elongated  so  as  to 


206  DISEASES    OF   THE    LIVER. 

lie  in  the  long  axis  of  the  column;  they  are  arranged  on  much  the  same 
pattern  as  in  a  small  bile-duct  around  a  potential  lumen.  It  is  indeed  open 
to  doubt  whether  similar  structures  containing  a  dUated  lumen  or  masses 
of  inspissated  bile  are  exactly  the  same  as  these  so-called  new  bUe-ducts; 
possibly  the  former  are  pre-existing  bile-ducts.  The  so-called  new  bile- 
ducts  twist  and  branch  in  the  interlobular  connective  tissue  and  form 
a  rough  network.  The  individual  columns  catch  one's  eye  as  minute 
worm-like  bodies  under  a  low  power. 

Special  importance  was  formerly  attached  to  the  presence  of  these 
so-called  new  bile-ducts  in  hypertrophic  biliary  cirrhosis,  but  they  may 
be  just  as  prominent  in  common  cirrhosis,  and  indeed  are  present  in  a 
number  of  conditions,  such  as  local  fibrosis  around  a  hydatid  cyst, 
gumma,  in  tubercle,  lymphadenoma,  acute  yellow  atrophy,  and  other 
lesions  which  have  in  common  destruction  of  the  liver  ceUs. 

A  considerable  amount  of  discussion  has  arisen  as  to  their  nature. 
It  has  been  thought  that  they  are  the  pre-existing  bile-ducts  of  the  portal 
spaces  and  lobules  of  the  liver  which  are  left  in  a  conspicuous  position 
by  the  atrophy  and  recession  of  the  Uver  cells;  the  brilliant  staining  of 
the  cells  is  explained  by  supposing  that  some  proliferation  of  the  ceUs 
normally  hning  the  ducts  in  the  interlobular  tissues  around  the  portal 
canals  extends  into  the  flat-waUed  ducts  between  the  fiver  cells.  Against 
this  view  are  the  facts  that  in  senfie  or  other  forms  of  simple  atrophy 
of  the  liver  ceUs  the  appearance  of  so-called  new  bile-ducts  is  not  seen, 
and  that  histologically  they  differ  from  normal  bile-ducts  in  that  they 
either  have  no  elastic  fibres  or  only  an  imperfect  development  of  these 
fibres  around  them.  (Flexner.*)  From  their  resemblance  to  small 
bile-ducts  it  has  naturaUy  been  suggested  that  they  are  due  to  prolifera- 
tion of  pre-existing  bile-ducts,  but  this  is  chiefly  based  on  the  facts  that 
they  are  usuaUy  prominent  features  in  cases  of  biliary  cirrhosis  and  have 
been  obser^'ed  after  experimental  ligature  of  the  ducts.  Against  this 
are  the  facts  that  these  so-called  new  bile-ducts  are  seen  in  very  diverse 
conditions  which  only  resemble  each  other  in  destroying  the  liver  ceUs, 
and  that  the  bile-ducts  may  be  fittle  or  not  at  all  affected  when  these 
so-caUed  new  bile-ducts  are  present. 

Another  suggestion  is  that  the  liver  cells  become  surrounded  by  the 
advancing  fibrous  tissue,  which,  so  to  speak,  shces  off  columns  of  hepatic 
ceUs  from  the  periphery  of  the  lobules.  {Vide  Fig.  28.)  The  liver  cells 
then  atrophy,  become  compressed,  and  are  said  to  reA^ert  to  the  type 
of  a  tubular  liver.  This  view  as  to  the  nature  of  the  change  is  supported  bj'' 
some  appearances,  but  is  opposed  to  the  fact  that  they  stain  deeph"  and  are 
evident^  actively  proliferating.  It  seems  more  probable  that  they  are, 
as  pointed  out  hj  Dreschfeld  f  3'ears  ago,  the  result  of  active  prolifera- 
tion of  the  liver  cells,  and,  as  Hanot  J  believed,  an  attempt  at  com- 
pensatory hj^Derj^Dlasia.  The  healthy  liver  cells  proHferate  in  order  to 
compensate  for  the  destruction  of  the  hepatic  tissues.     Appearances 

*  Flexner:    University  Medical  Magazine,  Philadelphia,  1900,  p.  617. 
t  Dreschfeld:    Journal  of  Anatomy  and  PhvsioL,  vol.  xiv,  p.  69. 
X  Hanot,  v.:    Gaz.  des  Hop.,  Paris,  July  10,  1S96. 


CIRRHOSIS    OF   THE   LIVER. 


207 


strongly  suggesting  hypeiplasia  of  the  cells  may  be  seen  at  the  periphery 
of  the  lobules,  and  the  columns  of  small  cells  may  in  fortunate  sections 
be  traced  into  continuity  with  a  liver  cell.  Since  at  any  rate  considerable 
doubt  exists  as  to  their  being  bile-ducts,  it  is  more  convenient  to  speak 
of  them  as  the  so-caUed  new  bile-ducts  or  pseudobile  canaliculi. 

The  liver  cells  in  the  early  stages  may  show  little  or  no  change,  and 
in  cases  where  the  disease  has  become  latent  or  compensated  they  may 
be  larger  than  natural  from  compensatory  hypertrophy.  When  the 
disease  is  well  established  or  advanced,  changes  in  the  cells  are  the  rule. 
The  normal  trabecular  arrangement  in  the  lobule  is  disturbed  by  the 
circumferential  pressure  exerted  by  the  contracting  fibrous  tissue,  and 


Fig.  32. — Slight  Multilobulak  Cirrhosis  with  Extensive  Fatty  Change  in  the 

Liver  Cells. 
The  vacuolation  of  the  liver  cells  is  irregular.     Some   groups  of  ceUs  are  unaffected,  while 
others  have  hardly  any  of  their  protoplasm  left.     X  72. 


disappears.  In  some  cases,  owing  to  backward  venous  pressure  from 
cardiac  failure,  the  capillaries  between  the  columns  of  liver  cells  become 
dilated  and  separate  single  columns  of  cells  from  each  other.  In  other 
cases  the  lymphatic  capillaries  are  dilated  and  the  lobule  becomes  oedema- 
tous.  When  cirrhosis  is  advanced,  the  liver  cells  show  degenerative 
changes.  Fatty  change  is  often  present  in  a  greater  or  lesser  degree, 
and  is  the  effect  of  the  action  of  alcohol  or  some  other  toxic  substance. 
It  has  been  thought  that  fatty  change  is  specially  related  to  excess  in 
beer  and  other  sugar-containing  beverages,  but,  plausible  as  it  appears, 
this  assumption  has  not  been  proved.     {Vide  p.  197.) 

The  degenerative  changes  are  extremely  marked  in  those  cases  which 


208  DISEASES    OF   THE    LIVER. 

run  a  rapid  or  an  acute  course.  The  protoplasm  may  show  cloudy 
swelling  and  become  granular,  while  the  nucleus  may  stain  badly  or  be 
obscured.  The  presence  of  pigment  granules  of  bile  is  seen  in  cases 
where  jaundice  has  existed,  while  in  malaria,  hsemochromatosis,  and  in 
other  examples  of  pigmented  cirrhosis  {vide  p.  299)  the  liver  cells  are 
crowded  with  pigment  and  are  markedly  degenerated. 

The  liver  cells  may  show  hsemosiderosis  quite  apart  from  the  existence 
of  general  hsemochromatoses. 

In  16  cases  of  cirrhosis  Abbott*  found  pigment  in  the  Uver  cells  in  6  cases, 
and  in  26  cases  examined  by  Kretzf  pigmentation  existed  in  14.  Since  this  pig- 
ment is  probably  due  to  the  hsemolytic  action  of  intestinal  bacteria,  it  is  curious 
that  it  is  not  more  constant  in  cases  of  cirrhosis. 

In  the  early  stages  of  cirrhosis  a  majority  of  the  liver  cells,  even  those 
cut  off  and  embedded  in  fibrous  tissue,  contain  glycogen.  This  observa- 
tion of  Brault's  %  helps  to  explain  the  absence  of  glycosuria  in  cases  of 
cirrhosis.  He  suggests  that  in  cirrhosis  there  may  be  excessive  glycogen 
storage  in  the  liver  cells  in  order  to  bring  about  compensation  for  the 
cellular  destruction. 

Compensatory  hyperplasia  of  the  liver  cells  in  cirrhosis  occurs  in 
two  forms:  (i)  the  earlier,  or  the  so-called  new  bile-ducts  already  de- 
scribed, and  (ii)  the  change  which  when  fully  developed  gives  rise  to 
the  multiple  adenomata.  In  both,  the  proliferation  of  the  liver  ceUs 
begins  at  the  margin  of  the  lobule,  probably  because  the  blood-supply 
to  the  cells  is  more  copious  there.  In  the  form  of  compensatory  hyper- 
plasia giving  rise  to  multiple  adenomata  the  liver  cells  become  indi- 
vidually larger  and  show  karyokinesis,  multiply,  and  lead  to  an  increase 
in  the  size  of  the  lobules  and  to  the  formation  of  actively  growing  masses 
of  liver  tissue.  Many  of  the  ''hobnails"  in  a  cirrhotic  liver  are  of  this 
nature.  When  the  process  is  well  marked,  the  condition  is  called  nodular 
cirrhosis,  or  cirrhosis  with  adenoma.  This  process  is  of  great  importance 
in  compensating  for  the  destruction  of  the  liver  cells  and  allowing  the 
disease  to  become  latent.  § 

Gall-bladder  and  Bile-ducts. — The  gall-bladder  and  larger  bile- 
ducts  do  not  show  any  constant  change  to  the  naked  eye.  In  some  in- 
stances the  walls  of  the  gall-bladder  are  thickened  from  past  or  from 
chronic  cholecystitis,  and  occasionally  there  is  inflammation  of  the  larger 
ducts.  In  cases  where  ascites  is  present  the  serous  coat  of  the  gall- 
bladder may  be  cedematous. 

Gall-stones  occur  slightly  more  frequently  in  cases  of  cirrhosis  than 
in  the  ordinary  run  of  cases.  Thus,  in  136  cases  of  cirrhosis  exainined 
after  death  at  St.  George's  Hospital  gall-stones  were  found  in  21,  or  15.4 
per  cent.;  but  in  many  of  these  cases  there  were  only  small  calculi  in 
the  gall-bladder,  and  in  a  few  only  bilirubin-calcium  calculi. 

*  Abbott,  M.:   Trans.  Path.  Soc,  vol.  li,  p.  79. 
tKretz:    Beitrage  zur  klin.  Med.  und  Chir.,  Heft  15,  1896,  Wien. 
i  Brault:    Archiv  de  Med.  experiment,  et  d'Anatom.  path.,  tome  xiv,  p.  453, 
1902.     La  Presse  M^dicale,  May  29,  1901.     Bull.  Soc.  Anat.  Paris,  1901,  p.  334. 
§  Hanot  et  Gilbert:    Bull,  de  la  Soc.  Med.  des  Hop.,  1S96,  p.  492. 


CIRRHOSIS    OF   THE    LIVER.  209 

The  small  intra-hepatic  bile-ducts  are  usually  healthy  or  show  little 
change.     In  some  instances  there  is  concomitant  catarrhal  cholangitis. 

In  one  case  microscopic  sections  of  a  cirrhotic  liver  with  some  perihepatitis 
showed  cystic  dilatation  of  the  bile-ducts  in  a  few  of  the  portal  spaces.  It  i.s  indeed 
remarkable  how  extremely  rare  any  dilatation  of  the  small  ducts  is  in  cirrhosis, 
especially  in  view  of  the  frequency  of  cysts  in  a  granular  kidney,  which  may  be 
considered  as  an  homologous  condition  to  hepatic  cirrhosis. 

Portal  Vein. — The  intra-hepatic  branches  of  the  portal  \ein  are  com- 
pressed, and  in  rare  instances  are  thrombosed.  The  trunk  of  the  portal 
vein  and  its  branches  are  dilated,  and  very  occasionally  varicosities  are 
seen  on  its  mesenteric  radicles.  The  walls  of  the  vein  are  thickened  by 
periphlebitis  and  there  is  opacity  of  the  intima  from  endophlebitis ;  in 
extreme  instances  secondary  calcification  may  occur  in  the  intima. 
These  changes  are  comparable  to  arteriosclerosis  and  are  connected  with 
increased  pressure  in  the  portal  vein,  or  possibly  with  the  presence  of 
poisons  in  the  blood.  Thrombosis  of  the  trunk  of  the  portal  vein  is 
more  often  associated  with  hepatic  cirrhosis  than  with  any  other  condi- 
tion, but  it  is  a  rare  complication,  occurring  in  about  3  per  cent,  of  the 
fatal  cases  of  cirrhosis. 

In  a  remarkable  case  of  calcification  of  the  portal  and  splenic  veins  in  a  man 
whose  case  is  referred  to  on  page  81,  the  liver  showed  old,  non-progressive  cirrhosis 
of  the  liver.* 

Dilatation  of  the  Communications  between  the  Portal  Vein  and  the 
General  Systemic  Veins. — This  is  important  as  providing  a  collateral 
circulation  for  venous  blood  which  would  otherwise  have  to  force  its  waj'' 
against  the  obstruction  offered  by  the  cirrhotic  liver.  On  the  develop- 
ment of  this  compensatory  anastomosis  great  importance  is  laid  as  one 
of  the  factors  which  enable  cases  of  cirrhosis  to  become  latent  or  to  appear 
cured.  The  normal  communications  between  the  portal  vein  radicles 
and  the  general  systemic  veins  are  (i)  general,  and  (ii)  local. 

(i)  General  communications  between  the  retroperitoneal  veins,  open- 
ing into  the  lumbar,  azygos  veins,  etc.,  and  the  veins  of  the  peritoneum, 
and  of  the  intestines  occur  especially  where,  as  in  the  case  of  the  duode- 
num, pancreas,  ascending  and  descending  colon,  areas  drained  by  the 
portal  vein  are  bound  down  to  the  abdominal  parietes.  The  veins  in  the 
fat  around  the  left  kidney  anastomose  to  some  extent  with  the  veins  of 
the  descending  colon,  and  venous  trunks  may  put  the  renal  vein  itself 
into  commimication  with  the  colica  sinistra  vein.  I'he  veins  of  the  de- 
scending colon  may  connnunicate  with  the  spermatic  plexus,  and  this 
has  been  thought  to  favour  the  development  of  varicocele  on  the  left 
side.  (Bennett. t)  Compensatory  dilatation  of  this  anastomosis  has 
been  recorded,  but  in  general  it  is  of  little  or  no  importance.  It  has  not 
appeared  to  me  that  varicocele  is  specially  coimnon  oi"  mai'kcd  in  ])atients 
with  cirrhosis. 

A  communicating  brancli  between  the  splenic  and  the  left  renal  \-eins  has  been 
seen,  and  in  Jacobson'sJ   case  of  compensated  hepatic  cirrhosis,   in  which  death 

*  Trevor,  R.  S.:    Trans.  Path.  Soc,  liv,  p.  302. 
t  Bennett,  W   H. :  On  Varicocele,  p.  43,  1891. 

j  Jacobson,  G.:    Archiv.  General,  de  Mddecine,  1893,  vol.  i,  p.  353. 
14 


210 


DISEASES    OF   THE    LIVER. 


occurred  from  urtemia  due  to  granular  kidneys,  a  vein  as  large  as  the  thumb  ran 
from  the  left  renal  A^ein  into  the  trunk  of  the  portal  vein.  A  somewhat  similar 
anastomosis  has  been  observed  by  Virchow  *  between  the  splenic  vein  and  the 
azygos  vein. 

In  some  cases  of  cirrhosis  the  greater  part  of  the  parietal  peritoneum, 
more  especially  on  the  posterior  wall  and  upper  part  of  the  abdominal 
cavity,  is  markedly  injected  and  in  some  areas  resembles  a  "claret 
stain"  on  the  skin.  The  significance  of  this,  and  also  the  fact  that  it  is 
not  due  to  a  terminal  peritonitis,  are  shown  by  the  absence  of  this  injec- 
tion from  the  peritoneum  covering  the  free  coils  of  the  small  intestine. 
This  subperitoneal  plexus  of  anastomoses  has  been  described  by  Retzius, 
after  whom  it  is  sometimes  called,  while  Sir  W.  Turner  f  specially  inves- 
tigated the  anastomoses  between  the  visceral  and  parietal  arteries. 
Peritoneal  adhesions  around  the  liver,  stomach,  omentum,  or  spleen  may 
become  markedly  vascular  and  thereby  assist  the  collateral  circulation. 

This  hint  on  the  part  of  nature  has  been  taken  in  a  surgical  sense  by  Drum- 
mond  and  Morison,J  who  artificially  produced  adhesions  between  the  liver  and 
abdominal  wall,  and  by  Talma, §  who  sutured  the  omentum  to  a  wound  in  the 
abdominal  wall,  and  thus  led  to  a  diminution  of  ascites. 

(ii)  Local. — (a)  Around  or  in  connexion  with  the  liver:  communica- 
tions may  develop  between  the  veins  in  the  substance  and  capsule  of 

the  liver  and  the 
phrenic  and  inter- 
costal veins,  where 
the  liver  and  dia- 
phragm are  uncov- 
ered by  peritoneum, 
i.  e.,  between  the 
layers  of  the  coron- 
ary ligament  and 
its  lateral  fringes, 
the  lateral  liga- 
ments. 

The  falciform 
ligament  of  the 
liver  may  contain 
a  large  vein  which 
runs  to  the  umbilicus  and  may  communicate  there  with  the  veins  of  the 
abdominal  wall,  and  so  establish  a  communication  between  the  portal 
vein  in  the  transverse  fissure  of  the  liver  and  the  deep  epigastric  and 
external  iliac  veins.  This  vein  is  comparable  with  the  epigastric  vein 
of  cold-blooded  air-breathing  vertebrates,  such  as  the  frog.  This  vessel 
may  be  a  greatly  dilated  parumbilical  vein,  which,  according  to  Luschka, 
normally  puts  the  portal  and  epigastric  veins  into  commimication,  and 

*  Virchow:  Quoted  in  Frerichs'  Diseases  of  Liver,  vol.  ii,  p.  41.  Transl.  New 
Sydenham  Soc. 

t  Turner,  W.:    Brit,  and  Foreign  Medico-chirurg.  Review,  vol.  xxxii,  p.  222. 
J  Drummond  and  Morison:    Brit.  Med.  Journal,  1896,  vol.  ii,  p.  479. 
§  Takna:    BerUn.  klin.  Wochenschrift,  Sept.  19,   1S9S,  S.  833. 


Fig.  33. — A  Cirrhotic  Liver  with  a  Large  Parumbilical 
Vein  (a)  in  the  Falciform  Ligament.  The  round  ligament 
is  also  shown.     (Drawn  by  L.  Jones,  M.B.,  F.R.C.S.) 


CIRRHOSIS   OF   THE   LIVER.  211 

runs  alongside  of  the  obliterated  umbilical  vein.  On  the  other  hand, 
this  vein  may  be  the  umbilical  vein,  which  has  become  pervious  again 
and,  so  to  speak,  has  reverted  to  its  foetal  function  of  carrying  blood, 
mth  the  difference  that  the  blood  runs  away  from,  instead  of  to,  the  liver. 
Sappey  *  insisted  that  the  large  vein  found  in  the  falciform  ligament  in 
some  cases  of  cirrhosis  was  always  independent  of  the  umbilical  vein, 
but  this  is  not  in  accord  with  cases  quoted  by  Champneys.f 

This  vein  may  be  extremely  large;  Wilks  J  mentions  a  case  where 
it  was  as  big  as  the  portal  A'ein,  and  in  Sappey's  case  and  the  case 
figured  here  it  admitted  the  little  finger.  This  big  vein  is  probably 
not  so  infrequent  as  would  appear  from  the  recorded  cases,  for  the  vein 
collapses  after  death  and  is  not  seen  unless  the  falciform  ligament  is 
specially  examined.  I  have  seen  it  full  of  carcinoma  in  a  case  of  carci- 
noma with  cirrhosis. 

As  a  result  of  the  anastomosis  thus  opened  up  the  veins  of  the  abdom- 
inal wall,  especially  around  the  umbilicus,  may  become  dilated  and  promi- 
nent. When  marked,  this  condition  is  spoken  of  as  a  "caput  medusse." 
It  is  hardly  ever  so  well  developed  as  the  caput  medusae  produced  by 
mechanical  obstruction  of  the  inferior  vena  cava.  There  is  a  difference 
in  the  situation  of  these  two  collateral  venous  circulations  in  the  ab- 
dominal wall;  that  due  to  portal  obstruction  is  most  marked  around  the 
umbilicus,  while  that  seen  in  obstruction  of  the  inferior  vena  cava  runs 
from  the  middle  of  the  groins  to  the  costal  arches  and  avoids  the  um- 
bilicus. 

It  may  be  pointed  out  that  in  healthy  subjects  the  round  Hgament  at  its  junc- 
tion with  the  right  branch  of  the  portal  vein  is  pervious  for  a  distance  of  J  to  1§ 
inches  and  then  becomes  occluded.  This  channel  is  no  doubt  utilized  in  the  forma- 
tion of  a  collateral  and  compensatory  circulation. 

In  very  rare  instances  the  ductus  venosus,  which  in  the  foetus  runs 
directly  from  the  umbilical  vein  into  the  inferior  vena  cava,  is  persistent, 
and  thus  provides  a  direct  communication  between  the  portal  vein  and 
the  inferior  vena  cava. 

In  an  interesting  case  of  hepatic  cirrhosis  with  olastruction  of  the  superior  vena 
cava  described  by  Duckworth  and  Garrod  §  there  were  great  by  dilated  veins  under  the 
skin  of  the  abdomen,  the  blood  running  into  them  in  both  directions,  but  it  is  note- 
worthy that  there  was  an  absence  of  these  veins  around  the  lunbilicus. 

In  ordinary  cirrhosis  extensive  ascites  may  so  compress  the  inferior 
vena  cava  as  to  lead  to  the  development  of  a  caput  medusse  comparable 
to  that  seen  when  there  is  obstruction  to  the  passage  of  blood  through 
the  inferior  cava.  An  extremely  rare  complication  of  cirrhosis  is  throm- 
bosis of  the  inferior  vena  cava,  which  would  produce  the  same  conditions. 

Councilman  II  has  met  with  a  terminal  streptococcal  infection  in  cirrhosis  in 
which  the  retroperitoneal  glands  and  tissues  were  suppurating  and  had  thus  caused 
thrombosis  of  the  inferior  vena  cava. 

*  Sappey:  Mem.  de  I'Acad.  Roy.  de  Med.,  xxiii,  p.  270. 

fChanipneys:    Journ.  Anat.  and  Physiol.,  vol.  vi,  p.  417,  1872. 

t  Wilks:  Pathological  Anatomy,  p.  467,  1SS9. 

§  Duckwortli  and  Garrod  :  St.  Bartholomew's  Hosp.  Reports,  vol.  xxxii,  p.  71. 

II  Councilman,  W.  T. :  Trans.  Assoc.  .American  Physicians,  vol.  xi,  p.  213,  1896. 


212  DISEASES    OF   THE    LIVER. 

Occasionally  there  may  be  a  kind  of  belt  of  dilated  cutaneous  venules 
over  the  line  of  attachment  of  the  diaphragm.  This,  however,  is  not 
pathognomonic  of  portal  obstruction,  as  has  sometimes  been  thought, 
but  occurs  in  emphysema,  bronchitis,  and  sometimes  in  elderly  men 
without  at  any  rate  any  manifest  morbid  lesion. 

(h)  At  the  terminations  of  the  intra-abdominal  parts  of  the  ali- 
mentary canal :  The  veins  of  the  oesophagus,  which  open  into  the  azygos 
veins,  communicate  at  the  cardiac  orifice  with  the  gastric  veins  and  so 
with  the  portal  vein.  This  communication  may  become  so  developed 
as  to  produce  varicosities  at  the  lower  end  of  the  oesophagus,  or  "oesopha- 
geal piles,"  and  from  ulceration  or  rupture  may  be  the  source  of  severe 
hsemorrhage.  Though  usually  developed  to  a  certain  degree,  it  is  only 
occasionally  that  there  are  large  varicosities.  This  may  be  explained 
on  the  ground  that  there  are  valves  guarding  the  entrance  of  the 
gastric  vein  (Macalister  *),  which  would  tend  to  prevent  reflux  of  blood 
from  the  portal  into  the  gastric  veins. 

It  should  be  noted  that  oesophageal  varix  may  occur  without  any  cirrhosis  of 
the  liver;  cases  of  fatal  hsemorrhage  have  occurred  from  this  cause  in  a  child  and 
in  a  boy  of  seventeen.! 

The  coronary  vein  of  the  stomach  communicates  with  the  phrenic 
vein,  and  it  w^ould  be  natural  to  expect  to  find  that  the  branches  of  the 
gastric  veins  would  be  often  dilated.  This  is  very  seldom  observed, 
though  it  is  possible  that  it  is  overlooked.  The  walls  of  the  vein  may 
undergo  chronic  inflammation,  and  from  the  results  of  fibrotic  atrophy 
local  dilatations  may  result.  These  become  adherent  to  the  mucosa  and 
the  raised  area  may,  as  the  result  of  traumatism,  toxic  irritation,  or 
microbic  infection,  become  ulcerated.  The  resulting  hsemorrhage  may, 
as  in  two  cases  of  cirrhosis  recorded  by  Letulle,t  be  fatal. 

Varicosity  of  the  gastric  veins  and  fatal  hsematemesis  may  occur  in  the  absence 
of  any  hepatic  disease.     (Barr,  §  Lancaster  ||.) 

Dilatation  of  the  anastomosis  between  the  superior  hsemorrhoidal 
vein  opening  into  the  inferior  mesenteric,  on  the  one  hand,  and  the  middle 
and  inferior  hsemorrhoidal,  which  pour  their  blood  into  the  internal  iliac 
vein,  on  the  other  hand,  may  also  occur.  It  would  if  excessively  devel- 
oped lead  to  piles,  and  from  a  friori  reasoning  it  has  been  assumed  that 
piles  are  common  in  cirrhosis.  As  a  matter  of  experience,  however, 
this  is  not  the  case,  and  it  must  be  admitted  that  constipation  is  a  far 
more  frequent  and  important  factor  in  the  production  of  piles  than 
cirrhosis. 

It  is  possible  that  the  compensatory  effects  of  these  anastomotic 
channels  have  been  somewhat  overestimated.  Thus  the  dilated  venous 
channels  may  be  absent  in  cases  of  latent  cirrhosis  dying  from  other 
causes,  and  may  be  well  developed  in  cases  dying  with  ascites.     In  the 

*  Macalister's  Anatomy,  p.  431. 

t  Graham:  Trans.  Assoc.  American  Physicians,  vol.  xi,  p.  215,  1896. 

J  Letulle:  La  Presse  Medicale,  Nov.  29,  1S9S. 

§  Barr:  Lancet,  1889,  vol.  ii,  p.  1226. 

II  Lancaster:  Trans.  Clinical  Soc,  vol.  xxx,  p.  32. 


CIRRHOSIS    OF   THE    LIVER.  213 

latter  instance  the  compensatory  process,  though  considerable,  cannot  be 
regarded  as  having  been  successful. 

In  an  examination  of  78  autopsies  of  cases  with  cirrhosis,  Sears  and  Lord  * 
found  this  cUlated  anastomosis  in  29  cases,  being  most  often  present  when  tlie  cir- 
rliotic  process  was  most  advanced.      But  in  22  out  of  the  29  cases  tlaere  was  ascites. 

Bad  Effects  and  Residts  which,  may  Depend  on  Excessive  Development 
of  this  Venous  Anastomosis. — The  development  of  a  free  communication 
between  the  portal  and  general  systemic  veins,  while  it  relieves  portal 
engorgement,  may  lead  to  bad  effects.  In  the  first  place,  if  the  com- 
munications are  extensive,  it  necessarily  follows  that  a  considerable  quan- 
tity of  blood  carrying  the  products  of  digestion  will  pass  directly  into  the 
general  circulation  instead  of  going  through  the  liver.  As  a  result 
poisons  absorbed  from  the  intestine  would  not  be  stopped  by  the  liver, 
but  would  pass  freely  into  the  general  circulation  and  set  up  toxaemia. 
If  the  anastomosis  is  very  free,  the  condition  would  resemble  that  in 
Eck's  fistula,  or  the  experimental  communication  between  the  inferior 
vena  cava  and  the  portal  vein,  which  results  in  all  the  portal  blood 
passing  into  the  inferior  vena  cava.  A  most  elaborate  and  interesting 
series  of  experiments  on  these  lines  was  carried  out  by  Hahn,  Nasse, 
Nencki,  and  Pawlow.f  In  animals  thus  treated,  effects  equivalent 
to  those  of  hepatic  insufficiency  naturally  resulted,  and  if  a  pro- 
teid  diet  was  adopted,  symptoms  comparable  to  those  of  uraemia 
developed,  which  were  regarded  as  due  to  the  presence  of  carbamic 
acid  in  the  blood.  In  man  excessive  development  of  the  collateral 
circulation  may  lead  to  a  toxemic  condition  verging  on  uraemia. 
This  has  been  insisted  on  by  Stockton, |  and  it  is  interesting  to  note 
that  one  of  Morison's^  patients,  after  the  operation  for  the  surgical 
relief  of  ascites,  was  alternately  excited  and  depressed  for  three  weeks 
after  the  operation.  Possibly  a  very  free  collateral  anastomosis  between 
the  portal  and  general  venous  systems,  while  relieving  portal  engorgement, 
may  lead  to  arteriosclerosis  and  granular  kidneys.  In  cases  where  the 
two  conditions  of  renal  and  hepatic  fibrosis  are  combined  the  patients 
usually  die  from  renal  disease  with  latency  of  the  hepatic  cirrhosis.  This 
was  the  termination  of  Jacobson's  1|  remarkable  case,  where  a  vein  as 
large  as  a  thumb  ran  between  the  portal  A^ein  and  the  left  renal  vein. 

In  the  second  place,  haemorrhage  may  occur  from  rupture  of  the 
dilated  venous  anastomoses.  This  generally  occurs  into  '  the  gastro- 
intestinal tract,  but  in  very  rare  instances,  of  which  examples  will  be 
given,  haemorrhage  may  take  place  into  the  abdominal  wall  or  into  the 
peritoneal  cavity.  Haematemesis  not  very  infrequently  results  from 
rupture  of  an  ulcerated  varicose  vein  in  the  oesophagus,  while  slight 
bleeding  from  piles  may  go  on  for  a  considerable  time. 

The  occurrence  of  a  ha^matoma  in  the  anterior  alidominal  wall  close 

*  Sears  and  Lord:  Boston  MccUcal  and  Sur<iical  Journ.,  vol.  cxlvii,  p.  2S.5,  Sept. 
11,   1902, 

t  Archiv  f.  experiment.  Path.  u.  Pharmak.,  Bd.  xxxii,  S.  1(31. 
X  Stockton:  Journ.  American  Med.  Association,  1901,  ]•>.  817. 
§  Morison:  Lancet,  1899,  vol.  i,  ]x  1426. 
II  Jacobson,  G. :  Archiv.  Ch'neral.  de  Med.,  1893,  vol.  i,  \-,.  3,5.3. 


214  DISEASES    OF   THE    LIVER. 

to  the  round  ligament,  though  a  rare  event,  is  another  iUustration  of  a 
pathological  event  in  the  course  of  this  compensatory  mechanism,  and 
may  be  considered  as  analogous  to  hsematemesis  from  dilated  oesophageal 
veins. 

A  case  is  recorded  by  Lefas  *  of  a  hEematoma  the  size  of  a  tangarine  orange  to 
the  left  of  the  middle  line  m  a  man  aged  fifty-five  -n-ith  cirrhosis.  There  is  an  inter- 
esting specimen,  380.8,  in  the  Musemn.  of  the  College  of  Medicine,  Newcastle- 
upon-Tyne,  showing  a  large  hsematoma  m  the  abdominal  wall  close  to  the  round  lig- 
ament of  the  liver,  which  contains  a  number  of  dilated  veins.  The  patient,  a  man 
aged  forty-eight,  had  been  tapped  two  and  one-half  years  before  his  death;  after 
this,  the  ascites  did  not  return.  Six  months  before  death  he  had  phlebitis  of 
the  right  femoral  vein,  and  one  month  before  death  he  had  a  sudden  attack  of  abdom- 
inal pain  and  swelling  to  the  left  of  the  umbilicus.  Ten  days  before  death  he  had 
epileptic  fits  and  died  with  pleuris}^  and  a  pyopneumothorax.  The  liver  showed  or- 
dinary portal  cirrhosis. 

In  extremely  rare  instances  traumatism  may  lead  to  rupture  of  dilated 
veins  in  peritoneal  adhesions  and  so  to  extensive  hsemorrhage  into  the 
peritoneum. 

A  man  aged  forty-five  received  a  blow  on  the  abdomen  and  died  in  St.  George's 
Hospital  after  being  in  a  condition  of  collapse  for  eleven  hours.  At  the  postmortem 
examination  there  was  cirrhosis  of  the  liver  (78  ounces)  with  marked  engorgement 
of  the  veins  in  the  substance  of  the  liver,  so  that  the  organ  had  a  nsevoid  appear- 
ance. The  abdominal  cavity  Avas  full  of  blood.  The  spleen  was  enlarged,  and  on 
section  showed  hfemorrhage  into  its  substance,  but  there  was  no  rupture  of  its 
capsule.  There  v\'as  laceration  of  some  vascular  adhesions,  from  which  the  blood 
probably  came.  Microscopically  the  liver  showed  multilobular  cirrhosis  of  old  date 
with  hardly  any  recent  prohferation  of  the  connective  tissues.  The  cirrhosis 
appeared  to  be  latent. 

Hepatic  Artery. — The  hepatic  artery  is  usually  considerably  enlarged, 
as  it  is  thought  to  supply  the  added  fibrous  tissue  with  blood.  Chronic 
endarteritis  is  not  a  special  feature  of  ordinary  cirrhosis,  but  it  is  seen  in 
cirrhosis  due  to  hsemochromatosis  and  sometimes  in  cases  of  cirrhosis 
in  syphilitic  patients  and  in  parasj^philitic  cirrhosis. 

Condition  of  the  Spleen  in  Portal  Cirrhosis. — The  spleen  is  enlarged 

in  portal  cirrhosis,  though  not  so  markedly  as  in  hypertrophic  biliary 

cirrhosis. 

In  147  cases  of  cirrhosis  examined  at  St.  George's  Hospital  the  average  weight  of 
the  spleen  was  10  ounces.  In  Keljoiack's  series  of  84  cases  of  cirrhosis  the  average 
weight  of  the  spleen  was  12.9  oimces.  So  that  if  the  weight  of  the  normal  spleen 
be  taken  as  7  ounces,  there  is  seen  to  be  a  very  definite  increase  in  cirrhosis.  The 
weight  of  the  spleen  varied  between  the  two  extremes  of  2  ounces,  in  a  case  of  latent 
cirrhosis,  and  48  ounces,  m  a  man  who  survived  thirty  months  after  the  operation  for 
producing  artificial  peritoneal  adhesions  had  been  performed.  This  weight  is  very 
exceptional  m  portal  cirrhosis,  though  not  in  hypertrophic  biliary  cirrhosis. 

In  cases  where  there  has  been  fatal  and  very  profuse  hgematemesis 
or  very  rapid  ascites,  the  spleen  may  be  small. 

In  latent  cirrhosis  the  enlargement  and  increase  in  the  weight  of  the 

spleen  are  much  less  than  in  cases  where  death  has  been  directly  clue 

to  cirrhosis. 

In  74  cases  where  cirrhosis,  though  present,  was  not  the  cause  of  death,  the  aver- 
age weight  of  the  spleen  was  9  ounces;  while  in  73  cases  where  death  was  referred  to 
the  effects  of  cirrhosis,  the  average  weight  of  the  spleen  was  11.5  ounces. 

*  Lefas:  Bull.  Soc.  Anat.  Paris,  1902,  p.  586. 


CIREHOSIS    OF    THE    LIVER. 


215 


•  The  fact  that  the  spleen  is  bigger  and  hea^'ier  in  cases  dying  from 
the  effects  of  cirrhosis  than  in  latent  cirrhosis  may  be  explained  as  de- 
pending on  two  factors  which  come  into  play  in  progressive  cirrhosis, — 
viz.,  (i)  general  toxaemia,  and  (ii)  increased  pressure  in  the  portal  vein, — 
but  are  either  absent  or  largely  obviated  in  latent  compensated  cirrhosis. 

In  very  exceptional  cases,  of  which  I  have  :^een  two,  the  spleen  is  greatly  enlarged 
and  the  liver  shows  slight  and  very  old  fibrosis.  One  of  these  cases  was  published 
by  Dr.  R.  S.  Trevor,*  the  other  was  atj'pical  case  of  chronic  splenic  anaemia  under  the 
care  of  my  colleague,  Dr.  Ewart.  This  combination  is  not  Banti's  disease,  for  in 
that  condition  cirrhosis  supervenes  as  a  terminal  phenomenon  in  the  course  of 
chronic  splenic  anaemia.  It  appears  indeed  to  be  the  reverse  of  Banti's  disease, 
and  to  be  a  continuation  and  exaggeration  of  morbid  changes  in  the  spleen  in  cases 
of  latent  or  practically  cured  cirrhosis. 


Morbid  Appearances  of  the  Spleen. — The  capsule  of  the  spleen  is 
often  thickened  and  shows  perisplenitis.  This  may  be  local,  the  thickened 
area  being  a  lamellar 
fibroma,  a  condition 
frequently  seen  in 
splenic  enlargement 
from  any  cause,  or  it 
may  be  general,  and 
then  usually  forms 
part  of  a  general 
chronic  peritonitis. 

In  131  cases  of  cirrho- 
sis analysed  by  Yeld  t  peri- 
splenitis was  present  in  4.3, 
or  33  per  cent. ;  and  in  23, 
or  29.5  per  cent.,  of  the  78 
cases  recorded  by  Sears 
and  Lord.  J 

The  spleen  is  fre- 
quently adherent  to 
the  parietal  perito- 
neum of  the  dia- 
phragm, abdominal 
wall,  stomach,  etc. 
When  the  spleen  and 
liver  are  both  consid- 
erably enlarged,  the  left  lobe  of  the  liver  may  overlap  the  spleen. 
Though  this  is  more  likely  to  occur  in  hy]3ertrophic  biliary  cirrhosis,  it 
may  occasionally  be  seen  in  multilobular  cirrhosis. 

On  section  the  organ  is  sometimes  firmer  than  natural  and  fibrosed ; 
in  other  cases,  probably  as  the  result  of  terminal  infections,  it  is  soft 
or  even  diffluent.     Occasionally  areas  of  extravasation  of  blood  are  seen. 

*  Trevor,  R.  S. :  Trans.  Path.  Soc,  vol.  liv,  p.  302. 

t  Yeld,  R.  A. :  St.  Bartholomew's  Hosp.  Reports,  a'oI.  xxxiv,  p.  215. 

t  Sears  and  Lord:  Bo-ston  Medical  and  Surgical  Journ.,  vol.  cxlvii,  p.  285. 


Fig.  34.- 


-Photomicrograph  Showing  Fibrous  Area  in 
THE  Spleen. 


Around  it  are  dark  masses  which  stained  blue  with  ferrocy- 
anide  of  potassium  and  hydrochloric  acid.  (By  S.  G.  Penny, 
Esq.) 


216  DISEASES    OF   THE    LIVER. 

In  a  case  of  fatal  cirrhosis  which  survived  Morison's  operation,  for  producing 
artificial  peritoneal  adhesions,  for  two  and  one-half  j^ears  the  spleen  was  greatly 
enlarged,  weighing  48  ounces,  and  contained  a  large  number  of  gritty  spots.  Micro- 
scopically these  areas  showed  fibrosis  surrounding  calcareous  granules  and  particles 
which  turned  blue  on  being  treated  with  ferrocyanide  of  potassium  and' hydro- 
chloric acid.  (Vide  photomicrograph.)  There  was  also  considerable  hyperplasia  of 
the  endothelial  cells  lining  the  sinuses. 

Microscopic  Appearances. — There  is  dilatation  of  the  blood-vessels 
generally,  which  spreads  to  the  capillaries  in  the  jNIalpighian  bodies  and 
is  followed  by  secondary  atrophy  of  the  lymphoid  tissue  in  the  Mal- 
pighian  bodies.  Some  difference  of  opinion  exists  as  to  proliferation  of 
the  splenic  pulp.  Oestreich  *  described  it  in  early  cases,  but  neither 
Sieveking  f  nor  Azzurrini  J  has  confirmed  this.  Fibrosis  of  the  spleen  due 
to  increase  in  the  trabeculse  occurs  in  cases  of  some  standing. 

The  Cause  of  Splenic  Enlargement  in  Hepatic  Cirrhosis. — There  are 
two  views  as  to  the  causation  of  the  splenic  enlargement. 

(I)  The  mechanical  view :  that  it  is  due  to  backward  pressure  and 
chronic  venous  engorgement  of  the  organ  brought  about  by  the  portal 
obstruction  existing  in  the  liver.  In  favour  of  this  is  the  fact  that  the 
enlargement  may  diminish  after  profuse  gastro-intestinal  haemorrhage  or 
diarrhoea.  The  manifest  objection  to  this  theory  is  that  in  the  chronic 
venous  engorgement  of  heart  disease  the  spleen,  though  firmer  than 
natural,  is  not  increased  in  weight.  This  is  w^ell  brought  out  in  a  com- 
parison drawn  up  by  Kelynack  ?  between  the  weights  of  the  spleen  (i) 
in  84  cases  of  cirrhosis  and  (ii)  in  56  cases  of  nutmeg  liver,  in  cases  of 
heart  disease  uncomplicated  by  any  febrile  or  other  conditions  likely 
to  affect  the  size  of  the  organ. 

Average  Weight. 


Males.         Females.     Both  Sexes. 

"  Hepatic  "  spleen 14.25  11.62  12.9.3 

"  Cardiac  "  spleen 7.32  7.32  7.32 

Some  explanation  of  this  difference  might  be  found  in  the  fact  that 
the  liver  would  act  as  a  kind  of  buffer  when  the  backward  pressure  is  due 
to  heart  or  lung  disease,  and  so  protect  the  spleen  from  excessive  venous 
engorgement,  whereas  in  cirrhosis  the  spleen  is  nearer  to  the  venous 
obstruction.  In  support  of  this  argument  of  Foxwell's  ||  it  may  be 
added  that  in  thrombosis  of  the  splenic  vein  the  spleen  is  very  markedly 
enlarged.  But,  on  the  other  hand,  the  splenic  enlargement  is  much  more 
marked  and  may  precede  any  manifest  change  in  the  liver  in  h}^3er- 
trophic  biliary  cirrhosis,**  in  which  the  obstruction  to  the  passage  of  blood 
through  the  liver  is,  as  shown  by  the  slighter  fibrosis,  much  less  than  in 
portal  cirrhosis.  It  appears,  therefore,  that  backward  pressure  does  not, 
at  any  rate  completely,  explain  the  splenic  enlargement. 

(II)  The  toxsemic  theory:   that  the  spleen  is  enlarged  as  a  result  of 

*  Oestreich :  Virchow's  Archiv,  Bd.  cxlii,  S.  285. 

t  Sieveking:  Centralblatt  f.  allg.  Path.  u.  path.  Anat.,  June.  1894,  S.  1017. 
X  Azzurrini:  Lo  Speriment.,  An.  56,  Fascic.  v-vi,  p.  597,  1903. 
§  Kelynack,  T.  N. :  Birmingham  Med.  Rev.,  Feb.,  1897. 
11  Foxwell,  .V. :  The  Enlarged  Cirrhotic  Liver,  p.  6,  1896. 
**Comparf  F.  P.  Weber:  I'xlinburgh  Med.  Journ.,  Dec,  1897,  vol.  ii,  p.  579. 


CIRRHOSIS    OF    THE    LIVER.  217 

poisons  circulating  in  the  blood  and  reaching  it  through  the  splenic  artery, 
and  that  there  is  an  active  inflammatory  swelling  of  the  spleen  like  that 
seen  in  bacterial  and  some  toxic  conditions,  such  as  the  early  stages  of 
syphilis,  Landry's  paralysis,  and  perhaps  exophthalmic  goitre.  In  favour 
of  this  view  is  the  fact  that  the  spleen  is  not  enlarged  in  cases  of  latent 
cirrhosis,  where  the  disease  is  arrested  or  compensated  for.  The  toxaemia 
responsible  for  the  enlargement  might  be  either  the  same  as  that  pro- 
ducing hepatic  cirrhosis  or  it  might  be  secondary  to  hepatic  insufficiency, 
the  cirrhotic  liver  allowing  poisons,  which  should  normally  be  arrested 
by  it,  to  pass  into  the  general  circulation. 

This  question  is  a  difficult  one.  The  spleen  and  liver  react  in  different 
degrees  to  hsemic  intoxication,  the  spleen  usually  to  a  greater  extent. 
Probably  the  spleen  may  suffer  to  some  extent  at  the  same  time  as  the 
liver  in  early  cirrhosis,  if  the  poison,  reaching  the  liver,  as  it  generally 
does,  from  the  portal  system  escapes  into  the  general  circulation.  But 
when  the  liver  becomes  unable  to  stop  poisons  and  general  toxaemia 
supervenes,  the  conditions  favourable  for  splenic  enlargement  have 
become  greatl}^  increased. 

Histologically  Oestreicli  *  found  proliferation,  of  the  splenic  i)ulp  and  concluded 
that  it  was  due  to  toxin es  reacliing  the  organ  by  the  splenic  artery. 

To  sum,  up:  Splenic  enlargement  in  cirrhosis  probably  depends 
primarily  on  microbic  or  other  poisons  setting  up  h}q3er]3lasia  and  in- 
flammatory softening  of  the  substance  of  the  organ  so  that  it  readil}' 
gets  overdistended  with  blood.  Though  chronic  venous  engorgement 
alone  is  not  enough  to  explain  enlargement  of  the  spleen,  it  favours  the 
stagnation  of  poisons  and  irritating  bodies,  and,  further,  it  supplies  blood 
to  distend  the  softened  splenic  blood  sinuses.  Hence  it  ma}'  be  con- 
cluded that  the  enlargement  of  the  spleen  is  primarily  clue  to  toxic  action 
and  is  aided  by  increased  venous  pressure  in  the  portal  S3'stem. 

Relation  between  the  Size  of  the  Liver  and  that  of  the  Spleen. — 
In  hypertrophic  biliary  cirrhosis  the  liver  and  spleen  are  both  very  con- 
siderably enlarged,  and  it  might  be  surmised  that  in  portal  cirrhosis 
there  would  be  a  general  relationship  between  the  size  of  the  liver  and 
that  of  the  spleen.  Careful  examination  of  cases  and  statistics  shows 
that  this  point  is  a  complicated  one,  and  that  no  rule  can  be  formulated 
to  the  effect  that  the  size  of  the  liver  and  spleen  varies  either  directly  or 
inversely.  Thus,  in  some  cases,  especially  those  running  a  rapid  course 
and  those  showing  a  mixture  of  portal  and  biliary  cirrhosis,  the  liver  and 
spleen  are  both  enlarged.  On  the  other  hand,  in  latent  or  compensated 
cirrhosis  the  liver  is  considerably  increased  in  size,  being  bigger  than  in 
cases  fatal  from  the  effects  of  cirrhosis,  while  the  spleen  is  either  of  normal 
size  or  but  slightly  heavier  than  normal.  Again,  in  cases  fatal  from 
cirrhosis  the  liver  is  sometimes  smaller  than  natural,  while  the  spleen 
is  almost  constantly  larger  and  heavier. 

In  order  to  sec  whether  any  relationsliip  exists  l)et\vcen  tlie  weight  of  tlie  hver 
and  of  the  spleen  in  eirrliosis  the  following  ])ercentagcs  were  extracted  from  a 
number  of  cases  examined  at  St.  (icorge's  Hospital. 

*  Oestreicli:  N'ircliow's  Arcliiv,  Pxl.  cxiii,  S.  285. 


218  DISEASES    OF   THE    LIVER. 

In  43  male  cases  in  which  the  liver  weighed  over  60  ounces  (averaging  79.6 
ounces)  the  spleen  averaged  1 1  ounces ;  while  in  7  males  in  which  the  liver  weighed 
under  50  ounces  (averaging  39.4  ounces),  the  spleen  weighed  9.4  ounces. 

In  11  female  cases  in  which  the  liver  w^eighed  over  55  ounces  (averaging  73.5 
ounces),  the  spleen  weighed  7.6  ounces;  while  in  9  cases  in  which  the  liver  weighed 
less  than  45  ounces  (averaging  35.4  ounces),  the  spleen  weighed  as  much  as  9.8 
ounces. 

Therefore,  in  male  cases  of  cirrhosis,  whether  fatal  from  the  disease  or  from 
other  causes,  large  livers  were  associated  with  a  more  considerable  enlargement  of 
the  spleen  than  is  seen  when  the  livers  are  small.  But  in  a  corresponding  collection 
of  female  cases  the  spleen  was  heavier  in  the  series  of  small  livers  than  in  the  large 
liver  series. 

A  consideration  of  the  whole  subject  shows  that  the  weight  of  the 
spleen  has  no  constant  relation  to  that  of  the  liver,  and  that  it  depends 
on  other  factors,  which  may  or  may  not  be  associated  with  increased 
weight  and  size  of  the  liver. 

Morbid  Appearances  in  other  Viscera. — Some  writers  have  spoken 
of  hepatic  cirrhosis  as  a  disease  which  is  not  strictly  limited  to  the  liver, 
but  is  part  of  a  general  change,  and  in  this  respect  it  might  be  compared 
to  the  condition  of  red  granular  kidneys  which  are  a  local  manifestation 
of  a  general  vascular  change — arteriosclerosis.  Portal  cirrhosis  might 
in  the  same  way  be  considered  to  be  part  of  a  general  change  in  the  ali- 
mentary system,  for  the  spleen,  the  intestines,  and  the  pancreas  com- 
monly show  changes  in  hepatic  cirrhosis.  Some  of  the  changes  are 
secondary  to  portal  obstruction,  but  this  does  not  account  for  the  visceral 
changes,  and  some  of  them  must  be  regarded  as  concomitant  effects  of 
a  general  cause,  in  many  cases  alcoholism.  As  bearing  on  this  concep- 
tion of  cirrhosis  as  part  of  a  widespread  change  in  the  alimentary  system, 
Klippel  and  Lefas  *  have  pointed  out  that  in  some  instances  of  cirrhosis 
the  changes  may  be  more  advanced  in  the  pancreas  than  in  the  liver. 
This  secondary  relationship  of  cirrhosis  to  a  general  cause  is  also  seen  in 
hsemochromatosis,  where,  as  a  secondary  result,  cirrhosis  of  the  liver  and 
pancreatic  fibrosis  may  occur.     {Vide  Pigmented  Cirrhosis.) 

The  (Esophagus. — There  may  be  chronic  oesophagitis  with  general 
thickening  of  the  mucous  membrane,  which  in  places  shows  localized 
elevations  due  to  hj^perplasia  of  the  epithelium — small  corns.  The  longi- 
tudinal veins  running  in  the  submucosa  of  the  oesophagus  in  its  lower  3 
or  4  inches  are  often  dilated  and  varicose.  {Vide  Collateral  Circulation 
Between  the  Portal  and  General  Venous  System.)  Inflammatory 
changes  in  the  varicose  veins  lead  to  adhesions  between  the  veins  and  the 
mucous  membrane,  and  the  veins  with  adherent  mucous  membrane 
covering  them  stand  up  as  elevations  on  the  surface  of  the  oesophagus. 
Ulceration  may  then  occur  and  give  rise  to  very  profuse  hajmorrhage. 

Stomach. — Portal  obstruction  induces  chronic  venous  engorgement 
of  the  stomach  which  nearly  always  shows  signs  of  chronic  gastritis. 
Mammillation  of  the  mucous  membrane  and  pigmentation,  especially 
near  the  pylorus,  are  often  present.  There  is  occasionally  dilatation  of 
the  gastric  veins  close  to  the  cardiac  orifice,  but  a  varicose  condition  of 
the  veins  of  the  stomach  is  very  rare.     Cases  of  hsematemesis  depending 

*  Klippel  and  Lefas:  Rev.  de  MM.,  Jan.,  1903,  p.  23. 


CIRRHOSIS    OF    THE    LIVER.  219 

on  ruptured  varicose  gastric  veins  have  been  described.  {Vide  p.  212.) 
Acute  gastritis  sometimes  supervenes  on  the  chronic  gastritis  and  small 
multiple  ulcers  which  are  quite  superficial  may  then  occur.  The  asso- 
ciation of  a  single  chronic  gastric  ulcer  with  cirrhosis  of  the  liver  is,  how- 
ever, rare. 

The  Small  Intestine. — There  may  be  signs  of  chronic  enteritis,  such  as 
thickening  of  the  mucous  membrane  with  tenacious  mucus  on  its  surface. 
Mere  engorgement  is  not  of  very  much  importance  after  death,  inasmuch 
as  it  may  be  largely  due  to  stagnation  of  venous  blood,  from  a  dependent 
position  of  the  intestinal  coils.  The  mucous  membrane  may  be  pig- 
mented from  the  effects  of  chronic  catarrhal  enteritis  and  venous  engorge- 
ment. This  is  often  more  marked  in  the  duodenum  and  the  upper  part 
of  the  jejunum  than  elsewhere.  Occasionally  the  mucous  membrane  is 
cedematous.  The  subperitoneal  tissues  of  the  intestine  may  also  be 
cedematous,  either  independently  of  or  in  association  with  oedema  of  the 
mucous  membrane.  Dilated  venules  and  submucous  haemorrhages  are 
sometimes  seen. 

The  small  and  large  intestines  become  diminished  in  length  in  severe 
cases  of  portal  cirrhosis ;  instead  of  25  feet,  the  small  intestine  may  only 
measure  15  feet,  while  the  colon  may  be  shortened  in  a  corresponding 
or  even  in  a  greater  degree.  This  fact,  originally  observed  by  Bright, 
has  been  explained  as  due  to  chronic  enteritis,  to  concomitant  chronic 
peritonitis,  or  to  chronic  inflammation  of  the  radicles  of  the  portal  vein. 
It  is  important  in  that  it  diminishes  the  area  of  the  mucous  membrane 
from  which  absorption  can  take  place.  In  rare  instances  the  colon  may 
be  cedematous. 

A  little  girl  aged  ten  years  was  admitted  under  the  care  of  my  colleague,  Dr. 
Ewart,  with  a  temperature  of  104°,  history  of  diarrhoea,  and  a  swollen  abdomen; 
the  next  day  the  abdomen  was  more  distended  and  it  was  thought  that  perforation 
of  a  typhoid  ulcer  might  have  occurred.  Mr.  Allingham  opened  the  abdomen  and 
found  a  clear  ascitic  effusion  and  a  cirrhotic  liver.  The  patient  died  the  next  day. 
At  the  autopsy  the  liver  (10  oz.)  showed  extreme  portal  cirrhosis  of  a  multilobular 
type;  there  was  no  portal  thrombosis.  The  mucous  membrane  of  the  colon  was 
enormously  swollen  from  oedema,  and  showed  a  little  follicular  ulceration.  There 
was  no  hsemorrhage  into  the  mucosa.  There  was  no  tubercle.  There  was  probably 
an  acute  infection  of  the  colon,  which  accounted  for  the  high  temperature  and  the 
acute  cedema  of  the  colon. 

The  rectum  occasionaUy  shows  dilated  veins,  but,  contrary  to  what 
might  be  expected  from  the  presence  of  a  communication  between  the 
portal  system  and  the  general  venous  system  in  the  hsemorrhoidal  veins, 
piles  are  rare  in  cirrhosis.  OccasionaUy  there  is  intense  congestion  of 
the  rectum  with  small  ulcers  which  may  give  rise  to  hemorrhage  of  con- 
siderable amount. 

The  Pancreas. — Changes  in  the  pancreas  are  extremely  frequent  in 
portal  cirrhosis. 

Steinhaus  *  found  chronic  interstitial  pancreatitis  in  11  out  of  12  cases;  Klippel 
and  Lefas  t  in  S  cases  of  portal  cirrhosis. 

*  Steinhaus:  Deutsch.  Archiv  f.  klin.  Mod.,  Bd.  Ixxiv. 
t  Khppel  and  Lefas:  Rev.  de  Mrd.,  Jan.,  1903,  p.  23. 


220  DISEASES    OF   THE    LIVER. 

The  pancreas  is  usually  enlarged  as  a  whole,  but  the  tail  is  relatively 
more  affected  than  the  body  and  head  of  the  gland.  In  his  first  series 
Lefas*  found  the  weight  increased  by  a  third.  Microscopically  there  is 
chronic  interstitial  pancreatitis,  the  fibrosis  being  either  perilobular, 
intralobular,  or  jDartly  periacinous,  but  chiefi}^  intralobular.  There  are 
scattered  areas  of  small-cell  infiltration.  The  fibrosis  resembles  that  in  the 
liver.  Occasionally  there  is  interlobular  oedema  present.  The  gland 
cells  undergo  fatty  and  pigmentary  degeneration;  but  according  to 
Steinhaus,  the  islands  of  Langerhans,  which  play  an  important  part  in 
the  production  of  the  internal  secretion  and  in  the  prevention  of  diabetes, 
remain  intact.  In  the  cirrhosis  of  hsemochromatosis,  how^ever,  which  is  an 
exception  to  this  rule,  the  islands  of  Langerhans  are  eventually  destroyed, 
and  as  a  result  there  is  diabetes  (diabete  bronze).  Klippel  and  Lefas  find 
that  there  is  no  relationship  between  the  size  and  consistency  of  the 
pancreas  and  these  changes  in  the  liver,  and  that  in  some  instances  the 
pancreas  shows  more  advanced  change  than  the  liver;  they  regard  the 
change  as  due  to  the  same  factors  as  cirrhosis,  but  independent  of,  and 
not  secondary  to,  hepatic  cirrhosis. 

In  a  case  of  latent  cirrhosis  in  a  -sA'oman  aged  seA'enty  fatal  hEPmorrhagic  pancre- 
atitis occurred.      (Pitt.j) 

Kidneys. — In  the  great  majority  of  cases  of  portal  cirrhosis  the  kidneys 
are  free  from  any  gross  old-standing  change,  but  show  hypertrophy  in 
about  50  per  cent,  of  the  cases. 

In  89  cases  of  fatal  cirrhosis  collected  by  Milian  and  Bassuet,t  the  kidneys 
were  perfectly  normal  in  19;  in  53,  or  59.5  per  cent.,  they  were  healthy  or  more  or 
less  hypertrophied.  Pitt  §  found  that  when  otherwise  healthy  the  kidneys  were 
enlarged  in  50  per  cent,  of  the  cases  of  cirrhosis. 

This  hypertrophy  of  the  renal  substance  is  a  point  of  some  interest  as 
regards  its  explanation.  In  some  instances  the  hypertrophy  may  merely 
be  due  to  overwork  from  excessive  drinking  on  tlie  part  of  the  patients. 
It  has  been  suggested  that  the  hypertrophy  is  a  compensatory  process 
with  the  object  of  removing  the  toxic  bodies  which,  owing  to  hepatic 
inadequacy,  have  flooded  the  circulation.  (MoUard.  ||)  In  some  in- 
stances enlarged  kidneys  are  fatty  or  affected  with  cloudy  swelling. 
The  kidneys  are  arteriosclerotic  (granular)  in  about  22  per  cent,  of  cases 
dying  with  cirrhotic  livers.  In  about  5  per  cent,  of  the  cases  there  is 
tubal  nephritis.  The  relation  of  renal  disease  to  cirrhosis  is  referred  to 
again  under  the  heading  of  associated  morbid  lesions.     {Vide  p.  223.) 

Diaphragm. — In  long-standing  cases  where  the  abdomen  has  been  for 
a  considerable  time  distended,  the  diaphragm  may  show  marked  mus- 
cular hypertrophy  from  overwork.  It  is,  however,  very  seldom  ob- 
served. 

*  Lefas:  Archiv.  General,  de  Med.,  Mav,  1900,  p.  539. 

t  Pitt:  Trans.  Clinic.  Soc,  vol.  xxxii,  p.  SO. 

X  Milian  and  Bassuet:  Bull.  Soc.  Anat.  Paris,  1903,  ]).  337. 

§  Pitt:  Trans.  Path.  Soc,  vol.  xl,  p.  349. 

II  Mollard:  Lvon  Medical,  t.  xcix,  p.  665,  1902. 


CIRRHOSIS    OF    THE    LIVER.  221 

There  was  great  hypertrophy  of  the  diaphragm  m  a  patient  avIio  survived  the 
Morison-Tahiia  operation,  performed  by  my  colleague,  Mr.  G.  R.  Turner  for  two  and 
three-quarter  years. 

ASSOCIATED  LESIONS. 

Tuberculosis. — Tuberculosis  is  met  with  in  the  bodies  of  patients 
with  cirrhosis  more  often  than  in  other  non-tuberculous  diseases. 

Thus  in  706  fatal  cases  of  cirrhosis  obtained  b}^  coml:)ining  the  statistics  given 
by  Lancereaux,*  Pitt,t  St.  George's,  Keljaiack,!  and  Yeld,§  209,  or  28  per  cent., 
presented  some  evidence  of  tubercle.  Taking  the  general  incidence  of  tuberculosis 
in  routine  postmortem  work  as  27.5  per  cent.  (Osier  ||),  and  deducting  the  large  num- 
ber of  cases  dying  directly  from  tuberculosis — about  14  per  cent. — it  is  evident  that 
tubercle  is  more  frequent  in  cirrhosis  that  in  ordinary  non-tuberculous  diseases. 

The  reason  why  tuberculosis  more  commonly  supervenes  in  cirrhosis 
than  in  other  non-tuberculous  diseases  is  probably  that  the  same  con- 
ditions favour  the  production  of  cirrhosis  and  tuberculosis.  Alcohol  and 
other  poisons  which  induce  cirrhosis  diminish  the  resistance  of  the  body 
and  so  dispose  to  the  invasion  of  tubercle.  Although  a  tuberculous 
cirrhosis  {vide  p.  191)  has  been  described  (Hanot  and  Gilbert  **),  there  is 
no  reason  to  think  that  ordinary  cirrhosis  is  ever  due  to  tuberculosis  or 
to  tuberculous  peritonitis,  and  when  tuberculosis  and  cirrhosis  are  asso- 
ciated, the  cirrhosis  is,  as  a  rule,  the  older  condition. 

Age  plays  some  part  in  influencing  the  incidence  of  tuberculosis  in 
patients  with  cirrhosis.  Thus  while  it  is  rare  in  the  somewhat  infrequent 
cases  of  hepatic  cirrhosis  in  childhood,  Pitt's  statistics  show  that  alco- 
holic cirrhosis  in  patients  under  forty  is  accompanied  by  tuberculosis  in 
two-thirds  of  the  cases.  The  lungs  and  the  peritoneum  are  the  most 
frequent  sites  of  tuberculosis  in  the  subjects  of  cirrhosis.  The  tubercle 
may  be  old,  acute,  chronic  or  recrudescent,  and  not  infrequently  escapes 
detection  during  life. 

Pulmonary  Tuberculosis. — In  patients  with  cirrhosis  pulmonary  tuber- 
culosis is  the  direct  cause  of  death  in  from  12  (Kelynack)  to  14.5  per 
cent.  (Rolleston  and  Fenton),  thus  agreeing  with  the  general  death 
incidence  from  tuberculosis.  In  cases  of  cirrhosis,  whether  fatal  from 
the  disease  itself  or  from  other  diseases  (excluding  tuberculosis),  the 
lungs  are  the  most  frequent  site  of  tuberculous  lesions,  and  are  more 
frequently  affected  than  in  persons  dying  from  other  diseases. 

In  .584  cases  of  cirrhosis  obtained  by  adding  together  the  figures  in  tlie  statistics 
of  Lancereaux,  St.  George's,  Kelynack,  and  Yeld,  tuberculous  lesions  were  found 
in  the  lungs  in  132,  or  22.6  per  cent.  On  the  basis  of  Heitler'sft  estimate  that 
tubercle  is  present  in  5  per  cent,  of  patients  dying  from  diseases  other  tlian  pul- 
monary tul)erculosis — a  low  estimate — there  is  a  marked  increase  in  the  incidence  of 
tubercle  in  the  lungs. 

Tubercle  is  more  often  found  in  the  lungs  in  patients  who  die  from 

*  Lancereaux:  Trait6  de  Maladies  du  Foie  et  du  Pancreas,  p.  302. 

t  Pitt,  G.  N. :  Trans.  Path.  Soc,  vol.  xl,  p.  350. 

X  Kelynack,  T.  N. :  Medical  Chronicle,  Jan.,  1897,  p.  262. 

§  Yeld,  R.  A.:  St.  Bart.'s  Hosp.  Reports,  vol.  xxxiv,  p.  215. 

II  Osier,  W. :  Practice  of  Medicine,  p.  270,  4th  ed. 
**  Hanot  and  Gilbert:  Archiv.  G('Mi6ral.  de  Med.,  tome  clxiv,  p.  513. 
tt  Quoted  by  Hilton  Fagge:  Practice  of  Medicine,  vol.  i,  p.  953,  1886. 


222  DISEASES   OF   THE    LIVER. 

the  effects  of  cirrhosis  than  in  patients  who  have  cirrhosis  but  die  from 
other  causes  (exchiding  tuberculosis). 

In  97  cases  of  cirrhosis  where  death  was  not  due  to  pulmonary  tuberculosis 
tubercles  were  found  in  the  lungs  in  17.  Of  these  97  cases,  47  were  fatal  from  the 
direct  effects  of  cirrhosis,  and  jDulmonary  tubercle  was  found  in  10,  or  21.2  per  cent. ; 
while  in  the  remaining  50  cases  where  cirrhosis  was  latent  and  death  was  due  to 
some  independent  cause,  pulmonary  tuberculosis  being  of  course  excluded,  tubercle 
was  present  in  7,  or  14  per  cent.* 

Tuberculous  Peritonitis. — The  peritoneum  is  next  to  the  kmgs  the 
most  frequent  situation  of  tuberculous  infection  in  cirrhosis.  In  584 
cases  of  cirrhosis  obtained  by  combining  the  statistics  of  Lancereaux, 
RoUeston  and  Fenton,  Kelynack,  and  Yeld  there  were  53  cases  of  peri- 
toneal tubercle,  or  9  per  cent.  In  a  large  number  of  cases  of  peritoneal 
tubercle  the  lungs  are  previously  infected.  Tuberculous  peritonitis  is 
rare  in  adults;  when  it  does  occur  in  males,  it  is  most  often  in  hepatic 
cirrhosis.  Probably  the  peritoneum  is  rendered  more  susceptible  to 
infection  by  the  chronic  portal  engorgement  and  possibly  by  pre-existing 
chronic  peritonitis  of  a  slight  degree.  In  121  cases  of  cirrhosis  Kelynack 
found  active  tuberculosis  of  the  peritoneum  in  12,  in  4  of  whom  the 
peritoneum  was  alone  affected,  thus  contravening  what  is  known  as 
Godalier's  law,  that  when  there  are  tubercles  on  the  peritoneum  they 
will  also  be  found  in  the  pleurae.  This  strongly  suggests  that  cirrhosis 
of  the  liver  disposes  to  the  local  invasion  of  the  peritoneum  by  tubercle. 

Chronic  Peritonitis. — A  certain  degree  of  chronic  peritonitis  is 
often  seen  in  the  bodies  of  those  who  have  died  from  cirrhosis  of  the 
hver,  but  a  high  degree  of  chronic  peritonitis  is  comparatively  rare  in 
association  with  well-marked  cirrhosis. 

In  Yeld's  131  cases  of  cirrhosis  simple  chronic  peritonitis  was  present  in  10.7 
per  cent.,  and  in  Sears  and  Lord's  t  78  cases  in  19  per  cent. 

Simple  chronic  peritonitis  may  be  associated  with  arteriosclerosis ;  in 
common  with  the  other  serous  membranes  this  low  form  of  inflammation, 
or  perivisceritis,  has  been  regarded  as  depending  on  arteriosclerosis. 
Alcoholism  and  venous  engorgement  have  both  been  regarded  as  causes 
of  chronic  peritonitis.  As  has  just  been  pointed  out,  tuberculosis  may 
supervene  in  the  peritoneum,  and  eventually  tuberculous  peritonitis  may 
result. 

Arteriosclerosis. — From  the  fact  that  cirrhosis  and  arteriosclerosis 
are  met  with  at  about  the  same  time  of  life,  it  is  natural  to  find  arterial 
degeneration  of  a  greater  or  lesser  degree  in  the  bodies  of  patients  dying 
from  cirrhosis.  There  is,  however,  no  direct  relationship  between  these 
two  conditions;  cirrhosis  is  accompanied  by  a  low-tension  pulse  and 
thus  does  not  tend  to  set  up  arterial  degeneration,  while  endarteritis  is 
not  a  cause  of  genuine  hepatic  cirrhosis.  In  some  exceptional  instances 
marked  sj^philitic  endarteritis  is  associated  with  hepatic  cirrhosis 
(probably    parasyphilitic)     in     children,    and     in     the     rare    disease 

*  Rolleston  and  Fenton:  Birmingham  Med.  Review,  Oct.,  1S96. 
t  Sears  and  Lord :  Boston  Med.  and  Surg.  Journ.,  vol.  cxlvii,  p.  285. 


CIERHOSIS    OF   THE    LIVER.  223 

liEemochromatosis,  cirrhosis  of  tlie  liver  and  endarteritis  of  the  hepatic 
artery  may  occur. 

From  the  statistical  point  of  view,  arteriosclerosis  is  the  commonest, 
and  one  of  the  least  essential,  morbid  changes  found  in  the  bodies  of 
patients  with  hepatic  cirrhosis. 

In  78  cases  of  cirrhosis  tabulated  by  Sears  and  Lord,  arteriosclerosis  was  noted 
in  49  instances ;  often,  however,  there  was  only  a  small  patch  in  the  aorta. 

Heart. — The  heart  is  frequently  flabby  and  dilated  and  the  muscular 
tissue  often  shows  cloudy  swelling  or  fatty  degeneration.  These  degen- 
erative changes  are  largely  due  to  concomitant  alcoholism. 

In  114  cases  of  cirrhosis,  obtained  by  uniting  Cheadle's,*  and  Sears  and  Lord's 
statistics,  there  was  fatty  degeneration  in  33,  or  28.9  per  cent.,  and  myocarditis  in  3. 

In  rare  instances  infective  endocarditis  may  occur  as  a  complica- 
tion. Chronic  A^alvulitis  is  common  just  in  the  same  way  that  arterio- 
sclerosis is  frequently  associated  with  cirrhosis. 

Renal  Disease. — The  kidneys  in  fatal  cases  of  cirrhosis  are,  generally 
speaking,  free  from  any  marked  structural  change;  they  often  show 
enlargement  from  overwork  (drinking),  chronic  venous  engorgement 
from  cardiac  failure,  or  some  degree  of  tubal  changes,  such  as  fatty  de- 
generation or  cloudy  swelling,  from  toxaemia  or  alcohol.  When  definite 
structural  change  is  present,  it  is  usual  to  find  that  the  kidney  is  granular 
from  the  effects  of  arteriosclerosis;  definite  lardaceous  disease  or  tubal 
nephritis  is  quite  rare.  The  association  of  granular  kidney  with  hepatic 
cirrhosis  is  intelligibly  explained  by  the  fact  that  the  two  diseases  are 
common  at  the  same  time  of  life,  and  are  therefore  met  with  together 
in  a  certain  number  of  cases.  As  Dickinsonf  expressed  it,  though  both 
the  liver  and  kidney  are  very  liable  to  fibrosis,  this  change  in  the  two 
organs  respectively  is  due  to  different  morbid  agencies. 

In  a  careful  analysis  of  78  fatal  cases  of  cirrhosis.  Sears  and  Lord  J  found  chronic 
nephritis  (interstitial  or  tubular)  in  23,  or  29.4  per  cent.,  fatty  change  in  15,  and  lar- 
daceous change  in  2. 

In  440  cases  of  cirrhosis  of  the  liver  obtained  by  adding  together  figures  obtained 
from  statistics  of  Pitt, §  Kelynack,  ||  Yeld,**  Cheadle,tt  and  myself  |t  there  Avere  110 
with  distinct  fibrosis  of  the  kidneys,  or  25  per  cent.  In  some  of  the  cases  the  renal 
change  was  not  very  marked,  and  as  the  average  age  for  death  in  cirrhosis  is  over 
forty-five  years,  it  is  probable  that  in  some  instances  the  change  in  the  kidney  was 
senile. 

The  incidence  of  marked  arteriosclerotic  change  in  the  kidneys  is 
lower.  Hawkins  §§  and  Dickinson  both  put  it  at  about  15  per  cent.  As 
would  be  naturally  expected  from  the  greater  frequency  of  both  hei'ialic 

*  Cheadle,  W.  B. :  Some  Cirrhoses  of  the  Liver,  p.  47. 

t  Dickinson,  W.  H. :  Med.-Chirurg.  Trans.,  vol.  hi. 

X  Sears  and  Lord:  Boston  Medical  and  Surgical  Journ.,  \()\.  cxlvii,  ]>.  285. 

§  Pitt,  G.  N. :  Trans.  Path.  Soc,  vol.  xl,  p.  348. 

II  Kelynack,  T.  N. :  Birmingham  Mod.  Review,  Feb.,  1897. 
**  Yeld,  R.  A. :  St.  Bartholomew's  Hospital  Reports,  vol.  xxxiv,  p.  215. 
tt  Cheadle,  W.  B. :  Some  Cirrlioses  of  tlie  Liver,  p.  51. 
tj  Rolleston  and  Fenton :  Birmingham  Med.  Review,  Oct.,  1890. 
§§  Hawkins,  H.  P. :  AUbutt's  System,  vol.  iv,  p.  180. 


224  DISEASES    OF    THE    LIVER. 

cirrhosis  and  arteriosclerosis  in  men,  the  two  conditions  are  more  often 
seen  associated  in  the  male  than  in  the  female  sex. 

The  question  whether  a  granular  kidney  is  more  often  associated  with 
a  large  or  with  a  small  cirrhotic  liver  has  been  referred  to  already  (p.  199). 
Pitt's  and  my  own  observations  point  to  a  small  cirrhotic  liver  as  more 
frequently  associated  with  a  granular  kidney;  Price's  statistics  were  to 
the  opposite  effect. 

Cirrhosis  Complicated  with  Carcinoma,  etc. — The  form  of  primary 
carcinoma  of  the  liver  described  by  Hanot  and  Gilbert  as  cancer  with 
cirrhosis  is  essentially  cirrhosis  first  with  a  secondary  hyperplasia  of  the 
liver  cells.  At  first  this  hyperplasia  is  compensatory  and  gives  rise  to 
cirrhosis  with  adenoma;  subsequently  the  cellular  proliferation  becomes 
so  riotous  as  to  be  malignant  and  constitutes  carcinoma.  It  is  very  hard 
to  draw  the  line  between  the  different  stages  of  cirrhosis,  cirrhosis  with 
adenoma,  and  carcinoma  with  cirrhosis.  The  latter  condition  is  un- 
doubtedly rare,  like  other  forms  of  primary  carcinoma  of  the  liver,  but 
Hanot  and  Gilbert  *  considered  that  one-third  of  the  cases  of  primary 
carcinoma  of  the  liver  were  of  this  nature.  A  full  description  of  primary 
carcinoma  with  cirrhosis  will  be  found  on  page  473. 

Secondary  Carcinoma  in  a  Cirrhotic  Liver. — Cirrhosis  of  the  liver  and 
carcinoma  elsewhere  in  the  body  are  both  so  common  that  at  first  sight 
it  would  appear  probable  that  the  occurrence  of  a  secondary  growth  in 
a  previously  cirrhotic  liver  would  not  be  rare.  It  must,  however,  be 
extremely  rare;  Hanot  and  Gilbert  f  refer  to  its  hypothetical  existence, 
but  say  no  more  about  the  subject.  I  have  never  seen  a  case.  Hale 
White  I  refers  to  a  case  of  sarcoma  of  bone  with  a  secondary  growth  in 
a  cirrhotic  liver.  Poulain  §  and  Achard  and  Laubray  ||  have  described 
cases  secondary  to  carcinoma  of  the  colon  and  stomach. 

Other  Accidental  Lesions  in  the  Liver. — In  a  few  cases  a  hydatid  cyst 
has  been  found  embedded  in  a  cirrhotic  liver.  {Vide  Hydatid  Disease, 
p.  395.)  Gummata  and  universal  cirrhosis  are  seldom  combined.  In 
86  cases  of  hepatic  gummata  collected  by  J.  L.  Allen  there  was  cirrhosis 
in  4,  or  4.6  per  cent.  {Vide  p.  356.)  Tubercles  are  sometimes  seen  im- 
planted in  a  cirrhotic  liver.  It  is  rare  to  find  cirrhosis  and  lardaceous 
disease  combined.  A  tight-laced  liver  may  become  cirrhotic.  This  con- 
dition is  figured  on  page  10. 

CLINICAL  COURSE. 

The  course  of  ordinary  cirrhosis  may  be  divided  into:  (1)  The  early 
or  pre-ascitic  stage,  which  is  often  divided  into  two  by  early  hsematemesis. 
(2)  The  late  or  ascitic  stage. 

Cases  may  die  from  intercurrent  diseases  during  the  course  of  cir- 

*  Hanot  and  Gill:)ert :  Etudes  sur  les  Maladies  du  foie,  p.  13. 
t  Hanot  and  Gilbert :  Etudes  sur  les  Maladies  du  foie,  p.  13. 
%  Hale  Wliite :  Allbutt's  System,  vol.  iv,  p.  208. 
§  Poulain:  Bull.  Soe.  Anat.  Paris,  Dec,  1899. 

II  Achard  and  Laubrav:  Mem.  et  Bull.  Soc.  Med  des  Hop.  Paris,  April  25, 
1902,  p.  335. 


CIRRHOSIS    OF    THE    LIVER.  225 

rhosis  or  ma}'  be  cut  off  by  a  very  profuse  gastro-intestinal  haemorrhage 
long  before  ascites  has  developed.  Again,  complications,  such  as  tuber- 
culosis, cardiac  failure,  peripheral  neuritis,  or  other  manifestations  of 
alcoholism,  may  supervene  and  prove  fatal  or  mask  the  symptoms  of 
cirrhosis. 

The  early  stage  begins  gradual^  and  vaguely;  though  in  some 
cases  it  may  be  dated  back  to  some  acute  illness  or  to  a  passing  attack 
of  gastro-enteritis.  The  symptoms  are  mainly  those  of  dyspepsia,  often 
of  an  alcoholic  nature,  with  loss  of  appetite,  occasional  nausea  and  vomit- 
ing, especially  in  the  morning,  flatulence,  abdominal  pain  or  unrest, 
and  looseness  or  irregularity  of  the  bowels.  Sometimes  symptoms  are 
absent;  at  other  times  they  are  those  of  chronic  alcoholism.  Bodily 
strength,  vigour,  and  energy  may  be  seriously  impaired,  and  the  con- 
dition resembles  neurasthenia;  or,  on  the  other  hand,  there  may  be 
little  or  no  complaint  of  altered  health. 

There  may  be  some  heaviness  or  tenderness  in  the  epigastrium  and 
hypochondrium,  especially  after  meals,  which  is  partly  due  to  dyspepsia 
and  perhaps  partly  to  hepatic  enlargement.  The  liver  is  generally 
somewhat  enlarged  and  may  be  slightly  tender.  The  enlargement  may 
vary  considerably  within  short  intervals,  and  is  chiefly  due  to  vascular 
engorgement.  The  spleen  is  usually  not  felt  to  be  enlarged,  but  it  may 
be  palpably  enlarged,  especially  shortly  before  hsematemesis  supervenes. 

Epistaxis  may  occur  now  and  then,  but  the  most  important  event 
in  the  early  stage  is  the  occurrence  of  hsematemesis.  This  may  come  on 
after  some  premonitory  discomfort  and  fever,  or  may  occur  with  little 
or  no  warning,  except  perhaps  slight  faintness  immediately  before  a 
large  quantity  of  blood  is  brought  up.  It  is  only  very  occasionally  fatal 
and  is  very  seldom  repeated  within  a  short  interval.  After  it  the  patient 
is  blanched  and  anaemic  for  a  time,  but  soon  recovers. 

Usually  some  months  or  even  years  elapse  after  hsematemesis  before 
ascites  develops,  especially  if  the  patient  has  taken  warning  and  altered 
his  manner  of  life.  The  disease  may  then  become  latent  from  the  devel- 
opment of  compensatory  processes.  But  in  cases  of  acute  cirrhosis, 
where  there  is  fever,  the  effects  of  hsematemesis  are  hardty  recovered 
from  before  the  abdomen  shows  signs  of  ascites. 

The  Late  or  Ascitic  Stage. — The  development  of  ascites  may  come 
on  somewhat  suddenly;  when  it  occurs  quite  suddenly  and  with  great 
rapidity  it  may  be  due  to  another  factor,  viz.,  thrombosis  of  the  portal 
vein.  The  development  of  ascites  may  be  preceded  by  gaseous  disten- 
sion of  the  intestines,  which  for  a  time  may  mask  the  presence  of  ascites. 
(Edema  of  the  feet  may  also  precede  instead  of  following  the  appearance 
of  ascites. 

When  ascites  occurs,  the  patient  has  undergone  a  considerable  amount 
of  wasting,  shows  marked  muscular  debility,  and  is  unfit  to  be  out  of  bed. 
The  wasting  of  the  temporal  and  facial  muscles  gives  a  characteristic 
appearance  to  the  patient.  The  atrophy  of  the  thoracic  muscles  shows 
up  the  bony  skeleton  of  the  chost,  Avhich  api^oars  as  a  prominent  object, 
like  a  bird's  thorax,  and  conti-asts  with  \]\v  swollen  abdomen.  The  skin 
15 


226  DISEASES    OF   THE    LIVER. 

becomes  dry,  harsh,  and  loses  its  elasticity,  and  may  show  petechise, 
while  there  may  be  haemorrhages  from  the  various  mucous  membranes  and 
oozing  from  the  gums.  The  ascites  may  require  tapping  once,  twice, 
or  even  oftener,  but  in  cases  of  cirrhosis  uncomplicated  by  chronic  peri- 
tonitis paracentesis  is  seldom  required  more  than  once.  The  patient 
emaciates  rapidly,  loses  strength,  becomes  stupid,  drowsy,  or  even  deliri- 
ous, and  dies,  sinking  down  in  the  bed  without  any  great  reaccumulation 
of  fluid  in  the  peritoneal  cavity.  A  patient  often  goes  down-hill  very 
rapidly  after  paracentesis,  not  because  of  the  tapping,  but  from  the  ad- 
vanced stage  of  the  disease.  Sometimes,  in  fact,  ascites  disappears, 
while  the  patient  becomes  more  drow^sy  and  urseixiic,  and  passes  into 
what  may  be  spoken  of  as  a  post-ascitic  stage.  The  patient  may  then 
linger  on  in  a  semicomatose  condition  for  some  weeks,  and  die  from  an 
acute  and  terminal  infection  or  gradually  from  mere  weakness. 

LATENCY. 

Cirrhosis  of  the  liver  is  not  uncommonly  latent  and  gives  rise  to  no 
symptoms.  It  may  be  found  in  the  bodies  of  persons  who  have  died  as 
the  result  of  accidents  or  from  other  diseases.  It  would  be  incorrect  to 
say  that  when  a  patient  dies  from  some  other  disease  the  cirrhosis  has 
necessarily  been  entirely  latent,  since  patients  wdth  cirrhosis  rapidly 
die  with  pulmonary  tuberculosis  and  are  very  bad  subjects  for  pneu- 
monia, erysipelas,  and  other  acute  infections.  The  fact,  however,  that 
out  of  166  consecutive  postmortem  examinations  at  St.  George's  Hospital 
in  which  the  liver  was  cirrhotic  86,  or  just  over  half,  died  from  other 
diseases  and  not  directly  from  cirrhosis,  shows  how  frequently  cirrhosis 
remains  latent.  It  thus  differs  from  universal  chronic  perihepatitis, 
which  is  practically  always  accompanied  by  ascites.  The  latency  of 
portal  cirrhosis  depends  on  the  compensator}^  processes,  i.  e.,  the  col- 
lateral circulation  between  the  branches  of  the  portal  and  general 
systemic  veins,  and  on  hyperplasia  of  the  liver  ceUs.  These  two  com- 
pensatory mechanisms  are  further  discussed  on  page  289  under  the 
heading  of  "Prognosis." 

When  cirrhosis  becomes  latent,  the  liver  is  enlarged  as  the  result  of 
compensatory  hyperplasia  of  the  liver  cells.  Hanot  and  Gilbert  *  have 
insisted  on  the  enlarged  liver  of  latent  cirrhosis,  and  speak  of  it  under 
the  title  of  hypertrophic  alcoholic  cirrhosis.  Cirrhosis  is  more  often 
latent  in  men  than  in  woman.  This  is  not  merely  due  to  the  fact  that 
cirrhosis  is  commoner  in  men  than  in  women,  for  the  ratio  of  women  to 
men  is  lower  among  the  cases  dying  independenth^  of  cirrhosis  than 
among  the  cases  fatal  from  the  direct  effects  of  cirrhosis. 

Thus  in  167  cases  in  which  the  hver  was  cirrhotic  at  the  autopsj^  at  St.  George's 
Hospital,  121  were  males  and  46  females,  or  a  ratio  of  5  to  2.  Of  these,  80  died  from 
the  direct  effects  of  cirrhosis,  50  being  males  and  30  females,  a  ratio  of  5  to  3;  Avhile 
of  the  87  who  died  from  other  factors  independent  of  cirrhosis,  71  were  males  and 
16  females,  a  ratio  of  4^  to  1. 

*  Hanot  et  Gilbert :  Soc.  Med.  des  Hop.,  May  23,  1890. 


CIRRHOSIS    OF   THE    LIVER.  227 


MINOR  SIGNS  AND  SYMPTOMS. 

Facial  Aspect. — The  face  may  be  bloated  and  show  acne  rosacea 
due  to  dyspepsia,  either  induced  by,  or  independent  of,  alcoholism;  the 
area  of  skin  affected  involves  the  nose  and  the  cheeks  and  roughly  corre- 
sponds with  the  common  site  of  lupus  erythematosus,  the  so-called 
"flush  area."  The  condition  of  the  skin  of  the  face  varies;  in  early  cases 
it  may  be  pale  and  clear,  but  often  it  is  sallow,  muddy,  and  dirty-looking. 
The  dirty  brown  aspect  of  the  skin  is  sometimes  so  accentuated  as  to 
suggest  that  the  cirrhosis  may  be  a  terminal  stage  of  hsemochromatosis. 
In  the  more  advanced  stages  of  the  disease  the  face  is  drawn  and  thin, 
the  eyes  deeply  set,  and  the  conjunctivae  congested  and  muddy,  or  slightly 
icteric.  The  wasting  of  the  temporal  muscles  is  often  very  manifest. 
The  skin  of  the  face  often  shows  clusters  of  dilated  vessels  or  stigmata; 
these  may  be  capillary  or  in  some  instances  arterial,  as  shown  by  pul- 
sation and  by  the  character  of  their  bleeding.  Haemorrhage  from  these 
stigmata  or  "spider  angiomata"  may  occur  on  slight  provocation.  It 
is  an  interesting  question  why  these  stigmata  should  develop  in  cirrhosis ; 
they  cannot  be  clue  to  increased  tension  in  the  portal  system.  It  has 
been  thought  that  they  depend  on  alcoholism;  Bouchard*  has  suggested 
that,  owing  to  altered  internal  secretion  on  the  part  of  the  liver,  the 
arteries  all  over  the  body  undergo  a  special  change  resulting  in  local  dila- 
tations or  naevi.  The  lips  are  usually  dry  and  apt  to  be  fissured;  the 
tongue  flabby,  furred,  or  dry,  and  sometimes  tremulous.  The  gums 
show  a  tendency  to  become  spongy  and,  when  hepatic  insufficiency  has 
become  established,  to  bleed.  The  throat  is  apt  to  be  chronically 
congested  and  pharyngitis  and  laryngitis  with  their  attendant  symp- 
toms are  frequently  seen. 

The  skin  of  the  body  is  often  dry  and  harsh  with  loss  of  elasticity. 
Local  haemorrhages  may  occur  as  the  result  of  slight  or  unnoticed  trau- 
matism. When  cirrhosis  is  advancing,  small  naevi  may  crop  up  all  over 
the  surface  of  the  body,  and  in  exceptional  instances  may  unite  to  form 
angiomatous  areas  of  considerable  extent.  Bouchard  t  records  a  case 
where  they  made  their  appearance  when  the  disease  was  advancing  and 
receded  when  improvement  took  place.  According  to  Gilbert  and 
Herscher,!  naevi  composed  of  capillaries  are  commoner  on  the  trunk, 
while  arterial  naevi  are  more  prone  to  occur  on  the  hands  and  face.  A 
zone  of  dilated  capillaries  on  the  chest  about  the  attachment  of  the  dia- 
phragm has  no  real  significance,  since  it  is  seen  in  many  men  of  middle 
age,  especially  those  with  emphysema,  who  have  nothing  wrong  with 
their  livers.  §  Dilatation  of  the  subcutaneous  veins  around  the  umbilicus 
(cirsomphalos)  points  to  portal  obstruction;  when  well  marked,  this 
is  spoken  of  as  a  "caput  medusae."     The  collateral  circulation  around 

*  Bouchard:  Rev.  de  MM.,  Oct.,  1902,  p.  837. 

t  Bouchard:  Rev.  de  M6d.,  Oct.,  1902,  p.  837. 

X  Ciilbert  and  Herscher:  Soc.  de  biolog.,  Jan.  31,  1903. 

§  For  further  information  about  this  "  costal  frinp;e"  tlie  reader  is  referred  to 
Solis-Cohen's  (Amer.  Jour.  Med.  Sc,  vol.  cviii,  p.  135,  1894)  and  F.  P  Weber's 
(Edinb.  Med.  Journ.,  April,  1904,  p.  346)  papers. 


228  DISEASES    OF   THE    LIVER. 

the  umbilicus,  due  to  portal  obstruction,  must  be  distinguished  from 
dilatation  and  varicosity  of  the  superior  and  inferior  epigastric  veins  in 
obstruction  of  the  inferior  vena  cava.  This  latter  anastomosis  is  often 
developed  in  a  minor  degree  as  the  result  of  ascites  pressing  on  the 
inferior  vena  cava. 

Jaundice. — Jaundice  is  not  a  prominent  feature  in  portal  cirrhosis, 
but  it  is  met  with  at  some  time  in  the  course  of  the  disease,  as  shown  by 
statistics,  in  more  than  one-third  of  the  cases. 

Thus,  in  293  cases,  obtained  by  combining  the  statistics  of  Fagge,*  Yeld,t  and 
Sears  and  Lord,J  jaundice  was  recorded  m  107,  or  36.5  per  cent. 

The  jaundice  is  usually  slight  and  often  transient.  It  may  be  merely 
an  incident  in  the  course  of  the  disease,  and  have  passed  away  before  the 
patient  comes  under  observation  with  indubitable  cirrhosis.  It  not 
uncommonly  happens  that  there  is  slight  jaundice  with  staining  of  the 
skin  and  blood  serum,  but  no  bile  pigment  in  the  urine.  To  this  condi- 
tion of  subicterus,  in  which  the  blood  serum  contains  bile  pigment,  the 
name  "acholuria  jaundice"  has  been  given.     (Gilbert  and  Herscher.§) 

Definite,  well-marked  jaundice  may  be  catarrhal  and  due  to  gastro- 
duodenal  inflammation — an  exceedingly  common  event  in  alcoholic 
subjects.  It  is  not  infrequent  in  cases  of  acute  cirrhosis,  and  is  then 
probably  due  to  inflammation  of  the  small  intra-hepatic  bile-ducts.  In 
rare  instances  it  is  dependent  on  a  gall-stone  in  the  common  duct,  or 
terminal  and  the  result  of  acute  and  widespread  degenerative  changes 
in  the  liver  cells  (icterus  gravis). 

Clubbing  of  the  Fingers. — This  condition,  spoken  of  as  ''hippocratic 
fingers,"  which  is  sometimes  seen  in  long-stancUng  cases  of  hypertrophic 
bihary  cirrhosis,  is  so  rare  in  portal  cirrhosis  that  it  may  practically  be 
regarded  as  a  curiosity. 

Bouchard  ||  described  it  in  a  case  in  1890.  I  have  watched  it  develop  in  a  patient 
in  whom,  two  and  one-half  years  before,  Morison's  operation  for  the  relief  of  ascites 
had  been  successfully  performed.  There  was  no  other  obvious  cause,  such  as  pulmo- 
nary or  heart  disease.  In  74  cases  of  Marie's  hypertrophic  osteo-arthropathy  col- 
lected by  Symes-Thompson  **  there  was  no  case  of  portal  cirrhosis. 

Debility. — Marked  weakness  and  languor  out  of  proportion  to  the 
physical  signs  are  not  uncommon ;  this  may  be  one  of  the  first  symptoms 
and  may  call  for  treatment  before  there  are  sufhcient  data  for  diagnosing 
cirrhosis,  and  long  before  ascites  has  developed.  Muscular  weakness, 
and  asthenia  are  usually  constant  late  in  the  course  of  the  disease  and 
are  only  natural  when  the  poor  state  of  general  nutrition  is  taken  into- 
account.  The  explanation  of  the  debility  is  partly  this  and  partly  a 
toxgemic  state  of  the  blood  due  to  hepatic  inadequacy. 

*  C.  Hilton  Fagge  and  Pye-Smith  :  Practice  of  Medicine,  vol.  ii,  p.  270,  1886. 
t  Yeld:  St.  Bartholomew's  Hosp.  Reports,  vol.  xxxiv,  p.  215. 
J  Sears  and  Lord:  Boston  Medical  and  Surgical  Journ.,  vol.  cxlvii,  p.  285. 
§  Gilbert  and  Herscher:  La  Presse  Medicale,  July  29,  1903,  p.  541. 
II  Bouchard  :  Quoted  by  Klippel  and  Vigouroux,  La  Presse  M(?dicale,  ^larch  21, 
1903. 

**  Symes-Thompson,  H.  E. :  Medico-Chirurg.  Trans.,  vol.  Ixxxvn 


CIRRHOSIS    OF   THE    LIVER.  229 

Wasting. — In  patients  with  advanced  cirrhosis  there  is  usually  very 
considerable  wasting;  the  muscles  of  the  trunk,  extremities,  and  face 
become  flabby  and  atrophy.  The  ribs  often  show  up  prominently  and 
the  wasted  thorax  contrasts  with  the  abdomen  distended  from  ascites. 
The  limbs  become  like  spindles.  The  face  gets  sharpened,  the  fat  disap- 
pears from  the  buccal  pads,  and  the  temporal  fossae  fall  in,  so  that  the 
face  often  has  the  aspect  of  a  case  of  advanced  pulmonary  tuberculosis 
or  of  malignant  disease.  In  latent  cirrhosis,  however,  bodily  nutrition 
may  be  very  good,  and  there  may  be  a  thick  layer  of  fat  over  the  body. 

I  have  several  times  seen  somewhat  fat  patients  with  latent  hepatic  cirrhosis  die 
from  rapid  or  generalized  tuberculosis.  In  such  cases  the  existence  of  cirrhosis  is 
very  hkely  to  be  overlooked.  The  large  size  of  the  liver  is,  however,  a  fairly  constant 
feature  of  such  cases. 

Offensive  Breath. — In  some,  but  certainly  not  in  all,  patients  with 
cirrhosis  the  breath  is  very  offensive  without  any  local  cause,  such  as 
decayed  teeth,  chronic  follicular  tonsillitis,  or  ozsena.  The  odour  is  often 
peculiar  and  is  described  as  cadaveric  or  earthy.  It  resembles  the  smell 
of  dried  and  decomposing  blood  and  is  sometimes  associated  with  oozing 
from  the  gums  or  epistaxis.  It  is  probably  due  to  failure  of  the  anti- 
toxic function  of  the  liver  and  to  the  passage  into  the  general  circulation 
of  poisons  manufactured  in  the  alimentary  canal.  In  other  words  it 
depends  on  hepatic  inadequacy,  and  is  therefore  of  bad  omen. 

Experimentally  Roger  and  Garnier  *  find  that  in  healthy  rabbits  a  hypodermic 
injection  of  sulphuretted  hydrogen  is  followed  by  excretion  of  the  gas  by  the  lungs, 
but  that  about  double  the  quantity  has  to  be  injected  into  the  rectum  before  it  jDasses 
through  the  lungs.  Wlien  the  functional  activity  of  the  rabbit's  liver  has  been  re- 
duced by  the  subcutaneous  injection  of  phosphorated  oil,  a  much  smaller  rectal  injec- 
tion of  sulphuretted  hydrogen  was  followed  by  the  excretion  of  the  gas  by  the  lungs. 

Saliva. — The  amylolytic  power  of  the  saliva  is  not  necessarily  re- 
duced; it  may  even  be  increased.  (Robertson. f)  If  there  is  ascites  or 
diarrhoea,  the  amount  of  saliva  will  tend  to  be  diminished. 

V.  Leube  %  mentions  a  case  of  excessive  salivation  where  as  much  as  3  litres  was 
secreted  in  one  twenty-four  hours,  and  as  a  result  ascites,  which  was  present,  disap- 
peared.    Cirrhosis  of  the  liver  was  found  after  death. 

Dyspepsia. — Dyspepsia  is  almost  constant  in  cases  of  portal  cir- 
rhosis, and  usually  precedes,  often  for  some  years,  the  first  striking  mani- 
festation of  the  disease,  namely,  hsematemesis.  It  may  be  irritative 
and  intermittent,  or  flatulent  and  very  persistent.  In  the  early  stages 
it  is  due  to  gastritis — often  of  alcoholic  origin — and  has  a  causal  relation- 
ship to  dyspeptic  cirrhosis,  inasmuch  as  the  chronic  gastric  catarrh 
manufactures  the  toxines  which  are  carried  to  the  liver  and  induce  cir- 
rhosis. Later,  when  portal  obstruction  and  engorgement  of  the  stomach 
and  intestines  have  come  on,  gastritis  and  indigestion  are  aggravated. 
The  portal  obstruction  disposes  to  infection  and  at  the  same  time  inter- 

*  Roger  et  Garnier:  Soc.  de  iMolog.,  1898,  p.  714. 

t  Robertson,  W.  G.  A.:  Journ.  Path,  and  Bacterid.,  vol.  A-ii,  p.  IIS. 

X  V.  Leube:  Deutsche  Archiv  f.  klin.  Med.,  Bd.  Ixvi,  1809. 


230  DISEASES    OF   THE    LIVER. 

feres  with  the  digestion  and  absorption  of  food.  Absor^Dtion  is  also  im- 
paired as  the  result  of  the  curtailed  length  of  the  intestinal  tract  (vide 
Morbid  Anatomy),  while  the  process  of  digestion  is  interfered  with  from 
a  deficiency  in  the  secretion  of  hydrochloric  acid.  There  is  loss  of  appe- 
tite for  solid  food,  especially  for  meat.  Morning  vomiting  may  be 
present  and  is  naturally  more  often  seen  in  alcoholic  subjects.  Occa- 
sionally acute  or  subacute  attacks  of  gastritis  may  supervene,  and  if  seen 
for  the  first  time  in  one  of  these  exacerbations,  the  underlying  condition 
of  cirrhosis  may  not  at  first  be  manifest. 

Diarrhoea. — Comparatively  early  in  the  disease  diarrhoea  or  excessive 
looseness  of  the  bowels  may  be  due  to  a  general  catarrhal  condition  of 
the  intestinal  tract  in  alcoholic  subjects,  and  to  diminished  and  delayed 
absorption.  In  other  cases  diarrhoea  may  alternate  vdth  the  more  usual 
state  of  constipation.  Diarrhoea  is  more  often  met  with  in  multilobular 
cirrhosis  in  chUdren. 

In  the  last  stage  of  the  disease,  when  the  patient  is  in  a  toxsemic 
state,  diarrhoea  may  set  in  and  be  very  rebellious.  It  may  continue 
until  the  patient  dies  of  exhaustion.  It  is,  however,  possible  that  the 
diarrhoea  is,  like  that  of  renal  disease,  of  use  in  getting  rid  of  toxic  sub- 
stances. 

Constipation. — A  sluggish  condition  of  the  bowels  and  constipation 
are  often  present.  Chronic  catarrh  of  a  certain  degree  may  cause  it 
instead  of  diarrhoea,  by  impairing  the  peristaltic  powers  of  the  intestine 
while  chronic  portal  engorgement  impairs  both  the  muscular  and  nervous 
activity  of  the  bowel.  In  the  later  stages  the  development  of  ascites 
tends  to  produce  constipation,  both  by  weakening  the  muscular  walls 
of  the  abdomen  and  by  withdrawing  water  from  the  bowel.  Thus  a 
patient  with  ascites  may  present  himself  chiefly  complaining  of  consti- 
pation. Moreover,  the  milk  diet  on  which  a  patient  vdth  cirrhosis  is 
placed  leaves  little  residue  for  the  faeces  and  may  thus  accentuate  this 
tendency.  Constipation  is  an  evil,  inasmuch  as  stagnation  of  food 
residues  in  the  bowel  leads  to  putrefaction  and  fermentation  and  so  to 
autointoxication. 

The  Urine. — The  urine  is  usually  diminished  in  amount  in  advanced 
stages  of  cirrhosis.  The  smaller  quantity  is  closely  associated  with,  in 
fact  mainly  depends  on,  low  arterial  tension,  which  in  turn  is  correlated 
with  increased  blood-pressure  in  the  portal  vein.  Normally  more  water 
passes  through  the  kidneys  during  digestion,  omng  to  increased  absolu- 
tion from  the  alimentary  canal;  in  cirrhosis,  absoi'ption  is  dela^^ed  on 
account  of  the  increased  A'^enous  pressure  in  the  portal  vein,  and,  as  a 
result,  the  normal  relation  between  the  amount  of  urine  excreted  during 
digestion  and  in  the  intervals  is  reversed,  more  urine  being  excreted 
during  fasting.  This  phenomena,  described  by  Gilbert  and  Lereboullet,* 
has  been  termed  "opsiuria." 

Another  abnormal  character  in  the  excretion  of  urine  in  cirrhosis,  described  by 
Chauffard  and  Castaigne,t  is  that  methylene-bhie  when  taken  by  the  mouth  is  ex- 
creted intermittently,  and  not  continuously,  as  in  health. 

*  Gilbert  et  Lereboullet:  Soc.  de  biolog.,  March  9,  1901,  p.  276. 
t  Chauffard  et  Castaigne :  Soc.  de  biolog.,  1898,  p.  359. 


CIRRHOSIS    OF   THE    LIVER.  231 

The  urine  is  strongh'  acid,  usually  of  a  high  specific  gravity,  high 
coloured,  often  reddish  orange,  and,  like  the  urine  of  cardiac  disease, 
commonly  precipitates  urates  on  standing. 

The  amount  of  urobilin  is  increased  in  cirrhosis,*  while  the  pigment 
described  as  urohsematoporphyrin,  which  is  in  reality  not  a  definite 
chemical  compound,  but  a  mixture  of  a  large  quantity  of  hsematopor- 
phyrin  with  a  small  quantity  of  urobilin,  has  been  said  to  occur  in  the 
urine  of  some  cases  of  cirrhosis  (McMunnf).  Indican  may  also  appear 
in  the  urine  without  any  evidence  of  special  intestinal  disturbance. 

Since  jaundice  is  somewhat  uncommon  in  portal  cirrhosis,  bile  pig- 
ment is  not  often  found  in  the  urine,  but  it  may  be  present  without  any 
manifest  pigmentation  of  the  skin.  I  have  seen  this  during  the  comatose 
condition  preceding  death.  The  converse  is  more  often  seen,  viz.,  slight 
icteric  colouration  of  the  skin,  due  to  small  quantities  of  bile  pigment 
in  the  blood  serum,  without  any  bile  pigment  in  the  urine,  though  the 
amount  of  urobilin  in  the  urine  is  increased.  Gilbert  and  Herscher,J 
who  call  this  condition  acholuric  jaundice,  believe  that  bilirubin  is  trans- 
formed by  the  kidneys  into  urobilin.  This  condition  was  formerly 
called  "urobilin  jaundice." 

In  cases  of  advanced  cirrhosis  a  port-wine  colouration  is,  in  rare  instances,  ob- 
tained when  hquor  ferri  perchloridi  is  added  to  the  urine,  m  the  absence  of  drugs, 
such  as  salicylates,  salol,  diuretin,  which  give  a  similar  colour  reaction;  this  is  due 
to  the  presence  of  diacetic  acid  (Gerhardt's  reaction). 

If  the  urine  is  previously  heated,  the  colouration  is  less  marked ;  this  is  due  to  the 
diacetic  acid  being  transformed  into  acetone,  which  does  not  give  this  colouration 
with  ferric  chloride,  although  it  is  commonly  spoken  of  as  the  acetone  reaction.  The 
presence  of  diacetic  acid  points  to  the  presence  in  the  blood  of  organic  acids,  such  as 
oxybutyric  acid,  or  to  an  acid  intoxication  (acidosis).  This  condition  is  one  of  great 
gravity,  inasmuch  as  it  may  pass  into  coma.  "Wlien  the  urine  gives  the  reaction  for 
diacetic  acid,  bicarbonate  of  soda  should  be  given  in  large  doses,  and  if  coma  begins  to 
appear,  transfusion  of  saline  solution  with  bicarbonate  of  soda  (2  drams  to  the  pint) 
should  be  performed.  As  is  well  known,  starvation,  especially  in  women  with 
gastric  ulcer,  may  induce  diaceturia  without  any  other  sign  of  acidosis. § 

When  the  disease  is  well  established,  the  amount  of  urea  excreted  is 
diminished,  while  that  of  uric  acid  is  increased.  The  diminution  in  the 
output  of  urea  accompanies,  but  is  not  a  direct  result  of,  destruction  of 
the  liver  cells;  it  is  correlated  with  an  increase  in  the  nitrogen  excreted 
in  the  form  of  ammonia  in  the  urine.  The  nitrogen  in  the  form  of  am- 
monia may  be  present  in  the  urine  in  the  normal  amount  (2  to  5  per  cent, 
of  the  total  nitrogen),  but  when  destructive  changes  in  the  liver  cells 
are  active,  it  may  rise  to  as  much  as  20  per  cent,  of  the  total  nitrogen. 
This  increase  in  ammonia  is  correlated  with  a  diminished  formation  of 
urea.  According  to  Herter,  ||  the  increase  in  ammonia  is  not  due  to  in- 
ability of  the  liver  cells  to  form  urea, — for,  as  shown  b}'  Weintraud,  if 
ammonia  is  given  to  such  patients  it  appears  in  the  urine  as  urea, — but 

*  Garrod  :  Lancet,  1900,  vol.  ii,  Bradshaw  lecture.  Durandeau:  These  de  Paris, 
1900,  No.  3-46. 

t  McMunn :  .Journal  of  Physiology,  vol.  x,  1SS9. 

X  Gilbert  and  Herscher:  La  Presse  M&licale,  Dec.  27,1902;  July  29, 1903,  p.  541. 

§  Vide  Rolleston  and  Tebbs,  Brit.  Med.  Jour.,  1904,  vol.  ii,  p.  114. 

II  Herter,  C.  A. :  Lectures  on  Chemical  Pathologj^,  p.  347. 


232  DISEASES    OF   THE    LIVER. 

to  the  fact  that  the  ammonia  is  seized  upon  by  organic  acids,  such  as 
lactic,  before  it  can  be  transformed  into  urea.  The  ammonia  neutral- 
izes the  organic  acid  and  so  tends  to  prevent  an  acid  intoxication.  In 
cases  where  there  is  extensive  destruction  of  the  liver  cells  leucin  and 
ty rosin  may  be  found  in  the  urine. 

The  chlorides  are  diminished  when  there  is  ascites. 

Albuminuria  is  comparatively  rare  in  cases  of  cirrhosis.  ^Vllen  it 
does  occur,  it  is  usually  due  to  some  concomitant  organic  renal  disease, 
such  as  granular  kidney,  tubal  nephritis,  or  lardaceous  change.  In  89 
cases  tabulated  by  Milian  and  Bassuet  *  albuminuria  occurred  in  three. 
Statistics  vary  with  regard  to  the  association  of  granular  kidneys  with 
a  large  or  with  a  small  liver,  and  the  point  cannot  be  considered  settled 
whether  a  small  or  a  large  cirrhotic  liver  is  most  often  associated  with 
arteriosclerotic  kidneys;  my  own  experience  is  rather  in  favour  of  the 
small  livers  being  more  often  seen  with  granular  kidneys. 

As  a  result  of  hepatic  insufficiency  a  toxsemic  state  commonly  occurs 
in  the  late  stages  of  cirrhosis.  Sometimes  this  toxaemia  so  affects  the 
renal  tubules  as  to  give  rise  to  albuminuria  and  casts  in  the  urine.  Albu- 
minuria is  sometimes  associated  with  cardiac  failure,  and  it  is  probable 
that  a  toxsemic  blood  state  combined  with  chronic  venous  engorgement 
of  the  kidney  are  the  most  favourable  conditions  for  the  production  of 
albuminuria.  In  rare  cases  albuminuria  may  be  mechanical  and  due 
to  the  pressure  of  a  considerably  enlarged  spleen  on  the  left  renal  vein 
and  possibly  on  the  left  kidney.  Falkenheim  f  in  1884,  and  in  1902 
the  writer,!  have  observed  that  intermittent  albuminuria  may  be  due 
to  this  cause  in  cases  of  cirrhosis.  In  these  cases  there  is  considerable 
albuminuria  with  high-coloured  and  lithatic  urine,  thus  resembling  that 
of  chronic  venous  engorgement,  when  the  patient  lies  on  the  left  side  or 
on  his  back;  while  when  the  patient  is  in  the  erect  position,  lies  on  the 
right  side  or  on  his  face,  the  urine  is  free  from  albumin  (Falkenheim). 

Albumose  is  very  occasionally  observed  in  the  urine  when  hepatic 
inadequacy  has  supervened  and  may  be  associated  with  albuminuria. 
(Teissier,  g) 

It  is  distinctly  rare  to  find  blood  in  the  urine;  it  may  be  due  to  con- 
comitant attacks  of  subacute  nephritis  in  an  already  damaged  kidney, 
or  it  may  be  due  to  toxaemia  and  occur  at  the  same  time  as  epistaxis  and 
oozing  from  the  gums. 

Glycosuria. — -It  is  rare  to  find  sugar  in  the  urine  in  ordinary  cirrhosis. 
Glycosuria  occurs  in  a  high  proportion  of  the  cases  of  pigmented  cirrhosis 
from  haemochromatosis  {diabete  bronze;  vide  ''Pigmented  Cirrhosis,"  p. 
300),  but  it  is  then  due  to  a  concomitant  fibrosis  of  a  very  intimate 
nature  in  the  pancreas  (involving  the  islands  of  Langerhans) — a  change 
which  is  not  present  in  ordinary  cirrhosis.     The  great  rarity  of  glycosuria 

*  Milian  and  Bassuet:     Bull.  Soc.  Anat.  Paris,  1903,  p.  3.37. 

t  Falkenheim:  Deutsch.  Archiv  f.  klin.  Medicin,  Bd.  x.xxv,  S.  446,  1S84. 

t  RoUeston:  Lancet,  1902,  vol.  i,  p.  585. 

§  Teissier:  LaSem.  Med.,  1899,  p.  282. 


CIRRHOSIS    OF   THE    LIVER.  233 

in  cirrhosis  is  certainly  curious,  since  the  Hver  is  usually  regarded  as 
stopping  sugar  reaching  it  from  the  alimentary  canal.  It  might  naturally 
be  expected  that  sugar  would  pass  through  the  cirrhotic  and  altered 
liver,  or  that  by  means  of  the  compensatory  venous  anastomoses  some 
sugar  would  a^'oid  the  liver  altogether,  and  pass  into  the  general  circu- 
lation and  so  appear  in  the  urine.  Brault's  *  histological  examinations 
of  cirrhotic  livers  show  that  the  glycogenic  function  of  the  liver  is  well 
maintained,  and  agree  with  the  clinical  fact  that  glycosuria  is  Very  rare. 
It  has  sometimes  been  observed  that  if  an  excessive  amount  of  sugar  in 
the  form  of  syrup  is  given  to  a  patient  with  cirrhosis,  alimentary  glyco- 
suria is  produced  when  it  would  not  occur  in  a  healthy  person.     (Roger.f) 

In  a  normal  person  3  ounces  (100  grams)  of  sugar  given  in  half  a  pint  of  water  or 
tea  on  an  empty  stomach  will  not  produce  alimentary  glycosuria.  To  test  for 
alimentary  glycosuria  this  quantity  of  sugar  should  be  given  before  food  and 
the  urine  should  be  obtained  after  six  hours  and  tested  for  sugar.      O''on  Noorden.  J) 

Alimentary  glycosuria  is  by  no  means  constant  in  cirrhosis,  and  even 
if  it  were  more  frequent  it  would  not  necessarily  show  that  the  liver  was 
at  fault ;  for  it  appears  from  Steinhaus'  §  work  that  it  is  to  be  correlated 
with  well-marked  changes  in  the  -pancreas.  The  majority  of  observers, 
such  as  Krause  and  Ludwig,  1|  Bloch,**  Colasanti,tt  Linoissier  andIloque,t  J 
Gorget,  §§  Strauss,  ||  ||  and  Ingelnans  and  Dehon,***  have  come  to  the  con- 
clusion that  alimentary  glycosuria  is  a  most  unreliable  sign  of  hepatic 
insufficiency.  The  glycogenic  function  may  be  retained  while  other 
functions  have  failed,  as  is  commonly  seen  in  cirrhosis;  again,  sugar 
taken  into  the  alimentary  canal  may  be  delayed  in  absorjDtion  and  undergo 
fermentation,  thus  vitiating  the  test. 

Urotoxic  Coefficient. — In  cases  where  hepatic  insufficiency  is  present 
and  due  to  destructive  changes  in  the  liver  cells,  the  toxicity  of  the  urine 
has  been  found  to  be  increased  (Sourmont,ttt  Gorget  JJJ),  as  shown  by  the 
fact  that  when  injected  into  dogs  it  appeared  to  be  decidedly  more  toxic 
than  healthy  urine  (Roger §§§). 

Symptoms  Connected  with  the  Vascular  System. — From  a  flabby, 
possibly  fatty,  condition  of  the  myocardium  the  left  ^^entricle  may  be 
dilated  and  a  systolic  apex  murmur  and  accentuated  second  sound  over 
the   pulmonary  artery,  due  to   mitral   regurgitation,  may  be  present. 

*Brault:  Archiv  de  Med.  experiment,  et  d'anat.  path.,  tomexiv,  p.  453,  1902. 
t  Roger:  Rev.  de  Med.,  1886. 
t  Von  Noorden :  XXtli  Century  Practice,  1903. 
§  Steinhaus:  Deutsch.  .A.rchiv  f.  klin.  Med.,  Bd.  Ixxiv,  S.  537. 
II  Krause  and  Ludwig:  Wien.  klin.  Wochens.,  1891. 
**  Bloch:  Zeitschrift  f.  klin.  Med.,  Bd.  xxii,  1893. 
tt  Colasanti:     Archiv.  Ital.  de  Biolog.,  t.  xvii. 

Xt  Linoissier  and  Roque:  Archiv  de  Med.  experiment,  et  d'anat.  patli.,  1S95,  p. 
228 

H  Gorget:  Rev.  de  Med.,  1897,  p,  545. 
nil  Strauss:  Berlin,  klin.  Wochens.,  May  2,  9,  1898. 
***  Ingelnans  and  Dehon:  Archiv  de  M6d.  experiment,  et  d'anat.  path.,  t.  xv 
p.  189,  1903. 

ttt  Sourmont:  Archiv  Gen^r.  de  M6d.,  1892. 
nt  Gorget :  Rev.  de  Med.,  1897,  p.  546. 
§§ij  Roger:  La  Presse  Mod.,  June  26,  1897 


234  DISEASES    OF   THE    LIVER. 

When  the  heart  is  displaced  upwards  by  ascites,  the  apex-beat  may  be 
found  in  the  fourth  or  even  in  the  third  left  intercostal  space,  and  from 
slight  kinking  of  the  pulmonary  artery  a  systolic  murmur  may  be  pro- 
duced in  that  area.  The  murmurs  at  the  apex  and  over  the  pulmonary 
artery  may  disappear  after  paracentesis  of  the  abdomen.  The  impulse 
is,  as  a  rule,  feeble.  The  second  sound  over  the  aorta  is  rather  less  dis- 
tinct than  in  health  and  is  correlated  with  the  low  arterial  blood-pressure. 
The  following  is  a  good  example  of  gradual  cardiac  failure  occurring 
in  the  course  of  cirrhosis. 

A  man  aged  fifty-six  who  died  under  vay  care  in  St.  George's  Hospital  had  gen- 
eral oedema,  sUght  jaundice,  albuminuria,  a  low-tension  pulse,  and  wandering  de- 
lirium. He  had  in  previous  years  had  jaundice  and  hsematemesis.  His  respirations 
were  very  rapid  (56) ;  he  had  signs  of  a  small  pleural  effusion  on  the  right  side  and 
haemoptysis.  The  autopsy  showed  marked  multilobular  cirrhosis,  kidneys  free  from 
old  disease,  right  pleural  effusion,  collapse  of  lower  lobe  of  right  lung,  but  no 
pulmonary  apoplexy  or  tubercle.  The  heart,  21  ounces,  was  dilated  and  hypertro- 
phied  and  showed  fatty  degeneration  in  both  ventricles.  The  valves  were  healthy. 
There  were  several  milk  spots  on  the  surface  of  the  heart  which  probably  accounted 
for  a  soft  double  murmur  heard  during  life  at  the  bottom  of  the  sternum. 

Fatty  degeneration  of  the  heart  may  account  for  sudden  death  in 
cases  of  cirrhosis. 

The  pulse-rate  is  usually  slightly  quickened;  in  the  late  stages  when 
there  is  a  general  toxsemic  condition  the  pulse  may  be  rapid  and  in  coma 
there  may  be  tachycardia.  The  tension  is  rather  low  when  the  disease 
is  active  or  producing  symptoms,  but  when  it  is  latent  or  compensated 
for  it  may  be  normal.  After  paracentesis  the  tension  of  the  pulse  is 
lowered;  according  to  Gilbert  and  his  pupils,*  this  is  a  mechanical  effect 
due  to  the  increased  portal  engorgement.  It  would,  however,  appear 
highly  probable  that  the  low  tension  is  a  toxic  effect.  The  low  tension 
pulse  is  associated  with  an  increased  rate  of  the  pulse  and  with  a  small 
output  of  urine.  Capillary  pulsation  with  perfectly  healthy  aortic  valves 
has  been  observed  (Bouchardf) ;  and  pulsation  of  the  veins  of  the 
forearm  (Hitschmann  J)  has  been  recorded. 

The  Blood. — In  early  or  latent  cases  when  the  general  health  is  well 
maintained  the  blood  is  practically  normal.  When  definite  symptoms 
appear  there  is  usually  a  secondary  ansemia  w^hich  becomes  more  marked 
as  the  disease  progresses.  From  repeated  haemorrhages  a  grave  secondary 
angemia  with  normoblasts  may  be  produced. 

In  a  case  quoted  by  Cabot  §  the  blood  count  was  as  low  as  1,300,000  red  and 
22  per  cent,  of  hsemoglobin.  v.  Limbeck  ||  refers  to  a  case  in  which  the  red  blood- 
corpuscles  were  reduced  to  1,500,000. 

Occasionally  a  grave  anaemia  develops  in  patients  with  cirrhosis 
without  any  manifest  cause,  such  as  haemorrhage.     A  distinction  should 

*  Gilbert  et  Gamier:  Soc.  biolog.,  Jan.  28,  1899.  Gilbert  et  Weill:  Sec. 
biolog.,  1899.     DeBrynine:  These  de  Paris,  1900. 

t  Bouchard:  Rev.  de  Med.,  Oct.,  1902,  p.  837. 

X  Centralbl.  f.  inn.  Med.,  1904,  S.  42,  Jan.  16. 

§  Cabot:  Examination  of  the  Blood,  p.  248,  1897. 

||v.  Limbeck:  Pathology  of  the  Blood,  p.  318.  Transl.  in  New  Sydenham  Soc, 
by  Latham  and  Nachbar. 


CIRRHOSIS    OF    THE    LIVER.  235 

be  drawn  between  secondan^  and  other  forms  of  anaemia  developing  in 
patients  with  cirrhosis,  and  cases  of  chronic  splenic  anaemia  in  which 
cirrhosis  subsequently  develops.  To  this  condition  the  term  Banti's 
disease  has  been  applied,  and  it  has  been  thought  that  the  cirrhosis  is 
due  to  poisons  manufactured  in  the  spleen  (Chauffard  *). 

Secondary'  anaemia  may  be  modified  by  cyanosis  which  leads  to  an 
increase  in  the  number  of  red  cells,  hence  if  cyanosis  is  due  to  ascites  the 
blood  count  may  be  lowered  by  tapping;  on  the  other  hand,  rapid 
ascitic  exudation  may  by  concentration  increase  the  blood  count ;  thus 
tapping,  by  favouring  the  recurrence  of  ascites,  has  been  observed  to  be 
followed  by  a  higher  blood  count.  Hence  a  patient  who  is  manifestly 
pale  and  anaemic  may  have  a  relatively  high  corpuscular  count.  Leu- 
cocytosis  does  not  occur  except  from  some  complication,  such  as  haem- 
orrhage or  inflammation.  The  blood  serum,  as  shown  by  Garrod's  test, 
may  appear  to  contain  uric  acid.  In  advanced  cases  the  alkalinity  may 
be  diminished  from  acid  intoxication. 

Respiration. — When  there  is  abdominal  distension  from  ascites  or 
flatulence,  the  upward  displacement  of  the  diaphragm  leads  to  shallow 
and  more  rapid  respirations.  Apart  from  this  there  is  nothing  noticeable 
about  respiration,  as  a  rule.  The  respiration  rate  may  be  slowed  from 
a  toxaemic  state  of  the  nerve  centres. 

The  Temperature. — As  a  general  rule,  the  temperature  is  not  raised; 
fever  is  much  less  frequent  in  multilobular  cirrhosis  than  in  h>73ertrophic 
biliary  cirrhosis,  and  when  it  is  met  with  should  at  once  suggest  the 
presence  of  some  complication,  such  as  tuberculosis,  pleural  effusion 
especially  on  the  right  side,  malaria,  infective  endocarditis,  or  other  in- 
fections. 

In  44  cases  tabulated  by  Carringtonf  the  temperature  was  irregular  in  18. 

Fever  is  usually  associated  -with  hepatic  enlargement  and  sometimes 
with  diarrhoea.  It  may,  in  fact,  depend  on  gastro-enteritis,  and  may 
then  simulate  enteric  fever  or  hepatic  suppuration.  (Vide  case  on  page 
219.)  Apart  from  manifest  secondary  infections  a  febrile  temperature  is 
more  often  seen  early  in  the  disease,  when  its  progress  is  somewhat 
rapid.  Fever  is  seen  in  the  acute  forms  of  multilobular  cirrhosis,  and 
therefore  makes  the  prognosis  worse.  It  may  be  difficult  to  decide 
whether  fever  in  any  given  case  is  due  to  some  undetected  complication, 
such  as  tuberculosis,  or  whether  it  depends  on  acute  progressive  changes 
in  the  liver. 

In  the  case  of  a  man  aged  forty-one,  whose  chart  is  attached,  admitted  for  ha;m- 
atemesis,  the  temperature  was  almost  constantly  raised,  and  in  a  few  weeks  ascites 
developed ;  it  appeared  to  be  a  case  of  acute  cirrhosis.  Mr.  G.  R.  Turner  performed 
the  operation  of  fixing  the  omentum  between  the  diaphragm  and  the  liver,  and  the 
man  greatly  improved,  the  temperature  fell,  and  he  went  out  of  the  hospital.  $  He 
died  from  cirrhosis  in  a  urtemic  state  about  two  and  three-quarter  years  later. 

*  Chauffard:  LaSem.  M^cL,  p.  177,  1899. 

t  Carrington :  Guy's  Hospital  Reports,  Series  iii,  vol.  xxvii,  1884. 

X  Vide  Rolleston  and  Turner:  Lancet,  1899,  vol.  ii,  p.  1660. 


236 


DISEASES    OF   THE    LIVER. 


< 

■^ 

w~ 

^~ 

~~ 

1       i 

, 

^?;" 

ffl". 

a; 

S- 

s 

S- 

" 

s 

"■ 

Vs' 

■%•■■■ 

o. 

s 

%■■ 

- 

g 

^ 

"■■ 

... 

.... 

^.... 

■~ 

g 

m 

ol 

■SJS- 

^ 

=> 

3 

sS- 

...."S 

.1.... 

- 

ts 

8 

r- 

" 

S 

£ 

V" 

... 

^ 

o 

S 

S 

r" 



Si 

'- 

S 

S 

r" 

™»!Hq">.i  vn-.T  -.       X 

S5 

■g 

J- 

I.... 

o 

s- 

•s 

" 

o 

1 

l> 

■s 

™ 

§ 

•3 

r' 

. .  .  .1 

o 

?i 

r 

> 

■S  S" 

"  r  ■ 

iibss 

,,c 

...|.... 

fSji 

c 

■  o 

..  i....rc 

=. 

1    1 

^, 

■CO  ^• 

....,.^ 

o 

.^ 

r:i..;r . 

,..i....r.. 

831  .ling  ^" 

jog 

!■•• 

s 

c. 

•o 

....|... 

....1....^ 

. .... 

- 

■o 

<M 

■.^ 

S- 

""l"" 

'■■1> 

-" 

■  tf 

?• 

g 

- 

■N 

...  ^^x^.. 

.... 

.... 

..<^. 

.|.... 

.... 

o 

.« 

P" 

— 

— 

—  ' 

— 

-^ 

o 

•s 

fad 

g 

g 

» 

.... 

— 

*- 

•g 

■"■ 

^ 

4- 

... 

c. 

s 

?■■ 

i-t 

•s 

-—U. 

§ 

i-t 

-ST  J                              ■■      ^^~~^ 

V- 

s 

- 

■S  r-     -...;ipr"''ir-K-0  ill!       ''^^~~ 

, 



s 

" 

Si;                                                    *°^> 

....|.... 

s 

" 

■?;'?      -n-vr.''il"-it-' ?.l'"  '  ■    ^~~^ 

,-  ■ 



S,' 

s 

- 

•  g;: 

§ 

«. 

•1! 

"• 

;." 

£='|'V''  l'n'-i''-.l''.'t"'     *°^~~~- 

»■■■■ 

§ 

». 

•a 

K" 

....,.,.             *^^~5i 

.1.... 

^ 

>- 

.c 

"■■ 

"=--^5, 

L.. 

«, 

■2 

?■■ 

;■  ■',^;   ^= — ^ 

-•■■ 

S,     i-              1 

■2 

"■■ 

fc-- 

^.^=:^ 

1 

■  s 

"•■ 

|...t!?.i 

g 

o 

b 

0 
0 

CCi 

H 

.-.= 

"■■ 

I....j....l....l....f^ 

.1.... 

CI 

^ 

s~ 

' — 

' 

-S. 

F 

s 

- 

1 

F 

— 

BOJiil'l 

M 

,'.'■ '.' '-^'',  ■    *=---., 

» 

s 

CO 

'        :;..,< 

s 

n 

g 

& 

<■, 

s 

1- 

„_----— ^ 

"• 

S! 

?J 

" 

?•■ 

i^: 

"q'-'ic.i  ^TCO  -r,«=::Z 

S 

»; 

CO 

Ah 

H. 

^ 

- 

■■■■r'"i"""T"" 

....|.... 

■o. 

te" 

M 

ss: 

••■•l^^- 

g 

r 

^ 

S-- 

..r  r. 

», 

- 

" 

.... 

........!....< 

..... 

g 

s 

" 

■  u. 

g 

" 

....J....J... 

■  ^ 

r^ 

1- 

"8 

s 

- 

.« 

s 

c. 

.« 

1:; 

kr 

~t" 

.... 

- 

^ 

s- 

K 

s 

<M 

g 

.- 

■s 

E- 

■1- 

S 

s 

- 

...  ,..^ 

:     1 

■s 

S- 

» 

-- 

.     1 

S; 

"■ 

....i....:,...f. 

.1... 

g 

3 

- 

'% 

"■ 

ii 

s 

c 

r- 

--I 

" 

...J..J.^' 

1 

■■■■r:jMr 

■s 

"■ 

> 

•s 

,...|......,;(. 

g  ?.  - 

s 

S 

\ 

luiSuJ  " 

o 

^'>-%  §.  s  i  i  2  '11  3  §  =  "  "  ""° 

3 

i 

^|i| 

Liver. — Clinically  the  liver 
is  more  often  enlarged  than 
diminished  in  size.  This  point 
has  been  specially  insisted  on 
by  Foxwell,*  who  considers 
that  "in  the  large  majority  of 
cases  of  hepatic  cirrhosis  at  all  • 
stages  of  the  disease  the  liver 
is  felt  below  the  ribs."  It  has 
often  been  assumed  that  en- 
largement of  a  cirrhotic  liver 
depends  largely  on  fat,  and 
that  this  is  more  likely  to  oc- 
cur in  beer  drinkers  than  in 
spirit  consumers.  But  Fox- 
well's  and  my  own  statistics 
do  not  bear  out  the  suggestion 
that  cirrhotic  livers  of  beer 
drinkers  are  usually  larger  than 
those  of  spirit  drinkers.  Fur- 
ther, it  is  far  from  being  uni- 
versally true  that  large  cirrho- 
tic livers  are  fatty. 

In  a  decided  minority  but 
still  in  a  certain  number  of 
cases,  chiefly,  I  believe,  in  per- 
sons whose  history  shows  no 
alcoholic  excess,  the  liver  is 
considerably  smaller  than  nat- 
ural. From  ascites,  flatulent 
distension,  or  from  obesity  it 
may  be  impossible  to  make  out 
the  enlargement.  Tympanites 
often  precedes  and  masks  the 
onset  of  ascites  and  prevents 
an  accurate  estimation  of  the 
size  of  the  liver.  Before  ascites 
has  appeared  the  liver  may  us- 
ually be  felt,  sometimes  several 
finger-breadths,  beyond  the 
costal  margin  in  the  right  nip- 
ple line,  its  surface  being  firm, 
slightly  irregular,  and  often 
tender.  In  other  instances  its 
rough  and  hard  margin  can  be 
reached  by  pushing  the  fingers 

*  Foxwell,  A. :  The  Enlarged 
Cirrhotic  Liver,  p.  20,  1896. 


CIRRHOSIS    OF    THE    LIVER.  237 

under  the  costal  margin,  while  in  other  cases,  although  conditions  are 
favourable,  the  liver  cannot  be  felt  on  deep  inspiration,  and  percussion 
may  show  that  there  is  definite  diminution  in  the  liver  dulness.  It 
should  be  remembered  that  percussion  is  subject  to  the  fallacy  that  a 
resonant  note  may  be  obtained  over  the  edge  of  the  liver  from  distended 
bowel  immediately  behind.  In  rare  cases  the  colon  may  pass  in  front  of 
■  the  liver  and  lead  to  great  diminution  in  the  apparent  size  of  the  organ. 
Palpation  is  therefore  more  reliable  than  percussion. 

It  has  been  widely  assumed  that  the  liver  is  enlarged  in  the  early 
stages  of  the  disease  and  that  subsecjuently  it  becomes  smaller  from 
shrinking  and  contraction  of  the  fibrous  tissue  inside  it.  This  sequence 
of  events  is  sometimes  noted  (Taylor*);  thus  a  considerable  time  before 
death  the  organ  has  been  found  to  be  large,  while  at  the  postmortem 
some  months  later  it  has  receded  behind  the  costal  arch.  At  the  same 
time,  it  is  by  no  means  certain  that  alterations  in  size  of  the  organ  can 
be  referred  solely  to  the  contraction  of  the  added  connective  tissue;  for, 
in  the  early  stage,  the  enlargement  may  vary  mthin  a  comparatively 
short  space  of  time,  thus  showing  that  the  increase  in  size  is  due  to  en- 
gorgement. Thus,  in  alcoholic  subjects  a  drinking  bout  may  lead  to 
rapid  increase  in  size  of  a  cirrhotic  liver,  the  organ  feeling  firm  and  being 
tender,  while  low  diet,  total  abstinence,  and  judicious  purgation  are 
followed  by  a  return  to  its  former  size.  Dilatation  of  the  heart  due  to 
alcoholic  excess,  or  cardiac  failure  induced  in  other  ways,  may  give  rise 
to  considerable  increase  in  the  size  of  a  cirrhotic  li^•er. 

It  has  been  noticed  by  many  observers  that  the  cirrhotic  livers  of 
people  dying  from  accident  and  other  causes  unconnected  with  the  dis- 
ease are  larger  than  those  of  patients  dying  from  the  disease.!  This 
might  be  thought  to  support  the  view  that  the  liver  is  enlarged  in  the 
early  stage  from  proliferation  of  the  interstitial  connective  tissue  and 
that  later  it  becomes  smaller  from  cicatricial  contraction.  But  it  is 
more  probable  that  these  cases  of  cirrhosis  were  latent  and  that  the  large 
size  of  the  livers  depended  on  compensatory  hyperplasia  of  the  liver 
cells,  than  that  the  cases  were  in  an  early  stage  of  progressive  cirrhosis. 
The  surface  of  the  liver  may  be  fairly  smooth,  esjDecially  when  it  is  con- 
siderably enlarged,  but  in  other  eases  its  surface  is  irregular,  and  some- 
times the  knobby  feel  of  the  "hobnails"  is  perceptible.  These  hobnails 
are  not  depressed  in  the  centre  or  umbilicated,  but  the  depressed  area 
of  liver  substance  between  two  adjacent  elevations  may  imitate  the 
umbilications  of  multiple  carcinomatous  nodules. 

Hepatic  Pain. — Some  discomfort  and  a  sense  of  uneasiness  in  the 
region  of  the  liver  are  very  common.  Pain  is  very  seldom  a  prominent 
symptom,  but  nevertheless  it  is  present  from  time  to  time  in  a  consider- 
able number  of  the  cases,  and  may  be  due  to  transient  attacks  of  perihepa- 
titis, as  shown  by  the  frec{uency  of  adhesions  between  the  liver  and  the  dia- 
phragm.    Pain  of  a  somewhat  severe  character  over  the  liver  may  be 

*  Taylor,  F. :  Guy's  Hosp.  Reports,  vol.  xlv,  p.  310. 

t  Fagge,  C.  Hilton:  Guy's  Hospital  Reports,  Series  iii,  vol.  xx.  Price,  J.  A.  P. : 
Series  iii,  vol.  xxvii. 


238  DISEASES    OF   THE    LIVER. 

due  to  right-sided  pleurisy.  Tenderness  over  the  liver  is  by  no  means 
constant;  it  is  often  present  over  large  cirrhotic  livers  after  bouts  of 
alcoholic  excess,  and  may  be  an  expression  of  passive  engorgement  from 
failing  heart. 

Venous  Bruits. — In  rare  instances  a  venous  hum  may  be  heard  over 
the  epigastrium  which  is  louder  on  inspiration.  It  has  been  explained 
as  the  result  of  the  compensator}^  dilatation  of  the  venous  communica- 
tions between  the  portal  and  the  general  systemic  veins.*  The  thin- 
walled  and  dilated  veins  may  readily  be  kinked  as  the  result  of  adhesions 
or  temporarily  distorted  by  the  descent  of  the  diaphragm  or  even  by 
the  pressure  of  a  wooden  stethoscope. 

In  a  man  aged  forty-three  who  was  under  my  care  in  St.  George's  Hospital  there 
was  a  continuous  bruit  in  the  epigastrium  resemjoling  the  bruit  de  diahle  in  the  neck. 
At  the  autopsy  the  hver  was  markedly  cirrhotic  and  the  round  ligament  contained  a 
thin-walled  vein  as  large  as  the  little  finger.      (Vide  Fig.  32.) 

It  has  also  been  thought  to  be  due  to  pressure  on  the  portal  vein  by 
enlarged  glands,  or  even  to  narrowing  of  the  inferior  vena  caA^a  where 
it  lies  in  contact  with  the  posterior  border  of  the  liver,     (v.  Gambarati.f) 

Spleen. — Enlargement  of  the  spleen  is  an  important  feature  in  portal 
cirrhosis;  it  has  been  shovTi  (p.  214)  that  the  spleen  is  almost  constantly 
enlarged  in  fatal  cases  of  progressive  cirrhosis,  though  not  to  such  a 
marked  degree  as  in  hypertrophic  biliary  cirrhosis.  The  amount  of 
splenic  enlargement  has  been  regarded  as  an  index  of  the  severity  of 
the  cirrhosis,  and  enlargement  in  cases  wdiere  the  cirrhosis  appears  to  be 
latent  or  compensated  for  should  always  be  an  indication  for  careful 
treatment  and  a  cautious  prognosis.  Considerable  enlargement  may 
precede  hsematemesis,  and  its  detection  may  therefore  be  regarded  as  a 
danger-signal  and  call  for  free  purgation.  In  some  cases  of  portal  cir- 
rhosis enlargement  of  the  spleen  is  easily  made  out  and  the  organ  can 
be  felt  to  be  firm  and  resistant.  In  other  instances  the  splenic  dulness 
is  increased,  though  the  organ  cannot  be  felt,  while  in  a  number  of  cases 
the  enlargement  of  the  spleen  is  obscured  by  tympanites  or  ascites.  Slight 
pain  or  discomfort  are  sometimes  experienced  in  the  splenic  region,  and, 
apart  from  the  referred  pain  of  flatulent  dyspepsia,  may  be  due  to  in- 
flammation of  the  capsule,  to  tension  and  engorgement  of  the  spleen,  or 
to  dragging  on  adhesions  between  the  spleen  and  neighbouring  parts. 

Venous  Bruits. — As  in  splenic  enlargement  from  other  causes,  such 
as  malaria,  splenic  anaemia,  etc.,  a  venous  bruit,  like  the  well-known 
bruit  de  diahle  in  the  neck  of  angemic  patients,  is  occasionally  heard  over 
the  spleen  in  cirrhosis.  It  has  also  been  compared  to  the  uterine  souffle. 
It  may  be  continuous  and  increased  during  inspiration,  or  may  only  be 
heard  during  inspiration.  Its  position  may  vary,  but  is  generally  in  the 
anterior  axillary  line.  It  may  be  due  to  temporary  or  prolonged  kinking 
of  the  dilated  splenic  vein  or  of  its  branches  in  the  hilum  of  the  spleen. 

*  Taylor,  F. :  Guy's  Hosp.  Reports,  vol.  lii,  p.  58. 
t  V.  Gambarati:  Riforma  Med.,  Feb.  11,  1903,  p.  153. 


CIRRHOSIS    OF    THE    LIVER.  239 

It  has  also  been  thought  to  be  due  to  pressure  on  the  inferior  vena  cava. 
(Martini.*) 

(Edema  of  the  Feet. — CEdema  of  the  feet  usuah}'  occurs  after,  but  it 
may  be  quite  independent  of,  the  development  of  ascites;  it  maj^  even 
come  on  in  the  latest  stages,  when  ascites  has  passed  away  and  the 
patient  is  in  a  toxsemic  state.  On  the  other  hand,  oedema  may  begin  in 
the  feet  before  the  appearance  of  ascites.  The  amount  of  oedema  is 
usually  small;  sometimes  it  is  very  soft,  probably  from  laxity  of  the 
skin  and  underlying  tissues  from  wasting  of  the. subcutaneous  fat  and 
of  the  muscles. 

CEdema  of  the  feet  is  often  referred  to  the  ascites  mechanicalh"  im- 
peding the  return  of  blood  through  the  inferior  vena  cava.  But  this 
explanation  will  not  fit  all  cases,  for  example,  those  in  which  oedema 
comes  on  before  the  advent  of  ascites,  or  when  there  is  so  little  peritoneal 
effusion  that  there  can  be  no  increased  intra-abdominal  tension.  In 
such  cases  the  toxic  origin  of  oedema  may  be  invoked ;  it  has  been  sug- 
gested that  there  is  a  poison  with  a  lymphagogue  action  present  in  the 
blood,  and  that  the  oedema  resembles  that  of  renal  disease  (Hale  White  t). 

It  has  been  thought  that  the  pressure  of  a  firm  cirrhotic  liver  on  the 
inferior  vena  cava  just  before  it  passes  through  the  diaphragm  may  be 
sufficient  to  give  rise  to  oedema  of  the  feet.  This  is  conceivable,  but 
if  it  is  a  factor  of  any  importance,  much  more  oedema  of  the  legs  than 
actually  occurs  would  be  expected  in  cases  of  malignant  disease  involving 
the  liver,  while  a  dilated  venous  plexus,  like  that  seen  in  mechanical 
obstruction  of  the  inferior  vena  cava,  should  also  be  present  under  the 
skin  of  the  abdominal  wall  to  provide  for  the  return  of  blood  from  the 
lower  limbs.  As  a  matter  of  fact,  dilatation  of  the  epigastric  and  mam- 
marv^  veins  may  occur  when  there  is  ascites,  but  hardly  ever  when  oedema 
of  the  feet  is  present  in  the  absence  of  ascites. 

In  some  cases  of  cirrhosis  oedema  of  the  feet  may  be  the  outcome  of 
complications,  such  as  the  backward  pressure  of  cardiac  failure;  thus, 
it  may  depend  on  alcoholic  dilatation  of  the  heart  or  on  concomitant 
valvular  disease.  Again,  it  may  be  due  to  alcoholic  neuritis;  in  the 
latter  contingency  there  will  be  muscular  tenderness  and  absence  of  the 
knee-jerks.  It  is  probable  that  a  slight  degree  of  peripheral  neuritis  is 
more  frequent  in  the  course  of  cirrhosis  than  is  generally  recognized, 
and  that  it  is  specially  likely  to  accompany  an  aggravation  of  the  liver 
symptoms  with  abdominal  pain,  tympanites,  and  dyspepsia.  When 
oedema  of  the  feet  occurs  in  association  -with,  a  considerable  degree  of 
ascites,  it  is  possible  that  it  is  brought  about  by  the  pressure  of  the 
fluid  on  the  inferior  vena  cava  and  the  lymphatic  vessels  going  to  the 
thoracic  duct. 

General  oedema  is  very  rare,  but  the  dropsical  condition  of  the  legs 
and  thighs  may  pass  up  onto  the  abdomen  and  appear  as  a  hunbar 
cushion  on  the  back. 

*  Martini :  Brit.  Med.  Journ.,  1893,  vol.  ii.     Leudct :  Rev.  de  Med.,  1S90,  p.  S6S. 
t  Hale  White :  Clinical  Journal,  April  26,  1899. 


240  DISEASES    OF   THE    LIVER. 

McCall  Anderson*  recorded  a  case  of  recurrent  attacks  of  universal  dropsy  in  a 
boy  aged  eighteen  who  had  no  renal  disease  and  whose  liver  (4  ]:)ounds)  showed 
changes  compatible  with  the  view  that  there  was  subacute  cirrhosis. 

ASCITES. 

Derivation. — a.<yy.i'>z  "a,  wineskin."  y/  aavJ-r^q  'yorrog^  "the  wine-skin 
disease/'  meaning  that  disease  in  which  the  abdomen  looks  hke  a  tense 
wineskin. 

The  words  "ascites/'  "tympanites/'  have  a  feminine  adjectival 
termination,  -ites,  like  -t-c7  in  neuritis,  peritonitis,  etc.,  which  agrees  with 
voffoe;^  "disease/'  understood.  In  the  case  of  -itis  an  entirely  secondar}^ 
meaning,  viz.,  "inflammation,"  has  been  evolved.f 

Definition. — Free  fluid  in  the  peritoneal  cavity. 

Incidence. — Ascites  occurs  in  50  per  cent,  of  all  patients  dying  with 
cirrhotic  livers.  Since  it  is  a  late  event  in  the  course  of  the  disease  it 
naturally  occurs  far  more  frequently  in  cases  fatal  from  the  effects  of 
cirrhosis  than  in  patients  who,  having  cirrhotic  livers,  die  from  indepen- 
dent disease,  such  as  ]3neumonia,  tuberculosis,  erysipelas,  etc.  Ascites 
occurs  in  the  vast  majority  of  the  cases  of  cirrhosis  which  run  their  full 
course,  but  a  certain  number  of  cases  who  die,  so  to  speak,  prematurely 
from  the  direct  effects  of  cirrhosis,  such  as  hgematemesis  or  melsena, 
do  not  present  ascites. 

In  Price's!  142  cases  ascites  occurred  in  72.  In  121  cases  of  cirrhosis  taken  from 
the  postmortem  records  of  the  Manchester  Royal  Infirmary,  Keljmack  §  found 
ascites  in  56  per  cent.  In  166  cases  of  cirrhosis  examined  after  death  at  St.  George's 
Hospital  ascites  was  or  had  been  present  in  84,  or  50.6  per  cent.  In  80  of  these  cases 
death  was  directly  clue  to  the  effects  of  cirrhosis,  and  in  68  of  them,  or  85  per  cent., 
ascites  was  present.  In  86  cases  where  death  was  due  to  other  factors  16,  or  18.6 
per  cent.,  had  ascites. 

Relation  between  Weight  of  the  Liver  and  the  Incidence  of  Ascites. — 
Ascites  is  much  more  often  found  in  association  with  a  comparative^ 
small  than  with  large  cirrhotic  livers.  This  is  due  to  two  factors:  (a) 
because  in  an  early  stage  the  liver  is  often  larger  than  it  is  later  in  the 
disease,  and  (6)  because  when  cirrhosis  becomes  latent  from  compensator}^ 
hyperplasia  of  the  liver  cells  the  organ  is  considerably  increased  in  size. 

Causes  of  Ascites. — ^The  factors  which  give  rise  to  the  peritoneal 
effusion  in  cirrhosis  require  some  discussion.  It  will  be  most  convenient 
to  refer  to  them  in  order  and  then  briefly  to  summarize  their  claims. 
The  factors  for  consideration  are : 

(I)  Mechanical  factors:  (a)  Obstruction  to  the  passage  of  blood 
through  the  liver,  due  to  fibrosis  and  contraction  around  the  intra-hepatic 
branches  of  the  portal  vein.  (6)  Thrombosis  of  the  radicles  of  the 
portal  vein  in  the  liver,  (c)  Thrombosis  of  the  trunk  of  the  portal 
vein. 

(II)  Toxgemia. 

*  McCaU  Anderson :  Contributions  to  Clinical  Medicine,  p.  345. 
t  Compare  Buzzard,  T. :  Trans.  Path.  Soc,  vol.  xl,  p.  347. 
X  Price,  J.  A.  P. :  Guy's  Hosp.  Reports,  Series  iii,  vol.  xxvii. 
§  Kelynack,  T.  N. :  Birmingham  Medical  Review,  Feb.,  1897. 


CIRRHOSIS    OF    THE    LIVER.  241 

(III)  Concomitant  inflammation  of  the  peritoneum  and  perihepatitis. 

(IV)  Associated  cardiac  failure. 

(I)  (a)  Obstruction  to  the  passage  of  Mood  through  the  cirrhotic  liver  is 
an  undoubted  fact,  and  leads  to  chronic  venous  engorgement  of  the  portal 
vein  area,  as  shown  by  the  development  of  a  collateral  circulation,  dila- 
tation, and  thickening  of  the  intima  of  the  portal  vein,  and  to  some  extent 
clinically  by  hsematemesis  and  melsena.  That  increased  pressure  in  the 
portal  vein  alone  does  not,  however,  necessarily  produce  ascites  is  shown 
by  experimental  ligature  of  the  portal  vein  in  animals.*  While  in 
patients  with  cirrhosis  it  is  noticeable  that  when  the  venous  pressure  in 
the  portal  vein  appears  to  be  high,  as  shown  by  hsematemesis  and  melsena, 
ascites  is  absent.  Further,  the  extreme  rapidity  with  which  the  effusion 
may  be  poured  out — a  pint  a  day  in  some  instances — is  hardly  compatible 
with  the  view  that  it  is  solely  due  to  increased  venous  pressure.  If  the 
peritoneal  effusion  was  due  to  the  fibrosis  in  the  liver,  it  would  come  on 
gradually,  pari  passu  with  the  cicatricial  contraction  of  the  fibrous  tissue 
around  the  portal  canals,  while  as  a  matter  of  fact  ascites  often  develops 
suddenly  and  rapidly. 

Since  the  collateral  circulation  is  a  compensatory  means  of  csirrying 
on  the  circulation,  great  importance  has  been  attached  to  it  as  preventing 
ascites.  But  ascites  is  often  present  in  spite  of  considerable  collateral 
circulation,  and  conversely  both  ascites  and  evidence  of  any  portal 
anastomosis  may  be  absent. f 

Levi  J  ill  a  case  of  cirrhosis  with  terminal  delirium  found  that  there  were  no 
ascites  and  no  collateral  circulation.  It  is  remarkable  that  there  was  peritoneal 
tuberculosis  in  addition,  which  in  itself  is  a  sufficient  cause  of  ascites. 

For  these  reasons  increased  venous  pressure  due  to  hepatic  obstruc- 
tion, though  very  frequently  associated  with  ascites,  is  not  alone  a  true 
cause  of  peritoneal  effusion. 

(I)  (6)  It  has  been  suggested  that  the  additional  factor  required  to 
'bring  about  ascites  in  cirrhosis  is  thrombosis  or  obliterating  endophle- 
bitis  of  the  terminal  branches  of  the  portal  vein,  either  in  the  liver  or 
where  the  portal  tributaries  anastomose  with  the  adjacent  systemic 
veins.     There  is,  however,  no  proof  of  this. 

(I)  (c)  Thrombosis  of  the  portal  vein  may  give  rise  to  ascites  in 
cirrhosis,  but  it  is  so  rare  that  it  has  no  claim  to  be  considered  among  the 
important  causes  of  ascites. 

In  334  cases  of  cirrhosis  examined  after  death  portal  thrombosis  was  present 
in  10,  or  3.3  per  cent.      (Langdon  Brown. §) 

(II)  The  Toxic  Nature  of  Ascites. — As  a  result  of  hepatic  inadequacy 
poisons  absorbed  from  the  alimentary  canal  or  possibly  produced  else- 
where are  no  longer  stopped  and  destroyed  by  the  liver,  but  pass  into 

*  Hale  White:  Brit.  Med.  Journ.,  1903,  vol.  i,  p.  535. 
t  Compare  Hanot :  Archiv.  Gi^neral.  de  Med.,  1886,  t.  cLxxvii,  p.  603. 
t  Levi:  Archiv.  Gh\6vd].  de  M6d.,  1886,  t.  clxxvii,  p.  221. 
§  Langdon  Brown:  St.  Bartliolomew's  Hospital  Reports,  vol.  xxxvii,  p.  62. 
16 


242  DISEASES    OF   THE    LIVER. 

the  general  circulation,  and  a  condition  of  hepatic  toxgemia,  analogous 
to  that  of  renal  toxaemia,  results ;  in  both  these  analogous  conditions  the 
patients  become  drowsy  and  may  have  numerous  hsemorrhages  in  various 
parts  of  the  body.  In  addition,  as  Hale  T\Tiite*  has  pointed  out,  oedema 
of  the  feet  and  sometimes  of  the  abdominal  vail  occurs.  By  regarding 
the  poison  of  hepatic  toxaemia  as  a  lymphagogue  the  occurrence  of  ascites 
in  cirrhosis  may  be  explained.  It  is  weU  to  lay  stress  on  the  fact  that 
oedema  of  the  feet  may  occur  before  ascites  develops,  inasmuch  as  this 
shows  that  the  oedema  of  the  feet  is  not  necessarily  a  mechanical  effect 
due  to  the  pressure  of  ascitic  fluid  on  the  inferior  vena  cava.  The  absence 
of  ascites  in  cases  of  biliarA^  cirrhosis,  where  there  is  some  reason  to  believe 
that  the  blood  is  toxic,  viz.,  the  considerable  splenic  enlargement,  is 
perhaps  explained  by  the  fact  that  the  liver  ceUs  remain  in  a  better 
state  of  nutrition  than  in  portal  cirrhosis,  and  that  the  poisons,  if  present, 
are  not  necessaril}^  of  the  same  nature  as  in  ordinary  cirrhosis. 

(Ill)  Ascites  due  to  Concomitant  Inflammation  of  the  Peritoneum. — In 
many  cases  of  cirrhosis  there  is  in  addition  chronic  peritonitis,  which 
accounts  for  the  ascites,  and  especially  for  ascites  which  continues  for  a 
considerable  time  or  recurs  again  and  again  after  tapping.  Bright,  in- 
deed, considered  the  ascites  of  cirrhosis  to  be  the  result  of  portal  obstruc- 
tion and  of  an  extension  of  chronic  inflammation  from  the  hver  along 
the  portal  vein  and  its  branches  to  the  peritoneum.  This  -view  in  a 
modified  form  is  held  by  many  authorities,  and  there  is  no  doubt  that 
ascites  is  very  often  satisfactorily  explained  on  this  hj^othesis.  But 
chronic  peritonitis  does  not  account  for  the  onset  of  ascites  in  aU  cases 
of  ordinar}^  cirrhosis,  for  it  is  often  absent  when  there  is  marked  ascites. 
In  some  cases  ascites  passes  away  when  the  patient  is  in  a  semi-comatose 
condition;  now,  since  chronic  peritonitis  would  give  rise  to  persistent 
ascites,  such  cases  may  be  expected  to  be  free  from  chronic  peritoneal 
inflanunation. 

The  i^ossibilit}'  that  ascites  is  due  to  a  low  form  of  secondan,-  infection 
will  require  consideration  when  more  is  knoT\Ti  about  the  bacteriology^ 
of  hepatic  cirrhosis  and  of  the  ascitic  effusion  which  occurs  as  a  terminal 
phenomenon.  This  suggestion  is  attractive  from  the  fact  that  secondare' 
infections  may  occur  in  other  parts  of  the  body  in  the  later  stages  of 
cirrhosis.  From  analog}'  it  appears  probable  that  the  peritoneum  would 
suffer  similarly,  since  it  is  decidedl}-  a  place  of  diminished  resistance  in 
cirrhosis,  and,  moreover,  infection  from  the  intestinal  tract,  which  is 
often  in  a  condition  of  chronic  catarrh,  might  easily  occur.  Again, 
ascites  ma}'  super^-ene  after  septic  processes  have  occurred  elsewhere  in 
the  bod}',  thus  suggesting  that  the  ascites  is  in  some  way  secondar}'. 

Although  as  seen  in  laparotomies  in  cases  mth  ascites  the  peritoneum 
is  highly  injected,  there  is  no  inflammation  or  acute  peritonitis.  So  if 
there  be  a  ixiicrobic  origin  for  ascites,  the  micro-organisms  are  not  pyo- 
genic, but  of  a  low  degree  of  virulence.  It  is  well  to  remember  that 
tubercle  of  the  pleura  and  peritoneum  may  give  rise  to  almost  pure  serous 
effusions,  and  that  in  these  cases  the  fluid  -withdrawn  may  be  almost,  if 
*Hale  White:  Clinical  Journ.,  April  26,  1899. 


CIRRHOSIS    OF    THE    LIVER.  243 

not  quite,  free  from  bacilli.  Possibly  the  same  ma}'  hold  for  ascites  of 
cirrhosis,  viz.,  that  it  is  due  to  a  micro-organism  which  does  not  appear 
in  the  fluid  ■^dthdrawn  by  paracentesis. 

Ascites  due  to  Concomitant  Perihepatitis. — Some  thickening  of  the  cap- 
sule of  the  liver  is  commonly  seen  in  cirrhosis,  and  in  some  instances  sat- 
isfactorily explains  ascites.  But  it  is  not  a  constant  cause;  this  is  shown 
by  the  fact  that  ascites  occurs  when  there  is  little  or  no  perihepatitis, 
and  that  it  may  be  absent  when  there  is  as  much  perihepatitis  as  there  is 
in  cases  where  the  peritoneal  effusion  is  thus  explained.  Parkes  Weber  * 
has  suggested  that  effusion  resulting  from  localized  areas  of  inflammation 
may  possess  sufficiently  irritating  properties  to  lead  to  a  copious  exuda- 
tion of  normal  or  nearly  normal  fluid  from  the  non-inflamed  surfaces. 
On  this  view  quite  local  perihepatitis  might  account  for  ascites.  Against 
this  view  is  the  fact  that  foci  of  perihepatitis  often  exist  in  the  absence 
of  ascites,  both  in  cirrhosis  and  in  other  conditions.  Weber  has  also 
suggested  that  transient  ascites  in  cirrhosis  may  be  due  to  local  peri- 
tonitis which  is  temporary  and  comparable  to  subacute  pleurisy  with  a 
serous  effusion. 

(IV)  Ascites  from  Cardiac  Failure. — In  cases  of  latent  cirrhosis  dila- 
tation of  the  heart  from  valvular  disease,  from  affections  of  the  myo- 
cardium, whether  chronic  or  acute,  or  from  obstructive  lung  disease  may 
develop  and  give  rise  to  ascites.  The  cirrhosis  and  ascites  are  therefore 
associated,  but  the  ascites  is  not  necessarily  dependent  on  the  cirrhosis. 
On  the  other  hand,  backward  pressure  very  probably  favours  the  onset 
of  ascites  in  patients  with  cirrhosis;  in  other  words,  an  amount  of  back- 
ward pressure  which  in  an  ordinary  case  would  not  produce  ascites  may 
be  the  cause  of  ascites  in  a  patient  with  progressive  cirrhosis.  Heart  dis- 
ease may  therefore  induce  ascites  in  cirrhosis  in  two  ways :  (I)  Merely 
by  backward  pressure,  as  in  some  cases  of  tricuspid  regurgitation;  (II) 
by  bringing  about  conditions,  such  as  venous  engorgement,  the  stagnation 
of  toxines,  or  damage  to  the  endothehal  cells  of  the  peritoneum,  which 
precipitate  ascites  due  to  cirrhosis. f 

In  conclusion,  ascites  may  be  merely  associated  with  cirrhosis  and 
directly  due  to  chronic  or  possibly  to  subacute  peritonitis  and  peri- 
hepatitis, or  to  cardiac  failure;  in  rare  cases  it  may  be  due  to  a  direct 
complication  of  cirrhosis,  i.  e.,  thrombosis  of  the  portal  vein,  or,  on  the 
other  hand,  it  may  be  due  to  cirrhosis  alone.  In  the  latter  case  it  may 
be  explained  as  being  due  to  a  toxic  condition  of  the  blood,  from  the 
presence  in  it  of  poisons  having  a  lymphagogue  action,  and  therefore  in- 
ducing an  exaggerated  flow  of  fluid  into  the  peritoneal  cavit}^  It  is 
probable  that  this  form  of  ascites  may  be  brought  about  prematurely 
by  cardiac  failure. 

The  onset  of  ascites  may  follow  so  soon  after  some  event,  such  as  a 
blow,  fall,  or  exposure  to  cold,  that  there  would  appear  to  be  a  definite 
connexion  between  them.  It  is  possible  that  by  a  blow  the  resistance 
of  the  peritoneum  may  be  so  reduced  that  the  real  responsible  cause  of 

*  F.  P.  Weber:  Brain,  1902,  p.  150;  E(linbur{j;h  Med.  Journ.,  April,  1903,  p.  322. 
t  Compare  Cheadl,  W.  B. :  Some  Cirrho.ses  of  the  Liver,  p.  103. 


244  DISEASES   OF   THE   LIVER. 

ascites  is  enabled  to  produce  its  effect  sooner  than  it  otherwise  would. 
As  the  result  of  a  chill,  vasomotor  paralysis  of  the  splanchnic  vessels 
results,  and  irdght  thus  precipitate  ascites,  so  to  speak.  These  cases 
have  been  spoken  of  as  acute  ascites.*  It  must  be  remembered  that 
what  appears  to  be  acute  ascites  may  prove  to  be  acute  peritonitis. 
Ascites  may  come  on  after  various  infections,  such  as  suppuration, 
erysipelas,  or  diseases,  such  as  influenza  or  typhoid. 

Though  it  may  be  sudden,  the  onset  of  ascites  is  usually  gradual, 
and  is  often  masked  by  flatulent  distension  of  the  abdomen.  It  thus 
contrasts  with  the  sudden  and  rapid  development  of  ascites  in  thrombosis 
of  the  trunk  of  the  portal  vein.  Ascites  occurs  late  in  the  course  of  un- 
complicated cirrhosis,  that  is,  in  cases  where  there  is  no  concomitant 
chronic  peritonitis.  The  gravity  of  ascites  in  such  cases  has  been  spe- 
cially insisted  on  by  Hale  White,  who  finds  that  the  patient  seldom 
survives  long  enough  to  require  tapping  more  than  once. 

Characters  of  Ascitic  Fluid .^ — The  ascitic  fluid  is  clear,  greenish  or 
yellow  in  tint,  and  sometimes  slightly  bile-stained.  Its  reaction  is 
alkaline  and  its  specific  gravity  between  1008  and  1015.  It  contains 
more  albumin  than  ascitic  fluid  of  renal  disease  and  less  than  that  of 
cardiac  ascites  (Dickinson  |).  If  there  is  any  added  peritonitis,  its 
specific  gravity  and  the  proportion  of  albuminous  matter  increase  and 
flakes  of  coagulated  fibrin  may  form  on  standing.  It  contains  from  0.2 
to  0.4  per  cent,  of  albuminous  material  and  occasionally  a  trace  of  sugar, 
urea,  urobilin.  The  large  amount  of  chlorides  present  in  ascitic  fluid 
is  associated  with  the  diminished  amount  in  the  urine.  If  the  specific 
gravity  is  above  1015,  contains  a  larger  amount  of  albumin,  and  micro- 
scopically shows  polymorphonuclear  leucocytes,  there  is  some  inflam- 
matory change  in  the  peritoneum. 

Character  of  the  Cells  in  the  Ascitic  Fluid. — Comparatively  little  work  has  been 
done  on  the  character  of  the  cells  found  in  the  ascites  of  cirrhosis,  and  the  results  are 
not  entirely  in  accord.  In  one  case  Dopter  and  Tantonf  found  a  majority  of  poly- 
morphonuclear leucocytes  and  a  few  endothelial  cells.  Grenet  and  Vitry  §  found 
endothelial  cells  and  a  few  lymphocj^tes.  Souques,  |1  and  Achard  and  Laubry,**  in 
two  cases  of  lactescent  ascites  in  cirrhosis,  found  lymphocytes  and  mononuclear 
leucocytes  chiefly  represented. 

Chylous  ascites  due  to  an  admixture  of  chyle  is  very  rare  in  cirrhosis. 
When  this  condition  does  occur,  it  is  usually  associated  with  malignant 
disease  in  the  abdominal  cavity. 

LetuUe  refers  to  3  cases  in  which  cirrhosis  was  associated  with  chylous  ascites ; 
in  Merklem'stt  case  of  cirrhosis  chylous  ascites  followed  a  fall,  and  thus  suggests  the 
possibility  of  laceration  of  l3Tiiphatic  vessels,  though  this  was  not  made  out  at  the 
autopsy. 

*  B.  Weill:  (Acute  Ascites)  These  Paris,  1899,  No.  278.       Potain:  (Ascites  a 
frigore)  La  Sem.  Med.,  1888,  p.  9. 

t  Dickinson,  W.  H. :  Allbutt's  System  of  Med.,  vol.  v,  p.  668. 

t  Dopter  and  Tanton:  Bull.  Soc.  Med.  d.  Hop.  Paris,  July  12,  1901. 

§  Grenet  and  Vitry:  T>a  Sem.  Med.,  1903,  p.  235. 

11  Souques:  Bull.  Soc.  Med.  d.  Hop.  Paris,  March  21,  1902,  p.  290. 
**  Achard  and  Laubry :  Ibid.,  p.  295. 
tt  Merklem:  La  Sem.  Med.,  May  12,  1897. 


CIRRHOSIS    OF    THE    LIVER.  245 

Resembling  true  chylous  ascites  in  appearance,  but  differing  from  it 
chemically,  are  the  two  following  forms  of  ascites:  (a)  the  chyliform  or 
fatty,  and  (6)  the  milky  non-fatt}^  ascites;  these  two  forms  are  not  very 
rare  in  cirrhosis. 

In  chyliform  or  fatty  (adipose)  ascites  the  fat,  which  is  present  in  larger 
globules  than  in  the  chylous  ascites,  is  probably  the  outcome  of  degen- 
erative changes  in  cells  suspended  in  the  ascitic  fluid.  In  cases  of  fatty 
ascites  in  cirrhosis,  Souques  and  Achard  and  Laubry  have  found 
both  fat  and  a  nucleo-albumin ;  the  latter  gave  rise  to  an  opalescent 
solution.  Fatty  ascites  would  thus  differ  from  the  next  form  only  in 
the  j)resence  of  fat,  since  it  has  been  thought  that  in  both  there  is 
a  nucleo-albumin  possessing  the  property  of  rendering  ascitic  fluid 
milky. 

In  opalescent,  milky  {non-fatty)  ascites,  of  which  Jousset  *  has  collected 
fourteen  cases  in  portal  cirrhosis,  there  are  a  large  number  of  mono- 
nuclear leucocytes  which  probably  give  rise,  as  the  outcome  of  degen- 
erative changes,  to  some  body,  such  as  nucleo-albumin  or  globulin,  which 
is  responsible  for  the  lactescent  appearance  of  the  fluid.  It  has,  however, 
been  suggested  that  lecithin  may  be  the  cause  of  the  lactescent  appear- 
ance. (Micheli  and  Mattirolo.t)  No  fat  can  be  extracted  by  ether  from 
the  ascitic  fluid  in  this  form.  In  both  the  fatty  and  the  non-fatty  forms 
of  milky  ascites  the  change  may  appear  on  the  second  tapping,  in  cases 
where  the  fluid  withdrawn  on  the  first  occasion  was  clear.  From  the 
presence  of  numerous  leucocytes  in  the  fluid  the  exudation  has  some- 
times been  spoken  of  as  purulent. 

A  hcemorrhagic  ascites  isA^ery  rare  in  cirrhosis.  It  is  not  due  to  mere 
hepatic  insufficiency,  like  the  oozing  from  the  gums  and  epistaxis.  Neither 
does  it  appear  that  it  is  usually  due  to  concomitant  tuberculosis  of  the 
peritoneum.  It  may  be  the  result  of  previous  tapping;  thus  in  cases 
where  the  fluid  is  serous  at  the  first  paracentesis  and  is  found  to  be  san- 
guineous at  subsequent  tappings,  it  is  probable  that  the  trocar  wounded 
some  of  the  vascular  adhesions  or  dilated  veins  in  the  peritoneum  forming 
the  collateral  circulation.  (Barjon  and  Henry. J)  In  some  instances  of 
cirrhosis  chronic  hsemorrhagic  peritonitis  occurs  and  possibly  may  be 
due  to,  at  any  rate  is  associated  with,  alcoholism.  Fernet  §  records  a 
case  bearing  this  interpretation. 

Bacteriology  of  Ascitic  Fluid. — More  observations  are  required  as  to 
the  bacteria  present  in  the  ascites  of  cirrhosis,  and  very  probably  may 
be  obtained  by  the  new  method  of  inoscopy.  It  consists  in  taking  the 
coagulum  of  the  fluid;  or,  if  there  is  no  spontaneous  one,  producing  one, 
dissolving  it  with  aseptic  gastric  juice,  and  examining  for  micro-organisms ; 
this  method  depends  on  the  fact  that  the  clot  filters  off  the  micro-organ- 
isms from  the  fluid.     By  this  method  Jousset  ||  has  found  tubercle  bacilli 

*  Jousset :  Quoted  by  Souques. 

t  Micheli  and  Mattirolo:  Wiener  klin.  WoHien.,  1900,  S.  56.  Epitome,  Brit. 
Med.  Jour.,  1900,  vol.  i,  No.  402. 

t  Barjon  et  Henry:  Lyon  Medical,  June  10,  1S9S. 

§  Fernet:  Bull,  de  la  Soc.  Med.  des  Hop.,  June  22,  1900,  p.  7S1. 

II  Jou.sset:  Archiv  de  M^d.  experiment.  et.d'anat.  path.,  tome  xv,  p.  289,  1903. 


246  DISEASES   OF  THE   LIVER. 

in  many  cases  thought  to  be  cirrhosis,  which  is  quite  in  accord  with  the 
comparatively  frequent  incident  of  tuberculous  peritonitis  in  cirrhosis. 

M.  Abbott  *  found  a  colon  bacillus,  of  the  same  type  as  Adami's  minute  diplo- 
coccus,  in  the  ascitic  fluid  of  three  cases  of  cirrhosis.  In  one  instance,  where  there 
was  chronic  peritonitis  as  well  as  hepatic  cirrhosis,  this  micro-organism  was  isolated 
from  three  tappings  during  life. 

Tension  of  Ascitic  Fluid.- — There  may  be  a  positive  pressure  inside 
the  abdomen  in  ascites,  as  shown  by  the  upward  displacement  of  the  dia- 
phragm. 

Pitres  t  has  measured  this  manometricaUy,  and  finds  that  it  may  vary  between 
30  and  6  miUimetres  of  mercury,  the  average  positive  pressure  being  about  12  miUi- 
metres. 

This  positive  intra-abdominal  pressure,  of  course,  varies  with  respira- 
tion and  is  associated  with  increased  tension  in  the  portal  vein  and  low 
arterial  pressure.     (Gilbert  et  Weill.  J) 

Physical  Signs. — The  abdomen  is  greatly  enlarged;  its  girth  may 
be  fifty  inches  or  even  more.  The  enlargement  is  uniform,  but  is  perhaps 
more  marked  antero-posteriorly  than  laterally.  The  parietes  are 
stretched  and  the  skin  often  shows  the  effects  of  distension  in  linese 
albicantes,  which  become  especially  visible  after  paracentesis.  The 
abdominal  muscles  become  lax  and  atrophied  and  the  umbilicus  may 
become  everted  and  project  like  a  tense  thin- walled  bladder;  it  may 
become  ulcerated,  and  has  been  known  to  burst.  The  veins  over  the 
umbilicus  are  sometimes  very  prominent.  The  loss  of  tone  in  the  ab- 
dominal parietes  allows  flatulent  distension  to  occur,  especially  after 
the  intra-abdominal  pressure  has  been  reduced  by  paracentesis.  The 
costal  margins  are  pushed  forwards  and  the  ensiform  cartilage  may  be 
carried  upwards  and  forwards.  The  subcutaneous  veins  of  the  ab- 
dominal walls  become  prominent  and  enlarged.  There  are  two  sets  of 
veins:  (a)  Those  around  the  umbilicus.  This  is  part  of  the  compensatory 
anastomosis  between  the  veins  of  the  abdominal  wall  and  the  parumbilical 
veins  in  the  falciform  ligament.  To  a  dilated  and  varicose  condition 
of  the  veins  around  the  umbilicus  the  term  cirsomphalos  has  been  applied. 
(b)  The  veins  running  up  from  the  middle  of  the  groin  (the  superficial 
and  deep  epigastric  veins)  towards  the  middle  of  the  costal  arch  (superior 
epigastric  and  long  thoracic  veins).  The  dilatation  of  these  veins  points 
to  obstruction  to  the  passage  of  blood  through  the  inferior  vena  cava. 
A  large  ascitic  effusion  may,  by  increasing  the  intra-abdominal  pressure, 
seriously  interfere  with  the  return  of  blood  from  the  lower  extremities, 
and  so  lead  to  opening  up  of  this  anastomotic  channel. 

The  ascitic  fluid  presses  the  diaphragm  up  and  diminishes  the  capacity 
of  the  thorax.  The  heart  may  thus  be  displaced  upwards  so  that  its 
apex-beat  is  in  the  third  interspace.  This  displacement  may  be  asso- 
ciated with  a  systolic  murmur  over  the  pulmonary  artery,  due  to  twisting 

*  Abbott,  Maude:  Journal  of  Path,  and  Bacterioh,  vol.  vi,  p.  315. 

t  Pitres:  Soc.  de  biolog.,  July  22,  1899,  p.  674. 

t  Gilbert  et  Weill :  Soc.  de  biolog.,  June,  1899,  p.  511. 


CIRRHOSIS    OF    THE    LIVER.  247 

or  kinking  of  its  trunk.     When  the  displacement  is  corrected  by  tapping, 
this  murmur  disappears. 

The  hver  dulness  is  displaced  upwards  into  the  thorax  and  anteriorly 
may  reach  to  the  fourth,  third,  or  even  second  rib,  while  posteriorly  the 
resonance  over  the  bases  of  both  lungs  is  also  encroached  upon.  If  there 
is  dulness  over  the  lower  lobe  of  the  right  lung  alone,  the  question  arises 
whether  this  is  due  solely  to  upward  displacement  of  the  liver  and  col- 
lapse of  the  lung  or  whether  there  is  not,  as  is  often  the  case  (tide  p.  282), 
an  effusion  into  the  right  pleural  cavity.  If  the  patient  be  directed  to- 
take  a  deep  breath,  the  dulness  will  remain  unaltered  if  there  is  an  effu- 
sion, but  will  diminish  somewhat  if  due  solely  to  the  liver;  in  addition, 
in  pleural  effusion  the  dulness  is  higher  in  the  axilla,  while  the  dulness 
due  to  the  liver  is  more  marked  behind. 

In  women,  the  uterus  is  pressed  forwards  by  the  fluid  in  Douglas' 
pouch,  and  depressed,  and  may  thus  become  prolapsed. 

The  fluid  collects  in  the  flanks  and  gives  rise  to  a  dull  note  on  percus- 
sion. In  order  to  distinguish  ascites  from  faecal  distension  of  the  colon 
the  patient  should  be  turned  over,  when  the  note  will  become  resonant; 
this  shifting  dulness  is  proof  of  free  fluid  in  the  peritoneal  cavity.  It 
should  be  pointed  out  that  in  a  certain  proportion  of  cases  of  ascites 
there  is  resonance  in  one  or  both  flanks,  due  to  gaseous  distension  of  the 
colon.  The  absence  of  dulness  in  the  flanks,  therefore,  must  not  be  taken 
as  absolute  evidence  against  ascites  and  in  favour  of  an  ovarian  cyst. 

After  collecting  in  the  flanks  the  fluid  rises  out  of  the  pelvis  and  gives 
rise  to  a  dull  note  on  percussion.  This  dull  area  gradually  increases  in 
extent  and  approaches  the  umbilicus.  The  stomach  and  intestines  are 
floated  upwards  against  the  abdominal  parietes  in  the  middle  line  be- 
tween the  umbilicus  and  the  ensiform  cartilage.  The  area  of  resonance 
eventually  roughly  corresponds  with  that  of  the  epigastric  region.  Chronic 
peritonitis  may  be  combined  with  cirrhosis,  and  if  well  marked  may 
lead  to  such  retraction  of  the  mesentery  that  the  intestines,  being  more 
or  less  tethered  to  the  spine,  are  unable  to  reach  the  anterior  abdominal 
wall ;  in  such  cases  there  may  be  complete  absence  of  resonance  over  the 
front  of  the  abdomen. 

When  there  is  more  than  a  small  quantity  of  ascitic  fluid  in  the  ab- 
domen a  thrill  is  readily  produced  by  flipping  the  abdominal  wall  in  one 
flank  with  the  flnger;  a  distinct  impulse  is  then  felt  by  the  other  hand 
laid  flat  on  the  skin  of  the  opposite  side.  In  order  to  prevent  the  impulse 
from  being  transiTiitted  merely  through  the  abdominal  walls,  an  assistant 
should  place  his  hand  or  a  piece  of  cardboard  on  the  linea  alba  in  the 
long  axis  of  the  body.  When  the  abdominal  wall  is  laden  with  fat  or 
swollen  from  subcutaneous  oedema,  the  precaution  is  especially  neces- 
sary. Wlien  old  peritoneal  adhesions  are  present,  the  ascitic  effusion 
will  very  probably  become  encysted.  The  physical  signs  ma}^  then  re- 
semble those  of  a  fixed  cyst,  and  are  very  difficult  to  interpret  correctly. 
Encysted  ascites  is,  however,  rarely  seen  in  connexion  with  hepatic  cir- 
rhosis. 

When  there  is  free  fluid  in  the  peritoneal  cavity,  it  is  found  under 


248  DISEASES    OF  THE   LIVER. 

certain  conditions  that  if  the  hand  is  placed  fiat  over  the  liver  and  a 
sudden  sharp  flexion  of  the  fingers  made,  a  sensation  of  displacement 
of  fluid  is  produced  and  the  finger-tips  come  in  contact  with  the  firm 
liver.  This  sign — ''dipping  for  the  liver" — often  cannot  be  obtained. 
It  depends  on  the  presence  of  fluid  between  the  liver  and  the  abdominal 
wall.  Hence  adhesions  between  the  liver  and  the  parietes,  or  the  fact 
that  the  liver  is  in  immediate  contact  with  the  abdominal  wall,  prevents 
this  manifestation  of  ascites. 

Symptoms  and  Effects  of  Ascites. — There  is  a  feeling  of  tightness 
and  discomfort  in  the  tense  and  stretched  abdominal  walls,  which,  like 
other  bad  effects  of  ascites,  are  due  to  the  pressure  exerted  by  the  fluid. 
The  upward  displacement  of  the  diaphragm  gives  rise  to  collapse  of  the 
lower  lobes  of  the  lungs,  and  so  to  dyspnoea,  and  even  to  orthopnoea  of 
slight  degree.  There  is  often  some  bronchitis,  and  in  rare  instances 
hsemoptysis  may  result  from  the  engorged  and  collapsed  lung.  In  cases 
where,  with  increasing  ascites,  signs  of  oedema  of  the  lower  parts  of  the 
lungs — rales — develop,  the  abdomen  should  be  tapped  without  delay. 

The  upward  displacement  of  the  heart  may  be  accompanied  by 
irregularity,  palpitation,  or  faintness.  The  pressure  of  ascites  on  the 
kidneys  and  their  vessels  may  help  to  diminish  the  excretion  of  urine 
and  possibly  to  produce  albuminuria,  but  the  diminished  amount  of 
urine  is  chiefly  due  to  the  low  arterial  pressure.  (Edema  of  the  legs 
may  be  accelerated  by  the  pressure  of  the  peritoneal  effusion  on  the 
inferior  vena  cava,  but  it  is  not  solely  due  to  this  mechanical  cause, 
inasmuch  as  oedema  of  the  feet  may  precede  the  appearance  of  ascites, 
or  indeed  occur  independently.  As  is  pointed  out  elsewhere,  toxaemia 
plays  an  important  part  in  the  production  of  oedema  of  the  feet. 

If  ascites  is  allowed  to  become  very  excessive,  the  umbilicus,  which 
has  become  everted  and  thin,  may  burst ;  this  spontaneous  discharge  has 
also  been  known  to  take  place  through  the  cicatrix  of  an  umbilical  hernia. 
(Merklem  and  Gougelet.*)  Such  an  event  should  never  be  allowed  to 
occur;  not  only  is  the  extreme  distension  ver}^  harmful,  but  the  rupture 
of  the  abdominal  wall  is  very  likely  to  be  the  means  of  introducing  in- 
fection, and  so  setting  up  fatal  peritonitis.  Most  of  the  recorded  cases 
occurred  years  ago,  when  paracentesis  was  postponed  as  long  as  possible. 

Differentiation  of  Ascites  from  Other  Abdominal  Conditions. — 
There  are  a  very  fair  number  of  conditions  that  have  at  one  time  or 
another  simulated  ascites.  The  most  likely  to  imitate  ascites  are  ovarian 
cysts,  large  peritoneal  lipomata,  and  encysted  peritonitis,  of  which  the 
first  is  the  only  frequent  cause  of  error. 

1.  A  large,  thin-walled  ovarian  or  parovarian  cyst,  if  so  large  as  to 
nearly  fill  a  great  part  of  the  abdomen,  may  give  rise  to  great  difficulties 
in  diagnosis.  In  the  case  of  an  ovarian  cyst  the  history  may  show  that 
the  swelling  was  definitely  noticed  to  begin  in  one  situation,  that  it  arose 
out  of  the  pelvis  and  then  spread  upwards.  The  outline  of  the  cyst 
may  be  felt  or  may  be  made  out  on  deep  inspiration.  In  a  doubtful 
case  a  vaginal  examination  may  reveal  a  cyst  with  pelvic  attachments. 
*  Merklem  and  Gougelet:  Bull.  Soc.  Med.  des  Hop.,  July  19,  1901,  p.  952. 


CIRRHOSIS    OF    THE    LIVER.  249 

The  abdomen  is  prominent  in  an  anteroposterior  direction,  while  in 
simple  ascites  the  bulging  is  also  in  a  lateral  direction. 

The  diilness  is  in  or  near  the  middle  line  of  the  abdomen  and  not  in 
the  flanks;  but,  as  already  pointed  out,  resonance  in  the  loin  may  persist 
in  ascites.  The  maximum  abdominal  girth  is  below  the  umbilicus,  while 
in  ascites  it  is  at  or  above  this  level.  In  ascites  the  umbilicus  is  in  its 
normal  position,  viz.,  one  inch  nearer  to  the  pubes  than  to  the  ensiform 
cartilage,  while  with  an  ovarian  cyst  this  relation  may  be  greatly  altered 
in  the  opposite  direction.  When  an  ovarian  cyst  is  situated  on  either 
side  of  the  middle  line,  it  may  displace  the  umbilicus,  so  that  it  is  nearer 
one  anterior  superior  spine  than  the  other.  This  displacement  may 
only  be  revealed  by  careful  measurement,  and  not  be  manifest  on  mere 
inspection. 

In  ovarian  cysts  the  thrill  may  be  absent,  and  when  present  is  less 
marked  than  in  ascites.  There  is  little  constitutional  disturbance  in 
ovarian  cysts,  the  ill  effects  being  almost  entirely  due  to  mechanical 
pressure.  When  an  ovarian  cyst,  as  is  sometimes  the  case,  is  complicated 
by  ascites,  the  diagnosis  is  extremely  difficult.  Rupture  of  the  cyst  with 
extravasation  of  its  contents  into  the  peritoneal  cavity  may  occur  spon- 
taneoush^  in  thin-walled  cystadenomata  and  parovarian  cysts,  or  from 
traumatism.  If  the  fluid  is  non-irritating,  it  is  absorbed,  with  the  result 
that  polyuria  follows;  but  if  irritating,  peritonitis  is  set  up.  A  rare  event 
is  fatal  intraperitoneal  haemorrhage.* 

2.  Solid  or  Semisolid  Abdominal  Tum,ors  Simulating  Ascites. — Fatty, 
fibro-fatty,  and  myxolipomatous  tumors,  though  comparatively  rare, 
may,  when  they  grow  to  a  considerable  size, — and  some  of  them  have 
weighed  as  much  as  40  pounds, — very  closely  imitate  ascites.  In  fact, 
many  of  the  recorded  examples  have  been  tapped  fruitlessly,  and  several 
of  them  more  than  once.  Of  the  fatty  tumors,  of  which  Aclami  f  has 
collected  42  examples,  about  one-third  arise  from  the  fat  around  the 
kidneys;  the  remainder  take  origin  from  the  retroperitoneal  and  other 
tissues.  The  tumors,  whether  originally  fatty  or  fibrous,  are  prone  to 
become  oedematous  and  undergo  myxomatous  degeneration  and  so 
readily  fluctuate. 

Diffuse  colloid  carcinoma  of  the  peritoneum  is  very  rare;  it  may  give 
rise  to  great'  enlargement  of  the  abdomen  and  to  clulness  on  percussion, 
but  fluctuation  and  thrill  are  not  present  unless  there  is  concomitant 
ascites.  In  some  cases  there  is  no  difficulty  in  feeling  definite  tumors, 
and  then  there  is  no  resemblance  to  ascites. 

Pye  Smith  %  refers  to  a  case  of  colloid  carcinoma  involving  the  peritoneum 
where  tapping  was  performed  thirty-six  times.  Sometimes  colloid  material  blocked 
the  cannula. 

Encysted  peritonitis  and  the  localized  tu])orculous  peritonitis  in  the 
lower  and  front  portions  of  the  abdomen^  (Tait's  allantoic  cysts)  differ 

*  Kelly,  H.  A. :  Operative  riyntpcology,  vol.  ii,  p.  253. 
t  Adami:  Montreal  Medical  Journal,  .Jan.,  Fell.,  1S97 
j  Pye  Smith:  Trans.  Path.  Soc,  vol.  xliv,  p.  117. 
§  Doran  A.:  Medico-chirurg.  Trans.,  aoI.  Iwxi,  p.  320. 


250  DISEASES   OF   THE   LIVER. 

in  the  extent  of  the  peritoneal  cavity  involved  and  in  the  fact  that  the 
dulness  due  to  the  effused  fluid  does  not  alter  with  changes  in  the  posi- 
tion of  the  patient. 

Hydatid  Cysts. — Murchison  describes  an  enormous  cyst  starting  from 
the  liver  and  passing  through  the  foramen  of  Winslow  into  the  general 
peritoneal  cavity,  which  it  almost  filled.  In  its  fully  developed  or  latest 
stage  it  resembled  ascites,  but  the  history  showed  that  the  abdominal 
swelling  was  at  first  localized  to  the  right  side. 

Various  abdominal  cysts,  such  as  pancreatic,  omental,  chylous, 
urachal,  mesenteric  cysts,  are  comparatively  seldom  so  large  as  to 
resemble  ascites.  A  large  pyonephrosis  or  hydronephrosis  is  so  uni- 
lateral that  it  should  not  be  mistaken  for  ascites.  In  very  exceptional 
instances  a  dilated  stomach,  a  dilated  gall-bladder,  and  a  very  large 
hepatic  abscess  have  been  diagnosed  as  ascites.  Cases  of  large  hepatic 
abscesses  which  were  at  first  thought  to  be  ascites  have  been  recorded 
by  Powell  *  and  Hatch.f 

From  a  Pregnant  Uterus  with  Hydrops  Amnii. — The  outline  of  the 
enlarged  uterus  may  be  made  out  by  palpation  through  the  abdominal 
walls.  Other  signs  of  pregnancy,  such  as  mammary  enlargement  and 
engorgement,  soft  and  patulous  os  uteri,  enlarged  uterus,  should  be 
looked  for. 

Obesity. — When  the  abdominal  walls  are  laden  with  fat,  the  detection 
of  a  small  amount  of  ascitic  fluid  is  difficult  and  often  impossible.  On 
the  other  hand,  a  feeling  of  semifluctuation  may  be  obtained  through 
the  pendulous  fatty  walls  and  suggest  ascites.  To  control  this  the  hand 
of  an  assistant  should  be  placed  with  the  ulnar  side  dowmwards  on  the 
abdominal  wall  between  the  two  hands  of  the  observer  so  as  to  prevent 
any  fluctuation  from  being  conducted  through  the  parietes.  Inspection 
alone  should  assist  in  the  diagnosis.  When  there  is  much  fat  in  the 
abdominal  parietes,  the  umbilicus  is  buried,  while  in  ascites  the  umbUicus 
tends  to  be  everted. 

Diagnosis  of  Ascites  Due  to  Cirrhosis  from  that  Due  to  Other 
Causes. — Under  the  following  heads  attention  will  chiefly  be  paid  to 
the  main  points  that  are  in  favour  of  the  various  conditions  which  may 
imitate  cirrhosis  by  inducing  ascites. 

Acute  peritonitis  can  hardly  be  confounded  with  the  ascites  due  to 
cirrhosis,  for  the  onset  is  sudden,  the  constitutional  symptoms  are  promi- 
nent, and  the  abdominal  distension  is  due  to  paralytic  dilatation  of  the 
intestines  with  gas  rather  than  to  the  quantity  of  fluid.  It  should  be 
mentioned,  however,  that  ascites  may  sometimes  come  on  rapidly  in 
the  course  of  cirrhosis,  especially  when  complicated  by  portal  thrombosis. 
Unlikely  as  it  would  appear,  sudden  ascites  developing  in  a  case  of  alco- 
holic cirrhosis  in  which  there  was  subacute  gastritis  has  simulated  in- 
testinal obstruction.     {Vide  p.  288.) 

The  ascites  due  to  the  various  forms  of  chronic  peritonitis  is  extremely 
likely  to  be  mistaken  for  that  of  cirrhosis.  Chronic  peritonitis  and  uni- 
versal perihepatitis  {vide  p.   164)  frequently  cause  ascites,  usually  in 

*  Indian  Med.  Gaz.,  Feb.,  1898.  t  Ibid.,  Aug.,  1898. 


CIRRHOSIS    OF   THE    LIVER.  251 

association  either  with  adherent  pericardium  or  with  arteriosclerosis 
and  granular  kidney.  The  physical  signs  of  these  conditions  should 
therefore  be  looked  for.  In  a  doubtful  case  albuminuria  is  there- 
fore against  the  existence  of  cirrhosis  as  a  primary  cause.  In  chronic 
peritonitis  the  ascites  recurs  again  and  again  after  tapping;  cases  are 
on  record  where  the  abdomen  has  been  tapped  fifty  or  even  a  hundred 
times.  This  is  the  most  reliable  criterion  in  distinguishing  chronic  peri- 
tonitis from  cirrhosis.  Enlargement  of  the  spleen,  which  is  compara- 
tively frequent  in  cirrhosis,  is  not  a  prominent  feature  in  chronic  peri- 
tonitis, unless  there  is  some  complication,  such  as  lardaceous  disease. 
Hsematemesis  hardly  ever  occurs  in  chronic  peritonitis;  hence  the  asso- 
ciation of  hsematemesis  and  ascites  points  to  cirrhosis.  In  cases  where 
hgematemesis  is  associated  with  frequently  recurring  ascites  chronic 
peritonitis  is  probably  complicated  by  some  other  condition,  such  as 
gastric  ulcer  or  cirrhosis. 

Tuberculous  peritonitis  may  supervene  as  a  secondary  infection  in  the 
course  of  cirrhosis,  and  is  then  very  likely  to  be  regarded  as  simple 
ascites.  Thus  in  121  cases  of  common  cirrhosis  in  adults  Kelynack 
found  that  active  peritoneal  tuberculosis  was  in  progress  in  12.  The 
primary  lesion  here  is  cirrhosis,  which  disposes  the  peritoneum  to  tuber- 
culous infection.  In  these  cases  the  liver  is  markedly  cirrhosed,  while 
the  peritonitis  is  of  more  recent  date.  In  cases  of  tuberculous  peritonitis 
a  slight  secondary  hepatic  fibrosis  is  sometimes  seen,  but  is  microscopic 
rather  than  macroscopic.  Tuberculous  peritonitis  alone  is  commoner 
in  children  than  in  adults,  while  cirrhosis  is  rare  in  children. 

The  mistake  that  has  often  occurred  is  to  do  laparotomy  on  a  child 
with  cirrhosis  and  ascites  in  the  belief  that  it  is  tuberculous  peritonitis. 
If  such  a  thing  occurs,  it  would  be  advisable  to  take  the  opportunity 
of  uniting  the  liver  and  great  omentum  to  the  abdominal  wall  so  as  to 
lead  to  vascular  adhesions.     {Vide  p.  257.) 

Tuberculous  peritonitis  in  adults,  except  when  secondary  to  cirrhosis, 
is  most  often  seen  in  women,  and  often  spreads  from  the  uterine  ap- 
pendages. Search  should  be  made  for  evidence  of  tuberculosis  elsewhere. 
The  following  points  are  in  favour  of  tuberculous  peritonitis:  abdominal 
pain  and  tenderness,  especially  in  the  lower  part  of  the  abdomen  and 
about  the  right  iliac  fossa;  pain  on  micturition;  fever;  palpable,  enlarged 
glands  in  the  abdomen  or  groin,  and  a  moderate  degree  of  effusion;  a 
hard  cord  due  to  the  roUed-up  transverse  colon;  induration  around  the 
umbilicus,  redness  of  the  skin,  and  evidence  of  a  small  abscess  in  this 
situation.  When  drawn  off,  the  fluid  is  more  turbid  and  is  often  sero- 
purulent,  of  a  higher  specific  gravity  (1020  instead  of  1010),  and  richer 
in  albumin  than  in  cirrhosis.  Ordinary  examination  for  tubercle  bacilli 
is  often  negative,  but  injection  into  guinea-pigs  gives  rise  to  tuberculosis. 
It  is  probable  that  the  method  of  inoscopy,*  or  bacterial  examination 
of  the  clot  formed  in  the  fluid,  will  give  positive  results  in  cases  where 
ordinary  methods  fail. 

In  ascites  due  to  multiple  nodules  of  malignant  disease  in  the  peritoneiuu 
*  Jousset:  Archiv  de  Mud.  experiment,  et  d'anat.  path.,  tome  x^-,  p.  289. 


252  DISEASES    OF   THE    LIVER. 

a  priman^  source  should  be  manifest  in  the  stomach  (symptoms  of 
dyspepsia,  pyloric  obstruction,  absence  of  HCl  in  vomit),  in  the  rectum, 
and  in  women  in  the  uterine  organs.  The  umbilicus  may  be  hard  and 
infiltrated  with  growth,  and  sometimes  small  subcutaneous  tumors  can 
be  felt  in  the  line  of  the  falciform  ligament  or  elsewhere  in  the  abdomen. 
It  must  be  remembered  that  small  masses  of  fat  may  very  closely  imitate 
these  minute  secondar\^  groT\i:hs.  In  malignant  disease  there  is  more 
emaciation  and  more  frequently  pigmentation  of  the  face  than  in  cir- 
rhosis. In  some  instances  of  malignant  disease  in  the  abdomen  there 
is  the  peculiar  warty  and  pigmented  condition  of  the  skin  known  as 
"acanthosis  nigricans."  The  spleen  is  not  enlarged  and  there  is  no 
histor}^  of  hsematemesis.  Sometimes  glands  in  the  groin  may  be  en- 
larged, and  occasionally  multiple  subcutaneous  tumors  are  present. 

In  malignant  disease  of  the  liver  the  presence  of  deep  jaundice  together 
A^dth  ascites,  the  enlargement  and  irregularity  of  the  liver,  the  progressive 
hepatic  enlargement  and  more  rapid  emaciation,  help  to  differentiate 
it  from  ascites  due  to  cirrhosis.  Other  points  in  favour  of  malignant 
disease  are  evidence  of  gro\\i;h  elsewhere,  induration  of  the  umbilicus,  and 
absence  of  splenic  enlargement.  In  cases  which  come  under  observ^ation 
at  a  late  stage  ^Aih  ascites  it  is  often  impossible  to  determine  w^hether 
there  is  cirrhosis  or  malignant  disease  of  the  liver  until  the  abdomen  has 
been  tajDped.     A  large  nodular  liver  points  to  new-growth. 

Syphilitic  disease  of  the  liver  may  give  rise  to  ascites.  The  presence 
of  syphilitic  lesions  elsewhere  should  always  be  the  signal  for  a  course 
of  antis}q3hilitic  treatment,  which  may  clear  up  the  diagnosis.  When 
enlarged  from  gummatous  or  lardaceous  change,  or  from  both  combined, 
the  liver  is  firm  and  may  be  irregular,  and  is  not  unlikely  to  be  mistaken 
for  malignant  disease. 

Lardaceous  disease  of  the  liver  does  not  often  give  rise  to  ascites.  The 
following  case  of  lardaceous  liver  closely  imitated  cirrhosis : 

A  -n-oman  aged  forty-seven  under  my  care  in  St.  George's  Hospital,  June-July, 
1900,  had  the  facial  aspect  of  cirrhosis;  there  were  signs  of  chronic  pulmonarj^  tuber- 
culosis at  both  apices,  oedema  of  the  feet  which  preceded  by  two  weeks  the  onset 
of  ascites,  and  albuminuria.  There  was  a  history  of  hgematemesis  -^^■hich  in  the  light  of 
the  autops}'  was  probably  hsemoptysis.  There  was  extreme  ascites  which  required 
tapping  twice;  the  liver  and  spleen  could  not  be  felt.  The  patient  was  thought  to 
have  cirrhosis.  Death  took  place  from  asthenia,  the  patient  being  semicomatose. 
The  autopsy  showed  lardaceous  disease  of  the  liver  (.53  ounces)  and  kidnej\s,  which 
was  accounted  for  by  chronic  pulmonary  tuberculosis,  with  .3  or  4  vomica?  in  both 
upper  lobes.  There  were  slight  thickening  of  the  capsule  of  the  liver  and  opacity  of 
the  peritoneum,  but  not  enough  chronic  peritonitis  to  accomit  for  the  ascites. 
There  was  no  cirrhosis  of  the  liver. 

The  history  of  past  suppuration  or  of  SA^ihilis,  evidence  pointing  to 
lardaceous  disease  of  the  kidneys  (albuminuria)  or  of  the  intestines  (diar- 
rhoea), are  important  points  in  making  a  diagnosis. 

Throvihosis  of  the  Portal  Vein. — This  is  a  rare  condition,  but  when  it 
does  occur  is  associated  with  portal  cirrhosis  of  the  liver  in  about  37  per 
cent,  of  the  cases.  T\Tien  the  trunk  of  the  portal  vein  is  affected,  ascites, 
if  not  already  present,  rapidly  de^'elops.     The  spleen  enlarges  from  oli- 


CIRRHOSIS    OF    THE    LIVER.  253 

struction  of  the  splenic  vein  and  haematemesis  may  occur.  The  severity 
of  the  symptoms  and  their  onset  in  a  person  whose  past  history  shows 
neither  cause  for  nor  evidence  of  cirrhosis  would  be  in  favour  of  primary 
thrombosis  of  the  portal  vein.  But  it  will  always  be  difficult  to  be  sure 
that  the  case  is  not  one  in  which  cirrhosis  has  remained  latent. 

The  difficulty  or  impossibility  of  a  correct  diagnosis  in  some  cases  of 
portal  thrombosis  supervening  in  the  course  of  cirrhosis  is  illustrated  in 
the  following  case: 

A  man  aged  fifty-six  in  a  state  of  great  weakness  and  considerable  emaciation 
was  admitted  under  me  at  St.  George's  Hospital  on  January  28,  1902,  complaining  of 
"dropsj^,  stoppage  of  the  bowels,  and  difficulty  in  passing  water."  He  had  noticed 
oedema  of  the  feet  five  weeks  before ;  this  was  followed  by  constipation  and  difficulty 
in  passing  water.  He  had  been  quite  a  moderate  consumer  of  beer,  and  denied 
syphilis.  He  was  fomid  to  have  marked  ascites;  nothing  abnormal  could  be 
felt  in  the  abdomen  and  he  was  thought  to  be  probably  the  subject  of  malignant 
abdominal  disease.  Almost  directly  after  admission  he  began  to  wander  in  his 
mind,  and  shortly  afterwards  became  moribimd,  dying  about  thirty-six  hours  after 
admission.  At  the  autopsy  there  were  chronic  peritonitis,  marked  portal  cirrhosis, 
and  thrombosis  of  the  portal  vein ;  the  liver  weighed  4  pounds  and  the  spleen  4  ounces. 

Ascites  from  ovarian  papillomata  may  recur  very  frequently,  and  is 
thus  different  from  the  ascites  of  uncomplicated  cirrhosis.  The  diag- 
nosis can  be  clinched  by  vaginal  or  rectal  examination  and  the  detection 
of  irregular  masses  of  growth  choking  up  the  pelvis,  or  by  the  recognition 
of  pieces  of  the  characteristic  villous  growth  in  fluid  withdrawn  from  the 
abdomen. 

Dr.  Pye  Smith  *  has  recorded  a  remarkable  case  of  papillomatous  tumors  of 
both  ovaries  which  gave  rise  to  ascites  in  a  woman  aged  thirty-five  lasting  nine 
years  and  necessitating  299  tappings.  At  the  autopsj^  there  were  numerous  im- 
plantation growths  over  the  parietal  peritoneum. 

Ascites  due  to  backivard  pressure  of  tricuspid  regurgitation,  etc.,  should 
be  recognised  by  examination  of  the  heart  and  the  recognition  of  mitral 
or  obstructive  lung  disease — emphysema,  chronic  interstitial  pneumonia, 
or  pneumonokoniosis.  In  some  cases  of  cirrhosis  failure  of  the  heart, 
such  as  may  occur  from  alcoholism,  may  induce  ascites,  so  that  cirrhosis 
and  ascites  are  associated,  though  not  necessarily  related,  as  cause  and 
effect.  In  such  cases  it  is  difficult  to  decide  their  relationship  until  the 
alcoholic  dilatation  of  the  heart  has  been  successfully  treated. 

In  renal  disease  ascites  is  part  of  the  general  dropsy  which  typically 
affects  the  face.  The  character  of  the  urine  and  the  cardiovascular 
changes  proper  to  renal  disease  should  prevent  any  mistake  in  diagnosis. 
As  pointed  out  elsewhere  (Associated  Lesions,  p.  223),  renal  disease  may 
coincide  with  portal  cirrhosis. 

In  splenic  ancemia  of  adults,  which  is  a  distinctl}'  rare  disease,  ascites 
very  occasionally  a])])ears  before  the  terminal  cirrhosis  of  the  liver,  which 
is  known  as  Banti's  disease,  has  developed,  as  shown  by  postmortem 
examination  of  cases  of  uncomplicated  splenic  anaemia.  Inasmuch  as 
periodic  haematemesis  also  occurs  in  that  disease,  the  resemblance  to 
cirrhosis  when  ascites  develops  might  be  thought  to  l)e  very  close.  Clin- 
*  Pye  Smith  :  Trans.  Path.  Soc,  vol.  xliv,  p.  111. 


254  DISEASES   OF  THE   LIVER. 

ically  the  anaemia  and  splenic  enlargement  are  so  much  greater  in  splenic 
anaemia  that  ordinary  cirrhosis  is  only  likely  to  be  diagnosed  by  those 
who  are  not  familiar  with  the  fact  that  ascites  and  periodic  attacks  of 
haematemesis  may  occur  in  splenic  anaemia. 

Prognosis  of  Ascites. — The  prognosis  of  ascites  due  to  cirrhosis  is 
very  bad;  as  a  rule,  death  fohows  within  a  short  time  of  its  onset — - 
usually  within  two  months,  and  sometimes  much  sooner. 

A  distinction  has  rightly  been  drawn,  more  especially  by  Hale  White  * 
and  Campbell  Thomson,!  between  ascites  due  to  cirrhosis  in  which  the 
prognosis  is  of  the  gloomiest  character,  and  ascites  associated  with  cir- 
rhosis, but  due  to  some  other  cause,  such  as  chronic  peritonitis.  In 
ascites  associated  with  chronic  peritonitis  tapping  may  be  required  fre- 
quently, and  occasionaUy  recovery  may  occur,  while  in  ascites  due  to 
cirrhosis  tapping  is  seldom  required  more  than  once,  and  is  soon  foUowed 
by  death. 

Since  oedema  of  the  feet  in  the  course  of  cirrhosis  is  a  sign  of  general 
toxaemia,  the  prognosis  in  a  case  of  cirrhosis  with  ascites  and  oedema  of 
the  feet  is  much  worse  than  in  cirrhosis  with  ascites  alone,  inasmuch  as 
the  latter  may  be  a  case  of  cirrhosis  associated  with,  ascites  clue  to  some 
other  factor,  such  as  chronic  peritonitis.  The  presence  or  absence  of 
oedema  of  the  feet  may  thus  be  useful  in  determining  whether,  in  any 
case  of  ascites  due  to  cirrhosis,  the  case  is  likely  to  terminate  rapidly, 
or  whether  several  tappings  may  be  required  with  a  possible,  though 
frail,  chance  of  recovery. 

In  the  section  on  the  general  prognosis  in  port.al  cirrhosis  the  prog- 
nosis of  ascites  is  referred  to  again. 

The  Treatment  of  Ascites. — The  treatment  of  ascites  may  be 
divided  into : 

(I)  By  paracentesis. 

(II)  By  the  operation  for  producing  vascular  adhesions  around  the 
liver. 

(Ill)  By  diuretics  and  purgatives. 

The  first  and  last  of  these  methods  are  merely  directed  to  the  removal 
of  the  ascitic  fluid.  The  production  of  artificial  Avascular  adhesions  is 
intended  to  prevent  the  peritoneal  exudation,  and  is  therefore  a  more 
radical  method. 

Advisability  of  Performing  Paracentesis. — Formerly  paracentesis  of 
the  abdomen  was  postponed  as  long  as  possible,  partly  because  infection 
of  the  peritoneum  sometimes  followed  tapping,  and  partly  because  the 
patient  often  went  down-hill  extremely  rapidly  after  the  withdrawal  of 
the  ascitic  effusion.  With  antiseptic  precautions  the  likelihood  of  peri- 
tonitis resulting  is  minimised,  while  the  occurrence  of  death  comparatively 
shortly  after  paracentesis  must  be  considered  to  be  due  to  the  natural 
course  of  the  disease,  and  not  to  the  removal  of  ascites. 

Other  reasons  given  for  only  adopting  paracentesis  as  a  last  resource 
were  that  (a)  the  removal  of  fluid  entailed  the  loss  of  a  considerable 

*  Hale  "White :  Guy's  Hosp.  Reports,  vol.  xlix,  1892. 

t  Thomson,  Campbell:  Medico-Chirurg.  Trans.,  vol.  Ixxxiv,  p.  251. 


CIRRHOSIS    OF   THE    LIVER.  255 

amount  of  albumin,  an  argument  that  might  also  be  used  against  opening 
an  abscess  (Murchison),  and  (6)  that  the  intra-abdominal  pressure  of 
ascites  prevented  further  transudation  of  fluid  (Frerichs).  Opinion  has 
changed,  and  at  the  present  time  tapping  is  performed  as  soon  as  it  is 
required  in  order  to  prevent  the  bad  effects  of  excessive  ascites.*  It  is 
a  much  more  effective  method  than  purgation  or  the  attempt  to  drain 
off  the  fluid  by  the  kidneys  and  does  not  tend  to  weaken  the  patient's 
strength  as  violent  purging  does. 

Bad  Effects  of  Excessive  Ascites. — ^The  results  of  ascites  have  been 
already  referred  to ;  they  are  largely  mechanical  in  the  first  instance  and 
due  to  pressure  on  the  abdominal  and  thoracic  viscera;  the  functions  of 
these  organs  are  interfered  with  and  are  therefore  imperfectly  performed. 
The  renal  veins  are  pressed  upon  and  the  urinary  excretion  impeded, 
much  in  the  same  way  as  in  the  backward  pressure  of  heart  disease.  It 
is  probable  that  this  mechanical  venous  engorgement  of  the  kidneys, 
due  to  the  pressure  exerted  by  the  ascitic  effusion  on  the  renal  veins, 
accounts  for  the  fact  that  diuretics  often  fail  to  remove  ascites  at  first, 
though  they  may  be  more  successful  in  producing  diuresis  when  given 
after  paracentesis  has  been  performed. 

Indications  for  Paracentesis. — When  the  patient  complains  of  marked 
discomfort,  the  abdomen  should  be  tapped,  but  apart  from  this  there  are 
other  conditions,  such  as  diminished  amount  of  urine  associated  with 
oedema  of  the  legs,  signs  of  thoracic  embarrassment,  such  as  dulness  at 
the  bases  of  the  lungs  due  to  collapse,  dyspnoea,  rales  at  the  bases  of 
the  lungs,  and  in  rare  instances  haemoptysis  from  collapse  of  the 
lungs,  which  should  make  the  practitioner  tap  the  abdomen.  In  cases 
where  with  abundant  ascites,  hsematemesis  occurs,  the  abdomen 
should  be  tapped,  as  by  this  means  venous  engorgement  may  be  dimin- 
ished. 

Method  of  Performing  Paracentesis. — ^The  most  satisfactory  treatment 
is  tapping  the  abdomen  with  a  Southey's  trocar  and  cannula  and  allowing 
the  fluid  to  drain  slowly  away  through  a  fine  india-rubber  tube  into  a 
bucket  which  is  placed  by  or  underneath  the  bed.  It  occasionally  hap- 
pens— I  have  seen  three  such  cases— that  the  abdominal  wall  is  so  enor- 
mously thick  that  a  Southey's  trocar  fails  to  reach  the  peritoneal  cavity, 
and  that  a  specially  long  trocar  is  required.  In  one  such  case  where  I 
used  the  trocar  of  a  Dieulafoy's  aspirator  the  abdominal  wall,  as  it  became 
lax  from  the  removal  of  the  ascitic  fluid,  collapsed  in  thick  folds  on  the 
trocar  and  bent  it  out  of  shape. 

The  skin  should  be  carefully  washed  and  an  antiseptic  dressing  (1  in 
40  carbolic)  put  over  the  area  where  the  trocar  is  to  be  introduced,  and 
the  trocar  and  cannula  should  be  boiled  in  a  test-tube  containing  water 
and  left  to  cool  in  a  solution  of  carbolic  1  in  40.  The  trocar  is  usually 
inserted  in  the  middle  line  between  the  symphysis  pubis  and  the  um- 
bilicus, but  sometimes,  from  the  presence  of  omental  or  other  adhesions, 

*  Austin  Flint  was  tlie  first  vigourous  advocate  of  tapping  comparatively  early 
in  the  course  of  the  disease.  Vide  American  Jour.  Med.  Sciences,  1863,  and  Brit. 
Med.  Jour.,  1883,  vol.  ii,  p.  565. 


256  DISEASES   OF  THE   LIVER. 

little  or  no  fluid  may  be  drawn  off  in  this  situation;  in  such  instances  it 
will  be  necessary  to  tap  the  abdomen  in  the  linea  semilunaris  on  one  or 
other  side.  It  has  been  suggested  that  the  spot  selected  should  be  on  a 
line  joining  the  umbihcus  and  the  anterior  superior  spine  of  the  ilium 
on  the  left  side,  so  as  to  avoid  any  danger  of  wounding  the  csecum  or 
the  liver  (Phcque*).  It  is,  of  course,  essential  that  the  area  selected 
should  be  dull,  and  it  should  be  ascertained,  if  necessary  by  passing  a 
catheter,  that  the  dulness  is  not  due  to  a  distended  bladder. 

Under  ordinary  conditions  and  with  reasonable  care  there  should 
never  be  any  danger  of  wounding  the  liver.  I  have,  however,  seen  its 
effects  at  a  postmortem  in  which  there  was  very  considerable  extrava- 
sation from  puncture  of  a  large  branch  of  the  portal  vein.  As  a  rule, 
little  or  no  harm  results. 

Goodhart,t  indeed,  refers  to  the  case  of  a  Avoman  who  when  apparently  in  a  very 
advanced  stage  of  the  disease  was  tapped,  but  only  blood  came  away,  and  it  was 
thought  that  the  trocar  had  passed  into  the  liver.  However,  from  that  time  the 
patient  steadily  improved.  Possibly  this  fortunate  result  was  due  to  the  wound 
producing  vascular  adhesions  around  the  liver. 

The  patient  lies  on  his  back  and  the  cannula  should  be  fixed  by  means 
of  plaster.  During  the  drainage  the  abdomen  should  be  compressed 
by  a  many-tailed  bandage,  or  by  a  binder  which  must  be  tightened  from 
time  to  time,  so  as  to  avoid  tympanites.  J  When  the  cannula  has  ceased 
to  run  from  the  small  amount  of  fluid  left  in  the  abdomen,  and  not 
from  displacement  or  blocking  of  the  tube,  which  can  be  ascertained  by 
passing  a  probe  down  the  cannula,  it  should  be  withdrawn  and  the  small 
wound  covered  with  a  plug  of  absorbent  cotton-wool  saturated  with 
collodion.  The  binder  should  be  kept  on  for  two  or  three  days  to 
prevent  flatulent  distension  of  the  intestines.  If  any  distension  occurs, 
a  dose  or  two  of  the  sulphates  of  magnesium  and  sodium,  a  drachm 
and  a  half  of  each,  should  be  given.  If  the  abdomen  is  nearly  emptied, 
the  small  trocar  wound  heals  up,  and  no  trouble  from  leakage  results. 
When,  however,  from  adhesions  the  fluid  is  not  satisfactorily  removed, 
I  have  seen  considerable  inconvenience  from  leakage  from  the  wound, 
although  the  cannula  had  ceased  to  run.  After  paracentesis,  from  the 
increased  absorption  of  fluid  from  the  bowel  and  from  the  flaccid  condi- 
tion of  the  abdominal  muscles,  there  is  occasionally  troublesome  constipa- 
tion. 

Use  of  a  Large  Trocar. — In  former  times  a  large  trocar,  like  that  emploj^ed  for 
withdrawing  the  contents  of  an  ovarian  cyst,  used  to  be  plunged  into  the  abdomen 
and  the  fluid  rapidly  drawn  off.  This  is  chiefly  of  historical  interest;  personally  I 
have  never  seen  it  employed.  The  rapid  withdrawal  of  fluid  sometimes  led  to  collapse, 
possibly  from  a  large  quantity  of  blood  being  drawn  into  the  splanchnic  veins. 

Treatment  hy  Continuous  Drainage. — The  wound  has  been  kept  open 
and  the  fluid  allowed  to  run  away  continuously  by  Caillie  of  New  York, 

*Plicque:  La  Presse  M^dicale,  Jan.  13,  1900,  p.  28. 
t  Gootlhart:  Guy's  Hospital  Gaz.,  June  7,  1897. 

X  This  practice  appears  to  have  been  first  employed  by  Dr.  R.  Mead.  See  "  The 
Gold-headed  Cane,"  2d  ed.,  p.  73,  1828. 


CIRRHOSIS    OF   THE    LIVER.  257 

Elliot  of  Boston,  Urso,  Cheadle,*  and  others.  This  has  also  been  recom- 
mended in  the  operative  treatment  of  ascites  due  to  cirrhosis  by  pro- 
ducing vascular  adhesions,  so  as  to  prevent  disturbance  of  the  adhesions. 
But  it  has  grave  drawbacks. 

In  9  cases  of  Urso's,  4  died  directly;  the  best  result  seems  to  have  been  pro- 
longation of  life  for  nine  months.  EUiot's  cases  were  both  fatal.  Cheadle  says  that 
in  some  of  his  cases  where  the  puncture  of  paracentesis  has  remained  open  the  results 
have  been  satisfactory  except  for  the  manifest  discomfort  involved. 

A  modification  of  permanent  drainage  is  described  by  Jaboulay  f  under  the  title 
' '  Cicatrice  a  filtration."  A  man  with  ascites  from  cirrhosis  was  operated  upon  in  the 
following  manner :  The  skin  of  the  abdomen  was  incised  transversely  below  the  left 
costal  arch,  the  muscles  and  peritoneum  were  divided  lower  down,  and  a  piece  of 
omentum  was  attached  outside  the  peritoneal  cavity,  and  the  wound  closed  with 
hardly  any  escape  of  ascitic  fluid.  The  skin  healed  over  the  artificially  produced 
interstitial  hernia  of  the  great  omentum  and  the  ascites  diminished  by  escaping  into 
the  subcutaneous  tissues  of  the  abdominal  wall.  About  a  week  after  the  operation 
a  small  external  fistula  in  the  stitch  wounds  developed  and  the  fluid  gained  an 
external  exit.     The  man  left  the  hospital  in  fair  health. 

The  Surgical  Treatment  of  Ascites  by  the  Production  of  Vascular  Peri- 
toneal Adhesions. — This  method  of  treatment,  as  conceived  by  Drummond 
and  Morison,{  was  based  on  the  assumption  that  ascites  was  due  to  portal 
obstruction,  and  was  an  attempt  to  increase  the  collateral  circulation 
between  the  radicles  of  the  portal  vein  and  the  general  systemic  veins. 
The  operation  was  original  in  Morison's  hands,  but  it  appears  that  it 
had  been  previously  planned  by  Talma  and  carried  out  by  Van  der  Meulen 
in  1889,  by  Schelkley  in  1891,  and  by  Lens  in  1892.  It  is  often  spoken 
of  as  Talma's  operation,  or  as  the  Talma-Morison  operation,  but  there 
is  no  doubt  that  Drummond  and  Morison  first  brought  it  into  notice  in 
England  and  America. 

Technique  of  the  Operation. — It  is  convenient  to  tap  the  abdomen 
before  the  operation  is  performed  so  as  to  remove  the  ascites,  though 
this  is  by  no  means  essential.  An  incision  parallel  to  the  right  costal 
margin  is  probably  more  convenient  than  one  in  the  long  axis  of  the 
body.  The  liver  should  be  examined  so  as  to  confirm  the  diagnosis  of 
cirrhosis,  for  the  operation  will  do  no  good  if  the  cause  of  the  ascites  is 
chronic  peritonitis.  The  peritoneum  over  the  liver  and  diaphragm  is 
scraped  or  curetted  so  as  to  set  .up  adhesive  inflammation,  and  the  surfaces 
are  brought  in  contact  by  stitching  the  round  ligament  to  the  abdominal 
parietes  or  by  passing  stitches  through  the  liver  itself.  It  appears  that 
it  is  a  distinct  advantage  to  utilise  the  great  omentum  as  a  means  of 
multiplying  the  vascular  adhesions;  in  order  to  accomplish  this,  the 
omentum  is  interpolated  between  the  diaphragm  and  the  convexity  of 
the  liver.  There  are  numerous  veins  in  the  great  omentum  which  will 
assist  in  the  development  of  a  compensatory  anastomosis.  No  bad  effects, 
such  as  intestinal  obstruction,  result  from  limitation  of  the  scope  of  the 
transverse  colon's  movement.     This  was,  I  believe,  first  carried  out  in 

*  Cheadle:  St.  Mary's  Hosp.  Gaz.,  May,  1S96.  Brit.  Med.  Journ.,  1900,  vol.  i, 
p.  895. 

t  Jaboulay :  Lyon  Medical,  tome  xciv,  p.  499. 
X  Drummond  and  Morison :  Brit.  Med.  Journ.,  1896,  vol.  ii,  p.  728. 
17 


258  DISEASES    OF   THE    LIVER. 

a  case  operated  upon  by  my  colleague,  Mr.  G.  R.  Turner.*  In  a  case 
operated  upon  by  Talma  f  the  spleen  remained  of  considerable  size  until 
he  did  a  second  laparotomy  and  sutured  the  spleen  to  the  abdominal 
parietes,  after  which  it  became  smaller.  It  has  therefore  been  thought 
that  the  peritoneum  should  be  scraped  widely  so  as  to  allow  of  vascular 
adhesions  forming  around  the  spleen  as  well  as  around  the  liver.  The 
peritoneal  cavity  should  be  drained  either  by  means  of  a  glass  tube  in- 
serted into  the  wound  or  by  a  separate  suprapubic  incision  into  the 
peritoneum  so  as  to  prevent  the  ascitic  fluid  separating  the  roughened  peri- 
toneal surfaces  and  interfering  with  the  formation  of  vascular  adhesions. 
The  patient  should  also,  as  far  as  possible,  be  kept  in  a  sitting  posture, 
so  as  to  prevent  re-accumulation  of  fluid  in  the  upper  part  of  the  abdomen. 

It  has  been  suggested  by  Murrell  t  that  the  development  of  a  collateral  circulation 
may  be  accelerated  by  rubbing  the  skin  of  the  abdomen  with  ung.capsici  or  with 
cajeput  oil.  Tlais  would,  of  course,  not  be  done  until  the  operation  wound  had 
completely  healed. 

Epiplopexy  is  the  name  applied  by  J.  B.  Roberts  §  to  a  slighter  opera- 
tion which  requires  less  manipulation  and  is  therefore  applicable  to 
advanced  cases  with  little  power  of  resistance.  Its  object  is  to  increase 
the  compensatory  collateral  circulation  between  the  radicles  of  the 
portal  veins  and  the  systemic  veins.  The  operation  consists  in  suturing 
the  great  omentum  to  the  anterior  abdominal  wall.  Roberts  performed 
this  operation  in  two  cases,  in  one  with  very  temporary  rehef,  in  the 
other  death  occurred  within  forty-eight  hours  of  the  operation. 

Discussion  of  the  Manner  in  which  the  Operation  Improves  the  Condi- 
tion of  the  Patients. — Does  the  improvement  which  sometimes  results 
both  in  the  general  health  and  in  the  local  condition — viz.,  the  disap- 
pearance of  ascites — simply  depend  on  the  collateral  circulation  relieving 
the  pressure  in  the  portal  vein?  This  was  the  assumption  on  which 
Drummond  and  Morison  planned  their  operation,  and  more  recently 
it  has  been  emphasised  by  Weir.  |1  Against  this  it  may  be  argued  (a) 
that  ascites  does  not  occur  when  the  blood-pressure  is  presumably 
highest  in  the  portal  vein — viz.,  earlier  in  the  course  of  the  disease 
when  hEematemesis  is  most  often  met  with,  and  that  experimental  hga- 
ture  of  the  portal  vein  does  not  necessarily  produce  ascites.  Cirrhosis 
may  exist  for  many  years  without  ascites,  which  may  appear  quite  sud- 
denly ;  while  if  ascites  was  a  purely  mechanical  effect  of  increased  venous 
pressure  in  the  portal  vein,  it  should  develop  gradually  and  earlier  in 
the  course  of  the  disease.  It  therefore  would  appear  that  the  good 
effects  of  the  collateral  circulation  are  not  solely  due  to  relieving  the 
pressure  in  the  portal  vein.  _(h)  That  ascites  is  a  late  manifestation  and 
appears  to  be  rather  a  result  of  a  toxemic  condition  of  the  blood  than  a 
mere  mechanical  result  of  increased  portal  blood-pressure,  and  that  it 

*  Rolleston  and  Turner:  Lancet,  1899,  vol.  ii,  p.  1660. 

t  Talma:  Berhn.  klin.  Wochen.,  Sept.  19,  1898,  S.  833. 

t  Murrell:  Lancet,  1902,  vol.  i,  p.  1602. 

§  Roberts,  .1.  R. :  Philadelphia  Med.  Journal,  Jan.  26,  1901,  p.  163. 

il  Weir:  Medical  Record,  1899,  p.  149. 


CIRRHOSIS    OF   THE    LIVER.  259 

is  the  outcome  of  a  poison  in  the  plood  exerting  a  lymphagogue  action.* 
The  toxsemic  state  depends  on  hepatic  insufficiency — ^in  other  words, 
on  the  cirrhotic  hver  being  unable  to  destroy  poisons  that  are  continually 
passing  to  it  from  the  alimentary  canal;  these  poisons,  therefore,  reach 
the  general  circulation  and  lead  to  oedema  of  the  feet,  ascites,  and  to  the 
constitutional  and  nervous  S3"mptoms  of  the  late  stages  of  cirrhosis.  If  the 
collateral  circulation  between  the  peripheral  parts  of  the  portal  vein  and 
general  systemic  veins  is  markedly  increased,  less  blood  will  go  through 
the  liver  and  the  toxaemia  will  be  increased.  In  fact,  the  collateral 
circulation  between  the  portal  and  general  venous  S3'stem  is  carried  to 
its  logical  conclusion  in  Eck's  fistula.  In  this  experiment  the  portal 
vein  is  interrupted  in  the  portal  fissure;  its  proximal  end  is  closed,  while 
its  distal  end  is  put  into  communication  with  the  inferior  vena  cava. 
In  other  words,  the  portal  circulation  through  the  liver  is  short-circuited 
and  all  the  blood  from  the  intestinal  area  enters  directly  into  the  inferior 
vena  cava.  As  shown  by  the  very  successful  experiments  of  Hahn,  Nasse, 
Nencki,  and  Pawlowj  on  dogs,  this  procedure  tends  to  induce  a  dispo- 
sition to  uraemia.  Thus  if  the  dogs  were  fed  on  meat,  severe  nervous  dis- 
turbance, depression,  asthenia,  clonic  and  tonic  spasms,  and  coma  were 
brought  on  and  sometimes,  indeed,  ended  in  death.  It  is  noticeable  that 
one  of  Morison's  J  patients  was  alternately  excited  and  depressed  for  three 
weeks  after  the  operation;  similar  depression  has  been  noted  in  other 
cases,  and  may  be  explained  as  being  due  to  the  passage  of  poisons, 
manufactured  in  the  intestine,  directly  into  the  general  circulation  with- 
out the  intervention  of  the  liver. 

Thus,  since  it  appears  that  the  increase  in  the  collateral  circulation 
between  the  portal  vein  and  the  general  systemic  system  would  tend  to 
induce  a  general  toxaemia,  the  improvement  in  general  health  that  follows 
the  operation  must  be  clue  to  some  other  cause  than  the  formation  of 
anastomotic  channels  betw^een  the  portal  vein  and  the  general  systemic 
veins. 

Thomson  §  has  suggested  that  the  operation  may  prevent  ascites  b}^ 
the  simple  method  of  producing  universal  adhesions  and  obliterating 
the  peritoneal  cavity.  That  this  is  a  possible  method  is  shown  by  the 
cases,  such  as  Dickinson's  ||  and  Weber's,**  in  which  ascites  disappeared 
and  cirrhosis  with  universal  peritoneal  adhesions  was  found  at  the 
autopsy. 

In  a  paper  written  in  1899  by  Mr.  G.  R.  Turner  and  myself  it  seemed 
probable  that  there  were  two  other  ways  in  which  the  development  of  a 
collateral  circulation  in  adhesions  around  the  liver  might  be  beneficial 
to  the  economy:  (1)  By  somewhat  diminishing  the  flow  of  l^lood  through 
the  liver  it  may  enable  that  organ  to  deal  more  satisfactorily  Avith  the 

*  White,  W.  Hale:  Clinical  Journ.,  April  26,  1899. 

t  Hahn,  Nasse,  Nencki,  and  Pawlow:  Archiv  f.  experiment.  Path.  u.  Pharmak., 
Bd.  xxxn,  S.  161,  1893. 

t  Morison:  Lancet,  1899,  vol.  i,  p.  1426. 

§  Tlionison,  H.  Campbell:  Medico-chirnrc;.  Trans.,  vol.  Ixxxiv,  p.  265. 
|l  Dickinson,  W.  H. :   .Mlinitt's  System  of  Medicine,  vol.  v.,  ]\  691. 
**  Weber,  F.  P. :  St.  Bart.'s  Hosp".  Reports,  vol.  xxxiv.  p.  321 . 


260  DISEASES   OF  THE   LIVER. 

blood  passing  through  it,  and  so  reduce  the  toxsemic  condition  of  the 
blood,  which  is  probably  the  important  factor  in  inducing  ascites.  (2) 
That  the  presence  of  vascular  adhesions  over  the  surface  of  the  Uver 
would  reheve  venous  engorgement  and  so  allow  a  freer  supply  of  arterial 
blood  to  the  hver.  The  nutrition  of  the  Uver  cells  would  thus  be  im- 
proved and  they  would  be  under  better  conditions  to  undergo  com- 
pensatory hyperjDlasia. 

The  compensatory  hypertrophy  of  the  liver  *  vnll  enable  the  organ 
to  perform  more  efficiently  its  important  antitoxic  functions,  and  so 
lead  to  a  latencj^  of  the  symptoms.  If  the  last  hypothesis  be  true,  it  is 
evidently  of  importance  that  any  operation  for  the  formation  of  vascular 
adhesions  around  the  liA'er  should  be  undertaken  before  the  liver  tissue 
is  so  disorganised  that  compensatory  hyperplasia  is  impossible. 

Early  Performance  of  Operation  Desirable. — It  is  important  that  the 
operation  should  be  done  comparatively  early  and  not  postponed  until 
the  patient  is  too  debilitated  to  withstand  it,  for  patients  vdth  cirrhosis 
are,  at  the  best  of  times,  far  from  good  subjects.  Thus  patients  may  die 
from  peritonitis  or  from  shock  immediately  after  the  laparotomy.  An- 
other reason  for  not  delaying  operative  interference  is  the  importance  of 
interA'ening  before  the  liver  tissue  is  so  degenerated  that  it  is  unable  to 
undergo  compensatory  hyperplasia  as  the  result  of  the  improved  blood- 
supply  provided  by  the  adhesions.  In  suitable  cases  for  operation  medical 
measures  should  only  be  persisted  in  while  the  diagnosis  is  open  to  doubt, 
and  they  should  always  be  directed  to  counteract  any  possible  syphilitic 
disease  of  the  lii^er.  When  medicab  treatment  and  a  course  of  iodide  of 
potassium  have  not  benefited  a  case  of  ascites  which  is  thought  to  be  due 
to  either  s\^hilis  or  cirrhosis,  the  question  of  operative  interference 
should  be  considered. 

IMien  cirrhosis  can  be  diagnosed  with  fair  certainty  in  the  pre-ascitic 
stage,  and  when  there  are  evidences  of  the  disease,  such  as  hsematemesis 
and  splenic  enlargement,  operative  interference  has  a  much  better  chance 
than  in  the  late  stages. 

Results  of  the  Operation. — A  large  number  of  cases  have  been  operated 
upon,  and  in  some  instances  the  operation  has  been  done  on  cases  in 
which  ascites  was  due  to  some  other  cause.  Statistics  show  that  no 
good  at  all  is  done  in  more  than  half  the  cases,  and  that  cure  occurs  only 
in  a  small  minority. 

Up  to  May,  1902,  Greenough  t  collected  122  cases  in  which  the  operation  had 
been  done.  After  deducting  17  in  which  the  disease  was  not  cirrhosis  and  one  case 
in  which  the  result  was  not  given,  there  are  104  cases  of  cirrhosis  in  which  the  operation 
had  been  performed.  Of  these,  31  died  within  thirty  days  of  the  operation  and 
29  were  in  no  way  improved,  so  that  60,  or  57  per  cent.,  not  only  received  no  real 
benefit  from  the  treatment,  but  possibly  had  their  lives  shortened;  44,  or  42  per 

*  It  is  interesting  to  note  that  in  a  case  of  hepatic  cirrhosis,  in  which  it  was  sug- 
gested that  the  symptoms  Avere  arrested  as  the  result  of  imiversal  peritoneal  adhe- 
sions, the  liver  weighed  89  omices  and  presented  nodules  on  its  surface  which  maybe 
interpreted  as  due  to  compensatory  hyperplasia  of  the  liver  cells.  The  patient  died 
from  poisoning  by  mussels.  (F.  P.  Weber :  St.  Bartholomew's  Hospital  Reports, 
vol.  xxxiv,  p.  321.) 

t  Greenough:  American  Joum.  Med.  Sciences,  vol.  cxxiv,  p.  979,  Dec,  1902. 


CIRRHOSIS    OF   THE    LIVER.  261 

cent.,  were  improved,  and  of  these  9  were  living  and  in  improved  health  two  years 
after  the  operation.  This  last  figure  does  not  include  one  of  Mr.  Turner's  and  my 
cases  operated  upon  on  July  31,  1899,  which  did  not  require  tapping  till  March  1, 
1902,  an  interval  of  more  than  two  and  one-half  years.  In  78  cases  collected  by 
Lejars,*  death  occurred  rapidly  in  36,  in  28  the  ascites  disappeared,  and  in  14 
notable  improvement  resulted. 

On  the  whole,  the  results  are  somewhat  disappointing,  but  this  may 
in  part  be  due  to  the  fact  that  the  operation  is  so  often  undertaken  as  a 
last  resource,  and  late  in  the  course  of  the  disease,  when  the  fatal  termi- 
nation is  already  near.  The  earlier  the  operation  is  undertaken,  the 
better  the  chance  of  improvement  or  even  arrest  of  the  disease.  It 
appears  that  it  does  give  the  patient  a  chance,  as  about  10  per  cent,  are 
alive  and  in  improved  health  two  years  after  the  operation. 

Treatment  hy  Diuretics. — When  ascites  is  small  in  amount,  diuretics 
may  be  tried;  it  is  also  advisable  to  give  them  directly  after  paracentesis 
has  been  performed.  It  appears,  however,  that  when  there  is  consider- 
able ascitic  effusion,  diuretics  have  very  little  effect,  possibly  because 
the  renal  veins  are  pressed  upon,  and  from  the  resulting  venous  engorge- 
ment the  kidneys  are  placed  at  a  disadvantage.  For  this  reason  they 
are  often  much  more  effective  after  paracentesis  than  before.  Diuretics 
may  be  tried,  but  should  never  be  employed  to  the  exclusion  of  para- 
centesis. 

A  large  number  of  diuretics  have  been  employed.  A  pill  containing 
digitalis,  squiUs,  and  mercury  is  one  of  the  most  successful  diuretics  in 
ascites;  the  mercur}^  may  be  in  the  form  of  calomel.  This  pill  is  called 
Baillie's  pill  at  St.  George's,  or  Addison's  pill  at  Guy's  Hospital.  Small 
doses  of  calomel  may  be  given  not  only  for  their  antiseptic  action,  but 
also  to  increase  the  output  of  urine,  especially  when  combined  with  citrate 
of  caffeine.  Potassium  salts,  such  as  the  acetate,  nitrate,  and  bitartrate, 
are  recommended  by  some,  but  their  diuretic  effect  is  inferior  to  that 
of  many  other  available  drugs,  and  the  depressing  and  toxic  effect  of 
potassium  is  a  distinct  drawback.  It  is  better  not  to  give  spirituous 
solutions,  such  as  spirits  of  juniper,  spiritus  setheris  nitrosi,  as  it  is  possible 
they  might,  like  alcoholic  drinks,  tend  to  do  further  damage  to  the  Uver. 

Copaiba  resin  in  10  to  15  grain  doses  has  been  advocated  as  a  valuable 
remedy  in  ascites.  It  should  be  given  in  keratin  capsules,  which  resist 
the  action  of  the  gastric  juice,  so  as  to  avoid  irritation  of  the  stomach. 
Apocynum  is  a  powerful  diuretic,  as  the  name  the  "vegetable  trocar," 
which  has  been  given  to  it,  implies.  It  has  the  disadvantage  of  irritating 
the  stomach;  in  order  to  prevent  this,  a  small  dose  of  cannabis  indica 
should  be  combined  with  it.  The  tincture  can  be  given  in  15  to  30 
minims  three  times  daily,  or  the  fluid  extract  (U.  S.  P.)  in  10  minim  doses 
may  be  employed  instead.  Musser  f  speaks  encouragingly  of  its  use, 
but  I  have  been  rather  disappointed  with  its  effects  in  the  ascites  of 
cirrhosis.  Asparagus  has  often  been  used  as  a  diuretic.  Hare  %  has  seen 
improvement  in  ascites  of  cirrhosis  after  a  drachm  of  a  liquid  extract  of 

*  Lejars :  La  Semaine  Mddicale,  March  25, 1903,  p.  93. 
t  Musser,  J.  H. :  Joum.  Amer.  Med.  Assoc,  Oct.  5,  1901. 
%  Hare,  H.  A. :  Therapeutic  Gaz.,  Oct.,  1899. 


262  DISEASES    OF   THE    LIVER. 

asparagus  given  three  times  daily.  Urea,  on  account  of  its  diuretic 
action,  has  also  been  recommended.  I  have  tried  it  vvithout  any  marked 
effect  in  several  cases,  while  Goggi  has  seen  bad  results  follow  its  admin- 
istration. Diuretin — a  salicylate  compound  of  theobromine — ^has  been 
tried,  but  is  not  of  any  particular  use  in  the  ascites  of  cirrhosis.  Liver 
substance  or  extract  has  been  given  by  the  mouth  or  by  subcutaneous 
injection.  Polyuria  and  diarrhoea  result,  and  ascites  may  be  much 
diminished.  In  14  cases  collected  by  Mouras  *  ascites  disappeared  in  7. 
(Vide  also  Treatment  of  Cirrhosis.) 

Treatment  by  Purgatives. — The  ancient  treatment  of  attempting  to 
remove  ascites  by  free  purgation  has  been  abandoned,  and  vigourous 
drugs  like  elaterium,  gamboge,  etc.,  are  no  longer  given.  The  excessive 
diarrhoea  thus  produced  necessarily  starves  and  weakens  the  patient, 
while  it  lessens  the  urinary  excretion  and  so  may  tend  to  induce  or  increase 
retention  of  toxic  substances  in  the  blood  and  lead  to  toxsemia.  Cheadle 
speaks  of  cases  being  "purged  to  death."  Further,  violent  purgatives 
readily  light  up  catarrh  of  the  intestine,  and  so  do  harm.  Repeated 
small  doses  of  calomel  may  be  given  and  exert  a  beneficial  antiseptic 
action  as  well  as  clearing  out  the  bowels.  Saline  purgatives  such  as 
sulphate  of  soda  or  magnesium  may  be  employed.  Jalap  powder  in  one- 
drachm  doses  is  an  effectual  purge  that  may  be  employed.  Turpeth, 
the  Ipomcea  turpethum  of  the  Colonial  and  Indian  Pharmacopoeias,  is 
recommended  in  20  grain  doses  (Murrellt)- 

Restriction  of  Fluid,  Etc.- — Dickinson  J  records  6  cases  of  ascites  due  to 
cirrhosis  treated  by  reducing  the  amount  of  liquid  taken  by  the  mouth 
down  to  one  pint  or  less.  In  two  cases  the  ascites  disappeared.  In  one 
death  occurred  two  years  later  from  cerebral  abscess,  and  the  patient,  a 
boy  aged  nine  years,  was  found  to  have  a  hobnailed  liver  and  universal 
peritoneal  adhesions.  The  treatment  was  recommended  not  as  a  sub- 
stitute for  tapping,  but  as  an  adjuvant.  The  diminished  fluid  has  dis- 
tinct disadvantages,  since  it  must  tend  to  produce  constipation,  thereby 
increasing  fermentation  and  the  tendency  to  autointoxication.  Further, 
it  must  curtail  the  urinary  excretion  and  so  tend  to  favour  the  onset  of 
toxgemia. 

It  has  recentlj'  been  urged  that  the  intake  of  chlorides  should  be  restricted,  as 
they  are  retained  and  tend  to  increase  ascites. § 

HAEMATEMESIS. 

This  may  be  the  earliest  warning  to  the  individual  that  he  is  the  sub- 
ject of  any  disease  more  serious  than  indigestion.  Perhaps  the  most 
frequent  sequence  of  events  is  that  a  man  who  for  years  has  lived  freely 
and  has  had  a  few  attacks  of  gastritis  and  dyspepsia,  due  to  alcoholic 
excess,  has,  while  in  his  usual  state  of  health  or  after  some  little  initial 
uneasiness  in  the  stomach  or  faintness,  a  copious  ha?matemesis. 

*  Mouras:  These  de  Paris,  1901,  No.  278. 

t  Murrell:  Lancet,  1902,  vol.  i,  p.  1602. 

t  Dickinson:  Allbutt's  System  of  Medicine,  vol.  v,  p.  691. 

§  Olmer  et  Audebort:  Rev.  de  M6d.,  Mars,  1904,  p.  199. 


CIRRHOSIS    OF    THE    LIVER,  263 

Hsematemesis  may  be  preceded  by  abdominal  discomfort,  febrile 
disturbance,  enlarged  spleen,  and  evidence  of  gastritis.  In  such  cases 
it  is  probable  that  infective  gastritis,  due  to  toxic  or  septic  agents,  is  the 
exciting  cause  of  the  haemorrhage.  The  hsematemesis  is  sometimes  re- 
peated in  the  course  of  the  next  few  days,  but  usually  there  is  a  single 
large  hsematemesis.  When  hsematemesis  is  often  repeated  the  condition 
is  either  not  cirrhosis,  or,  if  there  be  hepatic  cirrhosis,  it  is  complicated 
by  some  factor,  such  as  gastric  ulcer,  superficial  gastric  erosions,  or 
ulcerated  varicose  oesophageal  veins,  which  accounts  for  the  repetition 
of  the  hsemorrhages. 

Incidence. — Hsematemesis  does  not  appear  from  statistics  to  be  so 
frequent  in  the  course  of  cirrhosis  as  is  usually  imagined.  It  is  such  a 
striking  event  that  it  is  rather  surprising  to  find  that  it  occurs  less  often 
than  jaundice  and  in  rather  less  than  one-fourth  of  all  patients  dying 
with  a  cirrhotic  liver. 

In  163  cases,  obtained  by  combining  Yeld's*  (85)  and  Sears  and  Lord'sf  (78) 
cases,  haematemesis  occurred  in  38,  or  23.3  per  cent. 

It  naturally  occurs  rather  more  frec{uently  in  cases  who  died  directly 
from  the  effects  of  cirrhosis,  such  as  ascites,  toxaemia,  and  gastro-intes- 
tinal  haemorrhage. 

In  80  cases  of  cirrhosis  fatal  from  the  effects  of  the  disease,  examined  after 
death  at  St.  George's  Hospital,  26,  or  32.5  per  cent.,  had  had  hsematemesis.  In 
4  of  the  26  cases  death  was  directly  due  to  hsematemesis.  These  figures  showed 
that  men  suffered  more  frequently  than  women  from  hsematemesis;  thus,  of  51 
men,  19,  or  37  per  cent.,  had  hsematemesis,  while  of  the  29  women,  only  7,  or  14 
per  cent.,  had  had  hsematemesis. 

Hsematemesis  is  rare  in  children.  Possibly  this  may  depend  on  the 
fact  that  concomitant  alcoholism,  which  is  certainly  more  frequent  in 
adults,  favours  extravasation  of  blood  by  reducing  the  coagulability  of 
the  blood. 

Saunal,t  however  records  fatal  haemorrhage  from  an  cesophageal  varicose 
vein  in  a  girl  aged  twelve  years  with  cirrhosis.  In  the  Norfolk  and  Norwich  Hos- 
pital Museum  there  is  a  specimen  (No.  59)  of  dilated  oesophageal  veins  from  a  girl 
aged  eight  years  who  died  after  a  succession  of  hsematemeses.  The  liver  was  hob- 
nailed and  weighed  36  ounces,  the  spleen  weighed  18  ounces,  the  skin  was  slightly 
tinged,  but  there  was  no  real  jaundice.  This  case  somewhat  resembles  Banti's 
disease  or  cirrhosis  supervening  in  splenic  ansemia. 

After  hsematemesis  the  patient  is  left  in  a  condition  of  secondary 
ansemia,  the  degree  of  which  varies  with  the  amount  of  blood  l(^st.  It 
is  not  easy  to  estimate  the  amount  of  blood  lost,  for  though  a  considerable 
proportion  of  it  may  be  vomited  up,  some  always  passes  into  the  duo- 
denum and  gives  rise  to  melaena,  and  may  thus  escape  notice,  and  is 
necessarily  difficult  to  estimate.  After  the  hsematemesis  the  patient 
sometimes  feels  relieved  and  loses  any  feeling  of  oppression  and  heaviness 
that  he  may  have  previously  had  in  the  alxlomen. 

*Yeld:    St.  Bartholomew's  Hospital  Reports,  vol.  xxxiv,  p.  215. 

t  Sears  and  Lord:    Boston  Medical  and  Surgical  Journ.    vol.  cxlvii,  p    285. 

i  Saunal:    These  de  Paris,  1892. 


264  DISEASES   OF  THE   LIVER. 

Although  hsematemesis  is  usually  an  early  symptom  of  cirrhosis,  it 
may  supervene  late  in  the  course  of  the  disease,  and  even  prove  fatal 
in  a  patient  with  ascites.*     This  is  illustrated  by  the  following  case: 

A  man  aged  fifty-four  years  was  admitted  under  my  colleague,  Dr.  Ewart, 
into  St.  George's  Hospital  in  the  summer  of  1898.  He  had  jaundice,  ascites,  and 
albuminuria.  Paracentesis  to  lOJ  pints  was  performed,  and  after  this  the  fluid 
did  not  collect  again.  He  got  weaker,  and  eventually  died  immediately  after  a 
large  hsematemesis.  This  was  the  only  occasion  on  which  he  brought  up  blood. 
At  the  autopsy  the  liver  was  cirrhotic  and  weighed  6  pounds,  10  ounces.  The 
spleen,  10  ounces,  the  kidneys,  10  ounces  each,  appeared  normal. 

The  blood  is  probably  generally  poured  out  slowly  into  the  stomach, 
and  thus  has  time  to  clot  and  to  be  acted  upon  by  the  gastric  juice  and 
to  be  mixed  with  its  contents.  It  is  for  these  reasons  darker  in  colour 
than  the  blood  in  gastric  ulcer,  which  is  rapidly  extravasated  from 
branches  of  the  gastric  arteries.  The  quantity  of  blood  brought  up  in 
cirrhosis  is  practically  always  considerable,  for  the  vomiting  is  chiefly 
due  to  the  mechanical  distension  of  the  stomach  by  the  blood.  If  only 
a  small  quantity  is  poured  out,  the  blood  is  not  as  a  rule  vomited,  but 
passes  into  the  bowel  and  gives  rise  to  melsena.  This  accounts  for  the 
fact  that  melsena  may  occur  ^^dthout  any  hgematemesis  in  cases  of  haemor- 
rhage into  the  stomach.  Occasionally  w^hen  a  small  haemorrhage  has 
taken  place,  the  patient  may  vomit  from  some  other  cause,  and  a  little 
black  or  "coffee-ground"  vomit  may  be  brought  up,  but  this  is  somewhat 
exceptional. 

Very  large  amounts  of  blood  may  be  vomited  in  the  case  of  haemat- 
emesis  due  to  cirrhosis.  Thus  Osier  f  refers  to  a  case  where  10  pounds 
were  lost  in  seven  days.  It  is  noteworthy  that  collapse  is  not  so  frequent 
or  so  marked  a  symptom  as  in  the  hsematemesis  of  gastric  ulcer,  where 
blood  is  rapidly  poured  out.  When  a  varicose  oesophageal  vein  is  opened 
and  very  large  quantities  of  blood  are  lost,  sometimes  at  repeated,  in- 
terv^als,  death  may  follow,  but  this  does  not  invalidate  the  general  state- 
ment just  made  that  in  the  ordinary  haematemesis  of  cirrhosis,  often 
referred  to  capillary  oozing,  alarming  symptoms  are  rare.  In  fact, 
sometimes  the  patients  may  feel  relieved  by  it. 

The  temperature  after  haematemesis  is  subject  to  some  variations. 
As  a  rule,  it  is  depressed  from  shock,  but  after  a  few  days  it  becomes 
normal.  It  may  then  remain  normal  or  it  may  become  raised.  Fever 
after  haematemesis  should  suggest  the  existence  of  some  complication, 
such  as  tuberculosis,  a  pleural  effusion,  especially  on  the  right,  side, 
endocarditis,  or  some  septic  process  in  the  tonsils,  teeth,  or  elsewhere. 
Fever  may,  however,  depend  on  rapidly  progressing  changes  in  the  liver, 
especially  if  the  spleen  remains  enlarged  or  increases  in  size.  The 
haematemesis  and  the  rapid  progress  of  the  cirrhosis  may  be  due  to  an 
infection  faUing  on  a  liver  the  subject  of  latent  cirrhosis.  The  haemat- 
emesis may  therefore  be  followed  by  fever  and  ascites  may  soon  develop. 

Possibly  a  slight  and  transient  elevation  of  temperature  after  hsema- 

*  H.  Fagge:    Principles  and  Practice  of  Medicine,  1st  ed.,  1SS6,  vol.  ii,  p.  134. 
t  Osier:    Practice  of  Medicine,  p.  572,  4th  ed. 


CIRRHOSIS    OF    THE    LIVER.  265 

temesis  may  depend  on  the  retention  in  the  intestines  of  a  considerable 
quantity  of  blood  which  in  decomposing  liberates  fibrin  ferment.  This, 
if  absorbed  into  the  circulation,  ma}^  give  rise  to  an  elevation  of  tem- 
perature. Hsematemesis  may  act  as  such  a  severe  shock  to  a  patient 
who  has  previously  been  drinking  steadily  as  to  set  up  the  traumatic 
form  of  delirium  tremens  which  I  have  seen  prove  fatal. 

Etiology  of  Haematemesis  in  Cirrhosis. — (1)  Gastritis. — The  hsema- 
temesis may  foUow  a  debauch  and  be  due,  in  part  at  least,  to  an  exacer- 
bation of  a  chronic  gastritis.  In  such  a  case  the  after-history  will  indi- 
cate vfhether  acute  gastritis  alone,  or  whether  cirrhosis  and  gastritis 
together,  were  responsible  for  the  haemorrhage.  It  is  by  no  means  rare 
to  meet  vdth  cases  of  hsematemesis  apparently  solely  clue  to  gastritis, 
but  in  any  given  case  the  possibility  must  be  borne  in  mind  that  hsema- 
temesis may  after  aU  have  been  disposed  to  by  a  cirrhotic  condition  of 
the  liver,  which  subsecjuently  became  arrested  or  latent  and  gave  rise 
to  no  further  symptoms. 

Bad  teeth  and  pyorrhoea  alveolaris  are  not  infrequently  responsible 
for  infective  gastritis,  and  have  often  been  overlooked  in  the  days  before 
the  importance  of  oral  sepsis  was  recognised.  Toxic  gastritis  may,  of 
course,  be  set  up  by  a  drinking  bout.  In  hsematemesis  from  gastritis 
the  blood  is  thought  to  be  derived  by  oozing  from  the  capillaries  and 
small  veins  of  the  gastric  mucous  membrane.  The  hsemorrhage  is 
probably  determined  by  the  occurrence  of  minute  areas  of  necrosis  and 
ulceration  in  the  course  of  a  toxic  or  septic  gastritis.  In  cases  where  no 
source  for  haemorrhage  can  be  found  in  the  stomach  or  oesophagus  it 
may  depend  on  the  toxic  state  of  the  blood,  which  shows  itself  else- 
where by  hsemorrhage  from  the  gums,  into  the  skin,  etc. 

It  is  unlikely  that  hsematemesis  is  ever  due  to  mere  mechanical 
increase  of  venous  blood-pressure  in  the  walls  of  the  stomach;  some 
inflammatory  or  degenerate  change  in  the  gastric  mucosa  is  a  necessary 
factor.  It  is,  of  course,  true  that  often  no  determining  cause  is  forth- 
coming; but  sometimes  fever,  gastritis,  and  splenic  enlargement  may 
precede  it;  Gauthier  *  suggests  that  toxines  unaltered  l^y  the  liver  act 
on  the  intestinal  blood-vessels  and  so  set  up  haemorrhage. 

(2)  Minute  Erosions. — Haematemesis  in  cirrhosis  of  the  liver  may  be 
due  to  minute  superficial  erosions  of  the  gastric  mucous  membrane. 
These,  it  should  be  noted,  may  be  easily  overlooked,  especially  as  the 
stomach  is  blood-stained  and  somewhat  sodden.  In  order  to  detect 
them  the  stomach  should  be  allowed  to  remain  for  some  hours  in  jMiiller's 
fluid,  after  which  small  erosions  will  become  more  e^ddent. 

Deguyt  has  recorded  a  fatal  hajmatemesis  in  a  case  of  latent  cirrhosis  with 
a  minute  superficial  ulceration  x\>  oi  a  millimetre  in  size. 

MathieuJ  has  recorded  a  case  of  a  woman  aged  thirty  who  died  with  haema- 
temesis and  was  thought  to  be  the  subject  of  gastric  ulcer;  the  autopsy  showed 
cirrhosis,  varicose  oesophageal  veins,  and  numerous  hajmorrhagic  erosions  on  the 

*  Journ.  de  Med.,  March  10,  1S96. 

t  Deguy:    Bull.  Soc.  Anat.  Paris,  1S9S,  p.  7G7. 

t  Mathieu:    La  Semaine  M6dicale,   1897,  p.   170. 


266  DISEASES    OF   THE    LIVER. 

lesser  curvature  and  posterior  wall  of  the  stomach.     Microscopically  there  was 
acute  interstitial  gastritis,  which  was  the  apparent  cause  of  the  ulceration. 

(3)  Gastric  and  Duodenal  Ulcers. — Gastric  ulcer  rarely  occurs  in 
patients  with  cirrhosis  of  the  liver. 

In  the  j^ears  1894-1904  (JuljO  there  were  3094  autopsies  at  St.  George's 
Hospital,  among  which  Mr.  T.  C.  Enghsh  found  that  there  were  56  cases  of  gastric 
ulcer  and  19  cases  of  duodenal  ulcer;  in  two  of  the  56  gastric  cases  there  was 
hepatic  cirrhosis.  According  to  the  Fenwicks,*  cirrhosis  of  the  Hver  is  present 
in  9  per  cent,  of  cases  of  gastric  ulcer. 

It  is  indeed  remarkable  that  gastric  ulcer  is  so  comparativel}''  rare  in 
cases  of  cirrhosis,  where  the  chronic  venous  obstruction  would,  by  re- 
ducing the  resistance  of  the  part,  tend  to  render  it  more  vulnerable. 

Graham  Steele  t  refers  to  fatal  hsematemesis  from  gastric  ulcer  in  a  case  of 
cirrhosis. 

Duodenal  Ulcer. — In  rare  instances,  of  which  I  have  seen  one, 
copious  hsematemesis  may  occur  in  the  course  of  cirrhosis  from  a  duo- 
denal ulcer.  In  184  cases  of  duodenal  ulcer  collected  by  G.  M.  Cullen,J 
hepatic  cirrhosis  was  present  in  2.2  per  cent. 

(4)  Varicose  (Esophageal  Veins. — This  is  the  most  important  cause  of 
hsematemesis  in  cirrhosis,  as  shown  by  the  fact  that  it  is  found  to  be 
present  in  the  great  majority  (80  per  cent.)  of  the  fatal  cases,  where  a 
thorough  postmortem  examination  is  made.  (Preble. §)  In  exceptional 
instances  varicose  oesophageal  veins  insij  be  present  when  the  liver  is 
healthy. 

Graham  and  Weir  Mitchell  ||  have  recorded  cases  of  fatal  hsematemesis  from 
this  cause  in  a  boy  aged  seA-enteen  years  and  in  a  child  where  the  liver  was  healthy. 

In  adults  varicosity  of  the  oesophageal  veins  may  be  due  to  chronic  alcoholism 
without  any  cirrhosis  of  the  Hver  (LetuUe**).  It  has  Iseen  thought  that  this  alcohohc 
phlebectasis  is  due  to  the  local  caustic  action  of  alcohol  on  the  mucous  membrane 
of  the  oesophagus   (G.  Mullerft). 

In  most  cases  of  oesoj)hageal  varix  the  liver  is  cirrhotic  and  is  re- 
sponsible for  the  dilated  oesophageal  veins  in  the  manner  already  de- 
scribed. This  compensatoiy  collateral  circulation  serves  a  useful  end 
in  relieving  portal  engorgement,  but,  like  other  compensatoiy  mechan- 
isms, it  may  fail.  Severe  haemorrhage  may  occur  as  the  result  of  ulcera- 
tion of  the  mucous  membrane  coA-ering  the  varices,  and  may  be  pre- 
cipitated by  the  passage  of  rough  masses  of  food  through  the  oesophagus. 
These  cesoi^hageal  varices  and  severe  haemorrhages  are  commoner  in 
association  with  large  than  with  small  cirrhotic  livers. 

The  blood  may  well  up  from  the  oesophagus  when  the  patient  is 

*  S.  and  S.  Fenwick:    Ulcer  of  the  Stomach  and  Duodenum,  p.  76. 

t  Graham  Steele:    Medical  Chronicle,  vol.  xix,  p.  312. 

JCullen:    The  Scottish  Medical  and  Surgical  Journal,  vol.  i,  p.   637,   1S97. 

§  Preble:    American  Journ.  Med.  Sciences,  vol.  cxix,  p.  263. 

II  Graham,  Weir  Mitchell:  Trans.  Assoc.  American  Physicians,  vol   xi,  p.  215, 
1896. 

**  Letulle:    Soc.  Med.  des  HA  p.   Paris,  Oct.  24,  1890,  p.  783. 

tt  MuUer,  G.:    Gaz.  hebdom.  de  M6d.  et  de  Chirurg.,  May  20,  1900. 


CIRRHOSIS    OF    THE    LIVER.  267 

lying  quiet  in  l3ed,  and  not  be  vomited  up  as  it  is  in  gastric  ulcer.  But 
in  this  event  the  blood  does  not  enter  the  stomach  and  will  be  alkaline. 
As  the  varicose  oesophageal  veins  are  practically  always  close  to  the 
cardiac  orifice,  the  blood  usually  runs  into  the  stomach  and  is  vomited 
up  just  as  in  ordinary  hsematemesis. 

The  loss  of  blood  may  be  so  profuse  as  to  prove  fatal.  It  is  probable 
that  nearly  all  cases  of  fatal  hsematemesis  in  cirrhosis  are  due  to  ulcerated 
oesophageal  veins. 

In  Preble's*  analysis  of  60  cases  of  fatal  gastro-intestinal  hsemorrhage  in 
cirrhosis  the  condition  of  the  oesophagus  was  investigated  in  42  and  oesophageal 
varices  were  present  in  ,35,  or  SO  per  cent,  of  these  cases. 

It  is  highly  probable  that  in  many  of  the  cases  regarded  as  due  to  a 
general  venous  oozing,  an  ulcerated  oesophageal  varix  was  overlooked. 
The  ulceration  may  be  very  small  and  may  escape  notice  at  the  autopsy. 
Letulle  says  that  the  ulcer  may  only  become  apparent  after  the  oesophagus 
has  been  left  for  twenty-four  hours  in  Miiller's  fluid. 

The  first  haemorrhage  may  be  so  profuse  as  to  be  immediately  fatal. 
This  was  so  in  one-third  of  Preble's  t  60  fatal  cases  of  gastro-intestinal 
hsemorrhage  in  cirrhosis.  In  other  cases  repeated  haemorrhages  occur. 
In  rare  instances  there  are  considerable  intervals  of  good  health  between 
the  attacks  of  hsematemesis. 

GarlandJ  reports  a  case  in  which  hsemorrhage  took  place  at  intervals  for  seven 
years  and  at  the  postmortem  perforation  of  the  dilated  veins  was  found. 

Repeated  haemorrhages  may  occur  at  brief  intervals  and  kill  the 
patient  in  a  short  time  from  the  first  symptom  of  illness,  as  in  a  case  put 
on  record  ])y  Marmasse.§  In  cases  of  fatal  gastro-intestinal  haemor- 
rhage from  cirrhosis  the  primary  disease  is  often  latent.  The  latency 
of  cirrhosis  in  cases  where  varicose  oesophageal  veins  are  present  shows 
the  value  of  this  compensatory  mechanism.  In  only  6  per  cent,  of  35 
cases  of  cirrhosis  in  which  varices  were  present  were  the  clinical  symp- 
toms characteristic,  viz.,  ascites,  enlarged  spleen,  subcutaneous  abdomi- 
nal veins,  etc.     (Preble.) 

The  following  case  illustrates  the  latency  of  cirrhosis  imtil  fatal 
hsematemesis  from  an  ulcerated  oesophageal  varix  occurs: 

A  man  aged  thirty-three  years  was  brought  in  dead  into  St.  George's  Hospital 
on  September  10,  1900,  having  vomited  up  a  large  quantity  of  blood  shortly 
before  death.  There  were  dilated  varicose  veins  at  the  lower  end  of  the  cesopli- 
agus,  one  of  which  was  ulcerated.  The  veins  at  the  cardiac  end  of  the  stomach 
were  somewhat  varicose  and  there  was  a  very  minute  abrasion  of  the  mucosa  over 
one  of  them,  but  the  vein,  though  exposed,  was  not  perforated.  Tlie  intestines 
contained  blood.  There  was  no  ascites.  The  liver,  4^  pounds,  was  finelv  cirrhotic 
and  showed  bright  yellow  nodules,  fully  justifying  Laennec's  name,  '^cirrhosis" 
(=  full  of  yellowness).  Microscopically  there  was  multilobular  fibrosis  with  much 
fatty  degeneration  of  the  liver  cells.  The  gall-bladder  contained  a  small  bilirubin- 
calcium  calculus.     The  spleen,  9§  ounces,  was  shrunken  as  if  it  had  been  larger. 

*  Preble:  American  Journ.  of  Med.  Sciences,  vol.  cxix,  p.  263,  March,  1000. 
t  Preble:  American  Journal  of  Medical  Sciences,  vol.  cxix,  p.  263,  March,  1900. 
j  Garland:  Trans.  .Association  of  .American  Physicians,  vol.  .xi,  p.  206,  1896. 
§  Marmasse:    Bull.  Soc.  Anat.  Paris,   1899,  p.  75. 


268  DISEASES    OF   THE    LIVER. 

The  kidneys,  7 J  ounces  and  8  J  ounces,  were  hypertrophied  but  healthy.     There 
was  caseous  tubercle  at  the  apex  of  the  right  lung. 

In  the  following  instance  death  was  due  to  extensive  haemorrhage 
from  an  ulcerated  oesophageal  vein  in  a  patient  under  treatment  for 
cirrhosis : 

Charles  W.,  fifty-one  years,  a  farm  labourer,  was  admitted  under  my  care  in 
St.  George's  Hospital  on  September  15,  1900,  with  slight  ascites  and  oedema  of 
the  legs.  He  had  been  a  moderate  drinker,  and  had  never  had  syphilis.  In  July, 
1900,  he  had  hEeiuatemesis  and  melsena;  before  this  he  had  not  suffered  from  dyspep- 
sia or  morning  vomiting.  He  was  a  weatherbeaten  man  with  a  large  liver  and 
slight  ascites.  The  spleen  was  not  palpable.  There  was  oedema  of  the  feet,  but 
no  neuritis.  Pulse  96,  low  tension,  artery  tortuous  and  somewhat  atheromatous. 
Urine  1008,  no  albumin.  He  was  kept  in  bed  and  given  milk  diet  and  a  mixture 
containing  15  grains  of  the  iodides  of  potash,  soda,  and  ammonium  three  times 
daily.  The  oedema  of  the  feet  went  down  and  the  man's  condition  improved; 
he  was  indeed  feeling  particularly  well,  when  on  September  21  he  brought  up  a 
quantity  of  blood  from  the  stomach;  he  was  given  suprarenal  extract  by  the  mouth 
and  morphia  hypodermically;  on  the  next  day  he  again  had  hsematemesis  and 
became  very  blanched,  so  that  concealed  haemorrhage  was  suspected.  He  was 
transfused,  but  died  the  same  day.  At  the  autopsy  there  was  a  small  ulcer  in 
the  oesophagus,  elevated  so  as  to  look  like  a  miniature  volcano,  situated  about  one 
inch  from  the  cardiac  orifice  of  the  stomach.  This  opened  into  a  vein;  the  other 
veins  at  the  lower  end  of  the  oesophagus  were  not  dilated  or  varicose.  The  stomach 
was  fuU  of  blood  clot  (25  ounces) ;  the  intestines  were  also  filled  with  blood.  The 
fiver,  80  ounces,  was  pale,  finely  granular,  and  intensely  cirrhotic;  there  were 
numerous  hsemorrhagic  spots  in  it.  The  portal  vein  was  normal.  The  kidneys 
were  pale  but  free  from  arteriosclerotic  change.  Spleen  large.  The  cavity  of  the 
peritoneum  contained  two  pints  of  ascitic  fluid.     Testes  normal. 

(5)  Varicose  Gastric  Veins. — Haemorrhage  from  varicose  veins  in  the 
stomach  is  a  very  rare  event  in  cirrhosis.  Letulle  *  has  described  two 
fatal  cases  in  men  aged  twenty-three  and  thirty-nine  respectively.  Other 
cases  have  been  recorded  by  Machiafava,t  Hillier,  Blake,  Jackson, 
Revillout,  Minot. 

Hcemorrhage  from  the  Pharynx. — Bouchard  J  has  pointed  out  that 
small  nsevi  are  frequent^  present  at  the  back  of  the  pharynx  and  that 
haemorrhage  from  these  nsevi  may  give  rise  to  hsematemesis.  The 
pharynx  of  cirrhotic  patients  with  hsematemesis  should  therefore  be 
carefully  examined,  as  the  cause  of  the  haemorrhage,  if  found,  can  be 
satisfactorily  treated  by  local  styptics. 

It  has  thus  been  seen  that  hsematemesis  in  cirrhosis  may  occur  (i) 
when  there  is  no  morbid  lesion  visible  to  the  naked  eye  except  gastritis, 
(ii)  From  small  superficial  abrasions  of  the  gastric  mucous  membrane, 
(iii)  In  veiy  rare  instances  from  gastric  or  duodenal  ulcer,  (iv)  From 
rupture  or  ulceration  of  varicose  veins  at  the  lower  end  of  the  oesophagus; 
this  is  the  most  important  cause,  (v)  From  ulcerated  varicose  veins  in 
the  stomach,  (vi)  From  the  pharynx,  the  blood  being  swallowed  and 
subsequently  vomited. 

Diagnosis  of  Hsematemesis  of  Hepatic  Cirrhosis  from  that  Due 
to  Other  Causes. — Without  mentioning  all  the  possil^le  causes  of  hsema- 

*  Letulle:    La  Presse  M^dicale,  Nov.  29,  1898. 

t  Machiafava:    Boll,  delle  Soc.  Lancisiana,  Rome,  1S9S 

j  Bouchard:    Rev    de  Med.,  Oct.,  1902,  p.  837. 


CIRRHOSIS    OF   THE    LIVER.  269 

temesis  it  will  be  useful  to  refer  to  those  causes  that  are  common  and 
therefore  most  likely  to  be  confused  with  hepatic  cirrhosis. 

(A)  Gastric  ulcer  in  men  of  mature  years  runs  a  very  chronic  course, 
gives  rise  to  continued  pain  and  dyspepsia,  but  very  rarely  goes  on  to 
perforation.  In  some  cases  that  I  have  seen  there  was  an  absence  of 
tenderness  on  palpation,  although  the  ulcer,  as  verified  at  the  autopsy, 
was  large  and  adherent  to  adjacent  parts.  Haemorrhage  from  the 
stomach  in  these  cases  may  give  rise  to  a  suspicion  of  cirrhosis.  When, 
as  sometimes  occurs,  a  patient  with  entirely  latent  cirrhosis  dies  from 
very  copious  hsematemesis,  due  to  rupture  of  varicose  veins  at  the 
lower  end  of  the  oesophagus,  it  is  impossible  to  diagnose  the  condition 
from  gastric  ulcer  except  on  the  greater  probability  of  cirrhosis  giving 
rise  to  hsematemesis  in  a  middle-aged  man  than  gastric  ulcer. 

The  occurrence  of  repeated  haemorrhages  and  painful  dyspepsia  are 
against  cirrhosis.  If  the  spleen  is  palpable,  the  diagnosis  is  against 
gastric  ulcer.  In  young  women  gastric  ulcer  is  far  more  frequent  than 
cirrhosis.  When  cirrhosis  occurs  in  them,  there  is  usually  considerable 
enlargement  of  the  liver  and  spleen  and  distinct  evidence  of  alcoholic 
excess.  Pressure  over  the  gastric  ulcer  in  young  women  gives  rise  to 
sharp  pain,  compared  by  the  patient  to  that  of  a  knife;  this  is  quite 
different  from  the  diffuse  tenderness  elicited  on  deep  pressure  in  gastritis 
accompanying  cirrhosis.  The  character  of  the  blood  in  hsematemesis 
due  to  cirrhosis  is  a  point  of  some  importance.  It  is  black  from  the 
more  prolonged  stay  in  the  stomach  and  is  often  clotted,  forixiing  masses 
that  may  stick  in  the  patient's  pharynx.  In  gastric  ulcer  the  blood 
is  poured  out  more  rapidly  from  a  leaking  artery,  and  is  therefore  brighter, 
more  arterial,  less  acted  upon  by  the  gastric  juice,  and  not  necessarily 
coagulated. 

(B)  From  pore-like  erosions  of  the  gastric  arteries.  Very  free 
and  repeated  haemorrhages  may  take  place  from  minute  erosions.  In 
these  cases  there  is  no  deep  tenderness  and  there  is  a  comparative 
absence  of  antecedent  gastric  symptoms.  Attention  has  recently  been 
drawn  to  these  cases  by  Dieulafoy  *  and  Steven. f  It  is  important 
to  recognise  them,  since  the  proper  treatment  is  to  perform  laparotomy, 
open  the  stomach,  and  suture  the  bleeding  point.  The  chief  distinction 
from  the  hsematemesis  of  cirrhosis  seems  to  be  the  frequency  of  repeated 
and  copious  hsematemesis  in  a  patient  who  has  none  of  the  signs,  symp- 
toms, or  history  of  portal  cirrhosis. 

(C)  In  carcinoma  of  the  stomach  the  vomited  blood  is  black,  resem- 
bles ''coffee-grounds,"  and  is  usually  small  in  quantity,  so  that  melsena 
is  not  noticed.  In  carcinoma  of  the  pylorus  hsematemesis  is  in  rare  in- 
stances profuse;  in  such  cases  the  stomach  will  probably  be  dilated  and 
a  tumor  may  be  palpal)le.  As  a  rule,  carcinoma  of  the  stomach  is  accom- 
panied by  so  much  pain  and  the  ^•omited  blood  is  so  small  in  amount 
that  the  condition  is  not  likely  to  imitate  cirrhosis.     If  tested,  the  A-omit 

*  Dieulafoy:    (Exulceratio  simplex.)  La  Presse  Medicale,  Jan.   19,  1S98. 
t  Steven,  J.  L.:    (Pore-lilve  Erosions  of  the  Gastric  Arteries.)     Glasgow  Med 
Journ.,  vol.  li,  p.  5,  Jan.,  1899 


270  DISEASES    OP   THE    LIVER. 

will  probably  be  found  not  to  contain  hydrochloric  acid.  Another  im- 
portant point  in  the  diagnosis  of  gastric  carcinoma  is  the  presence  of  a 
tumor  near  or  at  the  umbilicus,  in  the  line  of  the  falciform  ligament,  or 
on  the  surface  of  the  liver. 

(D)  Periodic  hsematemesis  may  occur  for  years  in  splenic  ancemia; 
sometimes  there  is  very  fair  health  in  between  the  attacks;  in  some 
instances  recurrent  haemorrhages  have  occurred  over  a  period  of  ten 
years.  The  ansemia  is  more  marked  and  the  splenic  enlargement  more 
considerable  than  in  cirrhosis.  A  correct  diagnosis  from  cirrhosis  depends 
largely  on  this  fact,  and  is  of  importance  inasmuch  as  splenectomy 
appears,  from  Osier's  *  and  Harris  and  Herzog's  f  observations,  to 
offer  the  best  chance  of  cure.  These  cases  usually  occur  in  men  between 
thirty  and  forty  years  of  age,  and  so  might  easily  be  regarded  as  due  to 
latent  cirrhosis. 

Closely  allied  to  chronic  splenic  anaemia  of  adults,  and  probably  a 
late  development  or  complication  of  that  disease,  is  the  condition  de- 
scribed by  Banti,  and  often  spoken  of  as  Banti's  disease.  Splenic  anaemia 
is  after  some  years  complicated  by  secondary  cirrhosis  of  the  liver  and 
jaundice.  In  this  condition  severe  gastro-intestinal  haemorrhages  may 
occur. 

In  leukaemia,  hsematemesis  and  melaena  may  occur  and  be  associated 
with  both  splenic  and  hepatic  enlargement;  the  diagnosis  from  cirrhosis 
depends  on  an  examination  of  the  blood. 

Prognosis. — Haematemesis  is  rarely  fatal  in  cirrhosis;  in  80  cases 
where  cirrhosis  was  the  direct  cause  of  death  haematemesis  was  the  sole 
cause  in  only  4,  or  5  per  cent. 

Treatment  of  Haematemesis  from  Cirrhosis. — The  patient  should 
be  kept  perfectly  quiet  in  bed  and  for  three  or  four  days  nothing  whatever 
should  be  given  by  the  mouth.  Ice  should  certainly  not  be  sucked,  as 
an  indefinite  quantity  of  water  is  thus  taken,  which  necessarily  sets  up 
peristaltic  contractions  of  the  stomach,  and  so  may  give  rise  to  fresh 
haematemesis,  while,  further,  the  cold  water  must  abstract  a  considerable 
amount  of  heat  from  the  patient,  who  is  often  already  somewhat  collapsed. 
Thirst,  which  is  often  a  cause  of  distress  to  the  patients,  is  a  natural 
result  of  the  loss  of  blood  and  of  the  draining  of  the  tissues  to  replace 
the  fluid  part  of  the  blood.  The  mouth  should  be  cleaned  by  pads  of 
moistened  cotton-wool  and  enemata  of  warm  water  should  be  given  every 
four  hours  to  relieve  thirst.  If  necessary,  subcutaneous  transfusion  vnth. 
saline  solution  may  be  employed.  In  order  to  insure  rest  a  hypodermic 
injection  of  morphia  is  useful;  this  calms  the  natural  mental  disturbance 
and  anxiety  of  a  person  who  has  unexpectedly  brought  up  blood. 

The  administration  of  digitalis  or  digitalin,  ergot,  lead,  or  other  drugs 
which  constrict  the  vessels  and  raise  blood-pressure,  is  useless  if  not 
dangerous.  Nitrite  of  amyl,  which  dilates  the  small-  blood-vessels  and 
lowers  blood-pressure,  has  more  theoretical  grounds  in  its  favour,  but 
has  not  been  used  in  the  treatment  of  haematemesis.     Chloride  of  calcium 

*  Osier:    Trans.  Assoc.  American  Physicians,  vol.  xvii,  1902. 

t  Harris  and  Herzog:   Annals  of  Surgery   vol.  xxxiv,  p.  Ill,   Juty,  1901. 


CIRRHOSIS    OF   THE    LIVER.  271 

increases  the  coagulating  power  of  the  blood,  and  so  may  lead,  to  throm- 
bosis in  the  vessels  responsible  for  the  haemorrhage.  It  may  be  given  in 
a  dose  of  a  drachm  per  rectum  in  the  enemata  of  water  given  to  relieve 
thirst,  and  may  be  repeated  if  hsematemesis  recurs  and  the  patient's 
life  is  threatened  from  anaemia  and  exhaustion.  As  recurrent  hsema- 
temesis  in  cirrhosis  is  usually  due  to  ulceration  of  varicose  veins  at  the 
lower  end  of  the  oesophagus,  it  is  advisable  to  try  and  act  locally  on  the 
bleeding  area  by  the  administration  of  Ruspini's  styptic,  which  is  largely 
composed  of  gallic  acid ;  the  styptic  may  be  given  in  half  to  one  drachm 
doses  in  an  ounce  of  water  by  the  mouth.  Two  successive  half-drachm 
doses  may  be  given. 

The  various  preparations  of  suprarenal  gland  substance  may  also  be 
given  by  the  mouth  in  recurrent  hsematemesis  so  as  to  obtain  the  local 
vasoconstrictive  effect  on  the  bleeding  vessels.  It  should  not  be  given 
hypoderixdcally  or  per  rectum,  as,  its  general  effect  on  blood-pressure 
being  to  raise  the  tension,  it  would,  if  absorbed  into  the  general  circula- 
tion, tend  to  increase  haemorrhage  from  any  leaking  vessel.  Another 
remedy  which  may  be  given  by  the  mouth  is  turjDentine  in  twenty  minim 
doses  in  spirits  of  chloroform  ("ix)  and  water  (5j)  every  four  or  six 
hours. 

The  local  application  of  an  ice-bag  to  the  abdomen  is  recommended 
by  some  writers,  but  its  effect  is  open  to  some  doubt,  and,  on  the  whole, 
it  is  better  to  do  without  it. 

If  there  is  great  collapse  after  hsematemesis,  transfusion  of  normal 
saline  solution  subcutaneously  or  into  the  veins  should  be  performed. 

The  lower  bow^el  should  be  cleared  out  by  a  soap-and-water  or  by  a 
glycerin  enema,  or  when  there  is  no  recurrence  of  haemorrhage  and  there 
is  any  abdominal  distension  or  slight  fever,  a  blue  pill  followed  by  a 
saline  draught  containing  sulphate  of  magnesia  should  be  given  on  the 
third  day.  During  the  first  three  days  it  is  better  to  give  nothing  by 
the  mouth,  rectal  injections  of  water  (10  to  20  ounces)  being  given  to 
relieve  thirst  every  four  or  six  hours  as  seems  necessary.  Nutrient 
enemata  or  suppositories  may  also  be  given  every  six  hours,  but  in 
many  instances  this  is  not  really  necessary,  and  the  patient  is  more  com- 
fortable without.  In  fact,  the  mental  influence  of  nutrient  enemata  is 
often  more  valuable  than  their  physical  effect. 

If  there  is  nothing  to  suggest  gastric  ulcer,  cautious  feeding  by  the 
mouth  may  usually  be  begun  after  the  third  day,  ))rovided  there  has  been 
no  return  of  haematemesis.  Peptonized  milk  or  peptonized  milk  gruel 
should  first  be  given  and  the  diet  gradually  improved.  After  a  week 
or  ten  days,  according  to  his  general  condition,  the  patient  should  be 
allowed  to  get  up. 

A  most  important  point  is  the  after-treatment,  which  consists  in  a 
light,  simple  diet,  abstinence  from  alcoholic  stimulants  and  from  highly 
spiced  and  stinmlating  articles  of  food.  The  importance  of  change  of 
hfe  should  be  clearly  and  carefully  explained  to  the  patient,  and  he 
should  be  advised  to  become  a  total  abstainer. 

When,  as  sometimes  happens,  haematemesis  occurs  in  patients  with 


272  DISEASES    OF   THE    LIVER. 

ascites,  removal  of  the  fluid  b}^  paracentesis  may  be  followed  by  a  cessa- 
tion of  hsematemesis.  In  such  cases  congestion  may  be  aggravated  by 
the  intra-abdominal  pressure  of  ascites. 


HAEMORRHAGE  FROM  THE  BOWEL. 

Hsemorrhage  from  the  bowel  is  a  frequent  symptom  in  cirrhosis.  It 
may  be  divided  into  (i)  melsena  as  ordinarily  understood,  viz.,  blood  so 
altered  that  it  is  darkened  in  colour  by  the  action  of  sulphuretted  hydro- 
gen on  the  iron  of  the  haemoglobin,  and  by  other  factors,  such  as  the 
effect  of  the  secretions  of  the  aUmentary  canal  on  the  blood;  (ii)  hsemor- 
rhage from  piles  or  from  the  mucous  membrane  of  the  rectum,  the  blood 
being  more  or  less  of  its  normal  colour. 

Melsena  {r,  ix^lav^a  -Mmuq^  "the  black  disease")  commonly  accompa- 
nies or  follows  hsematemesis.  The  blood,  which,  by  distending,  mechan- 
ically irritates  the  stomach,  is  expelled  in  two  directions — ^into  the 
oesophagus  and  into  the  duodenum.  In  other  words,  while  hsematemesis 
is  going  on  the  patient  vomits  into  the  duodenum.  The  hsemoglobin  of 
some  of  the  blood-corpuscles  is  acted  upon  by  the  gastric  juice  and  re- 
duced to  acid  haematin;  there  is  hardly  sufficient  time  for  this  to  take 
place  in  the  mass  of  the  blood  that  is  driven  into  the  duodenum,  so  that 
the  blackness  and  tarry  appearance  of  the  motions  are  largely  the  result 
of  the  iron  of  the  hsemoglobin  being  acted  upon  by  sulphuretted 
hydrogen  in  the  intestines  and  converted  into  some  compound  contain- 
ing sulphide  of  iron. 

Melsena  from  gastric  hsemorrhage  may  occur  without  concomitant 
hsematemesis.  This  depends  on  the  fact  that  the  stomach  is  not  over- 
distended  by  the  blood  poured  out  into  it.  When  the  volume  of  blood 
poured  out  into  the  stomach  is  small,  it  will  pass  into  the  duodenum 
mixed  with  the  contents  of  the  stomach  and  appear  in  the  motions.  In 
such  cases  the  fact  that  melsena  has  occurred  may  escape  observation 
or  only  be  found  out  accidentally,  and  may  then  be  regarded  as  due  to  a 
latent  duodenal  or  intestinal  ulcer.  It  may  be  difficult  or  impossible  to 
diagnose  the  source  with  certainty  in  the  absence  of  other  signs  of  cir- 
rhosis. In  duodenal  ulcer  there  should  be  deep  tenderness  in  the  situation 
of  the  duodenum  and  pain  two  or  three  hours  after  food.  Duodenal 
ulcer  may  complicate  cirrhosis  and  give  rise  to  melsena  without  hsemat- 
emesis. I  have  seen  one  case  in  a  man  aged  forty  years  in  which  this 
coincidence  was  present.  The  duodenal  ulcer,  undiagnosed  during  life, 
gave  rise  to  very  acute  pain  in  the  right  loin. 

Melsena  in  cirrhosis  may  depend  on  hsemorrhages  of  considerable  size 
from  the  mucosa  of  the  intestines.  This  event  is  analogous  to  the  gastric 
hsemorrhages,  and  is  related  in  a  similar  fashion  to  the  abnormal  condi- 
tions of  the  portal  circulation  and  to  the  inflamed  and  altered  state  of 
the  mucous  membrane  of  the  intestine.  Melsena  in  cirrhosis  is  usually 
seen  about  the  same  time  as  hsematemesis,  viz.,  in  the  pre-ascitic  stage, 
but  it  may  occur  after  ascites  has  come  and  gone,  and  be  a  terminal 
phenomenon. 


CIRRHOSIS    OF    THE    LIVER.  273 

In  the  following  cases  extensive  haemorrhage  from  the  rect-mn  imme- 
diately preceded  death : 

A  woman  of  alcoholic  habits,  aged  forty-nine,  under  my  care  in  St  George's 
Hospital,  was  tapped  for  ascites  twice  within  a  fortnight  after  admission.  After 
this  she  lived  for  seven  and  one-half  weeks  in  an  extremelj'  drowsy  condition, 
but  did  not  again  become  ascitic.  The  day  before  her  death  she  passed  two  pints 
of  blood  from  the  bowel.  There  were  no  subcutaneous  heemorrhages  at  any  time. 
At  the  autopsy  the  mucous  membrane  of  the  lower  6  inches  of  the  rectum  was 
inflamed,  and  though  no  definite  ulcer  could  be  found,  the  rectum  must  have 
been  the  source  of  the  hemorrhage;  for  no  blood  or  blood  staining  was  found  higher 
up  in  the  bowel.     The  liver  was  cirrhotic. 

In  a  man  aged  forty-four  j-ears  death  was  immediately  preceded  b}^  mela?na. 
He  had  twice  been  tapped  for  ascites  due  to  cirrhosis;  his  case  is  referred  to  else- 
where (p.  274),  as  he  had  successively  hsematuria,  epistaxis,  and  lastly  mehena. 

Melsena  of  slight  degree  may  occur  from  small  multiple  haemorrhages 
taking  place  from  the  mucosa  of  the  intestines  and  due  to  hepatic  in- 
sufficiency. These  extravasations  are  analogous  to  the  multiple  haemor- 
rhage occurring  under  similar  conditions  into  the  skin  and  other  tissues. 

Piles  occasionally  occur  in  cirrhosis  and  may  give  rise  to  some  bleed- 
ing. It  is  certainly  remarkable  that  piles  are  not  more  common  in  cir- 
rhosis, as  it  would  naturally  have  been  expected  that  portal,  obstruction 
would  almost  constantly  lead  to  a  varicose  condition  of  the  haemor- 
rhoidal  veins.  FrerichS;*  Sappey,  Thierfelder,  Nothnagel,t  and  others 
are  all  agreed  on  the  comparative  rarity  of  piles  in  cirrhosis.  It  has  been 
thought  that  haemorrhage  from  piles  in  cirrhosis  serves  a  useful  purj^ose 
by  relieving  hepatic  engorgement,  and  that  their  cure  by  operation  may 
be  followed  by  hsematemesis  or  by  advance  in  the  downward  course  of 
the  disease;  in  other  words,  that  piles  in  cirrhosis  is  a  condition  that  it 
is  dangerous  to  cure. 

Treatment  of  Melaena. — For  considerable  melaena  without  any 
haematemesis  a  tuipentine  enema  may  be  given.  The  patient  should  be 
kept  quiet  and,  if  necessary,  given  mori^hia.  If  bleeding  occurs  from 
piles,  the  local  condition  should  be  attended  to. 


HAEMOPTYSIS. 

Haemoptysis  in  the  course  of  cirrhosis  is  somewhat  infrequent.  When 
it  does  occur,  it  is  usually  comparatively  slight  in  amount.  It  may  be 
due  to  various  causes : 

1.  False  Hcemoptysis. — This  may  depend  on  epistaxis  from  the 
posterior  nares,  or  on  haemorrhage  from  the  mucous  membrane  of  the 
naso-pharynx.  These  haemorrhages  are  not  uncommon  in  the  late  stages 
of  the  disease  and  may  be  due  to  the  general  toxa?mic  state.  Bouchard  | 
has  insisted  on  the  frec^uency  of  naevi  in  the  pharynx,  from  which  haemor- 
rhage may  occur  independently  of  grave  toxaemia. 

2.  Hcemorrhage  from  the  larynx  may  be  due  to  concomitant  tuber- 
culous disease,  or  to  venous  oozing  depending  on  hepatic  insufficiency. 

*  Frerichs:   Diseases  of  Liver,  vol.  ii,  p.  47.     Transl.  New  Sydenham  Soc. 
t  Nothnagel:    Diseases  of  Intestines.     English  translation,  p.  298. 
I  Bouchard:    Rev,  de  Med.,  Oct.,  1902. 
18 


274  DISEASES    OF   THE    LIVER. 

Drey  fuss  observed  a  bleeding  tumor  in  the  larjaix  of  a  patient  with 
cirrhosis. 

3.  Hcemorrhage  from  the  lungs  due  to  (a)  pulmonary  tuberculosis; 
(b)  extreme  congestion  accompanying  pulmonary  collapse  secondary  to 
abdominal  distension;  (c)  venous  oozing  depending  on  hepatic  insuffi- 
ciency. 

The  occurrence  of  haemoptysis  in  patients  with  cirrhosis  should 
always  arouse  a  strong  suspicion  of  pulmonary  tuberculosis.  It  is,  how- 
ever, not  always  justified.  In  an  alcoholic  woman  under  my  care  who 
said  she  had  had  slight  haemoptysis  for  years,  the  lungs  showed  no  trace 
of  tubercle  at  the  autopsy. 

BIBLIOGRAPHY. 

Drevfuss:    Miinchener  med.  Wochen.,  No.  32,  Bd.  xlv,  S.  1022,  1898. 
Galiiard:    Union  Medicale,  Nov.,  1889. 

Lubet  Barbon:    Annal  de  laryngol.  et  d'otolog.,  1897  (Laiynx). 
Dieulafoy:    Manuel  de  Interne.  Path.,  t.  ii,  689  (Larynx). 

EPISTAXIS. 

Bleeding  from  the  nose  is  by  no  means  an  infrequent  symptom  of 
cirrhosis.  It  may  be  part  of  the  general  tendency  to  haemorrhage  de- 
pending on  hepatic  insufficiency,  but  it  may  supervene  before  there  is 
any  other  evidence  of  this  toxaemia  or  be  the  first  sign  of  this  complica- 
tion. It  occurs  from  one  nostril — usually,  as  was  pointed  out  long  ago, 
from  the  right.  It  usually  comes  from  a  point  near  the  anterior  extremity 
of  the  septum  which  can  be  easily  compressed  (Bouchard  *).  The 
haemorrhage  may  be  due  to  ulceration  of  an  arterial  naevus,  and  may  if 
uncontrolled  be  so  severe  as  to  lead  to  syncope.  Relapses  are  very 
prone  to  occur.  In  a  patient  of  Dieulafoy'sf  repeated  haemorrhages 
occurred  from  an  ulcerated  naevus  in  the  nostrils. 

Epistaxis  may  alternate  with  haemorrhages  from  other  sources. 

In  a  case  under  my  care  a  man  aged  forty-four  had  first  liEematuria,  then 
epistaxis,  and  just  before  death  melsena.  His  liver  was  markedly  cirrhotic  and 
had  given  rise  to  ascites,  which  had  been  tapped  twice. 


HAEMORRHAGES  FROM  OTHER  SITUATIONS. 

Haematuria  may  occur  from  hepatic  insufficiency  and  be  comparable 
to  epistaxis,  but  it  is  rare. 

In  a  man  aged  fifty  years  who  was  under  my  care  in  1903,  with  cirrhosis,  tran- 
sient hsematuria  occurred  at  the  same  time  as  epistaxis  and  oozing  from  the  gums. 

The  following  case  is  of  interest  as  an  example  of  haematuria  and 
other  forms  of  haemorrhage. 

Cirrhosis.     Hcematuria  due  to  Nephritis.     Epistaxis.     Fatal  Melcena. — A  man 
aged  forty-four,  of  alcoholic  habits,  was  admitted  to  St.  George's  Hospital  under 

*  Bouchard:    Rev.  de  Med.,  Oct.,  1902,  p.  837. 

t  Dieulafoy:  Manuel  de  Intern.  Pathologic,  t.  ii,  p.  669,  1901. 


CIRRHOSIS    OF   THE    LIVER.  275 

my  care  on  June  20,  1900,  with  swelling  of  the  abdomen,  flatulence,  pain  near  the 
umbilicus,  swelling  of  the  legs,  and  loss  of  flesh  and  strength  dating  from  an  attack 
of  pneumonia  eighteen  months  previously.  He  had  the  signs  of  cirrhosis  with  a 
large  liver,  but  had  very  distinct  haematuria  with  casts  and  a  sp.  gr.  of  1009.  The 
question  arose  whether  it  was  a  case  of  cirrhosis  with  intercurrent  nephritis 
or  one  of  primary  malignant  disease  of  the  kidney  with  secondary  growths  in  the 
liver.  There  were  no  haemorrhages  elsewhere  in  the  body  and  there  was  nothing 
to  show  that  the  haematuria  was  due  to  hepatic  insufficiency.  The  abdomen 
manifestly  contained  fluid  and  required  tapping  twice  _  With  rest  in  bed  the 
haematuria  passed  away,  but  the  patient's  general  condition  got  worse.  On  July 
9  there  was  only  a  trace  of  albumin,  and  on  July  11  none  at  all.  On  July  11  and 
12  he  had  epistaxis,  and  on  the  latter  day  rapidly  become  comatose;  though  he 
revived  a  httle  after  transfusion,  he  died  on  July  14  with  considerable  melaena. 
At  the  autopsy  the  liver,  68  ounces,  was  cirrhotic  and  finely  granular;  the  portal 
vein  was  free  "from  any  thrombosis.  The  kidneys  weighed  7J  and  8  ounces  each, 
and  showed  parenchymatous  nephritis.  The  mucous  membrane  of  the  small 
intestine  was  pigmented,  the  change  being  more  marked  near  the  stomach.  The 
spleen  weighed  10  ounces. 

Menorrhagia  and  Metrorrhagia. — In  the  early  stages  of  cirrhosis 
metrorrhagia  is  often  seen;  very  possibly  this  is  partly  connected  with 
chronic  alcohohsm.  In  the  later  stages  of  cirrhosis  there  is  usually 
amenorrhcea,  though  when  hepatic  insufficiency  supervenes,  haemor- 
rhages may  occur  from  the  uterine  mucous  membrane. 

The  occasional  formation  of  a  hematoma  in  the  rectus  abdominis 
muscle  has  already  been  referred  to  as  a  possible  evil  effect  of  the  collateral 
circulation  in  connexion  with  the  veins  in  the  round  ligament.  {Vide 
p.  213.) 

In  a  case  recorded  by  Lefas*  in  which  portal  cirrhosis  was  comphcated  by 
jaundice  and  grave  toxaemia  (icterus  gravis)  the  cause  of  the  haematoma  was 
thought  to  be  fatty  degeneration  of  the  endothelium  of  the  intramuscular 
capillaries. 

General  Haemorrhages. — In  the  late  stages  of  cirrhosis  when  the 
hver  has  become  incapable  of  stopping  poisons  absorbed  from  the  ali- 
mentary canal,  a  condition  of  hepatic  toxaemia  results.  The  blood- 
vessels suffer  and  haemorrhages  may  occur  from  their  damaged  walls  all 
over  the  body.  The  general  haeniorrhagic  condition  may  in  some  in- 
stances be  due  to  haemic  infection.  Thus  in  a  remarkable  case  of 
cirrhosis  with  hsemorrhagic  bullae  Monnierf  cultivated  Bacillus  coh  and 
streptococci.  In  such  cases  there  is  naturally  some  fever.  Petechial 
haemorrhages  into  the  skin  are  frequent,  while  haemorrhages  are  often 
seen  from  the  mucous  membrane  of  the  mouth,  blood  oozing  from  the 
gums  or  from  cracks  on  the  dry  dorsum  of  the  tongue.  The  sordes  thus 
produced  give  rise  to  an  offensive  odour  of  the  breath. 

In  an  exceptional  case  recorded  by  WebberJ  htemorrhage  took  place  from  the 
external  ears,  in  addition  to  haemoptysis  and  bleeding  from  the  gums.  Leudet§ 
also  reports  haemorrhage  from  the  external  ear  in  cirrhosis. 

In  the  following  case  thrombosis  and  haemorrhages  were  combined. 
These  two  conditions  are  usually  associated  with  opposite  conditions  of 

*  Lefas:    Bull.  Soc.  Anat.  Paris,  1902,  p.  .586.. 
t  Monnier:  Compt.  rend.  Soc.  de  biol.,  1896,  p.  65. 
t  Webber:    Lancet,   1894,  vol.  i,  p.  1000. 
§  Leudet:   Ann.  Mai.  de  I'or,  Oct.,  1890 


276  DISEASES    OF  THE   LIVER, 

the  blood  as  regards  coagulation,  the  blood  coagulating  more  rapidly 
in  thrombosis  and  less  rapidly  than  normal  in  haemorrhage. 

An  alcoholic  woman  aged  forty  years  was  admitted  under  my  care  in  March, 
1900,  for  severe  hEematemesis  thought  to  be  due  to  cirrhosis;  in  two  days'  time  she 
developed  typical  delirium  tremens,  from  which  she  recovered  under  the  adminis- 
tration of  hyoscine  yV  gr.  subcutem.  After  her  recovery  from  delirium  she  had 
nmnerous  hsemorrhages  all  over  the  body;  it  was  noticeable  that  there  were  several 
small  tlirombosed  veins  in  the  neighbourhood  of  some  large  cutaneous  hgemorrhages. 
There  were  tlirombosed  veins  on  the  front  of  the  abdomen,  on  the  right  mamma, 
and  right  arm.     The  veins  of  the  legs  were  not  affected. 

The  treatment  of  haemorrhages  is  partly  local  and  partly  general;  the 
local  treatment  consists  in  the  appHcation  of  reniecUes  such  as  adrenalin 
to  bleeding  spots  where  they  can  be  reached,  while  the  general  treatment 
consists  in  giving  chloride  of  calcium  in  half-drachm  closes  three  times  a 
day  for  six  doses,  and  in  attempting  to  reduce  the  general  toxaemia  by 
getting  the  kidneys  to  act  "udth  citrate  of  caffeine,  etc.,  draughts  of  water, 
etc.  The  bowels  should  be  kept  open,  and  subcutaneous  transfusion 
may  be  employed  if  it  is  thought  necessary. 

NERVOUS  SYMPTOMS. 

A  considerable  number  of  nervous  manifestations  may  occur  in  the 
course  of  cirrhosis;  as  a  rule  the  more  striking  are  noticed  late  in  the 
disease  and  are  associated  with  advanced  toxaemia.  The  shghter  ner- 
vous symptoms,  such  as  headache,  giddiness,  muscular  weakness  and 
tremor,  disturbance  of  mental  power,  disordered  sensation,  pruritus, 
may  occur  earher  in  the  course  of  cirrhosis.  It  may  not  be  easy  to 
determine  satisfactorily  in  every  case  whether  sjaiiptoms  supervening 
in  cirrhosis  are  solely  due  to  the  liver  and  its  functional  failure,  or  whether 
they  depend  on  other  factors,  such  as  alcoholic  excess  or  renal  disease, 
or  whether  the  symptoms  are  the  outcome  of  hepatic  inadeciuacy  com- 
bined with  one  of  these  additional  factors.  Thus,  dehrium  tremens  is 
due  to  recent  alcoholic  excess,  wliile  other  forms  of  delirium  may  be 
most  satisfactorilv  explained  as  due  to  hepatic  or  renal  inadequacy. 
As  long  as  the  kidneys  excrete  toxic  bocUes  which  the  liver  fails  to  stop, 
the  patient  may  remain  fairly  free  from  marked  nervous  symptoms, 
but  headache,  mental  torpor,  and  depression  are  readily  produced  by 
food  which  has  no  bad  effects  in  a  healthy  person.  Failure  in  the  ex- 
cretion of  urine  gives  rise  to  increased  toxaemia  and  often  precedes  the 
development  of  acute  nervous  phenomena. 

Slight  mental  disturbance  is  conmion  in  patients  with  cirrhosis,  but 
it  is  natural  to  ascribe  loss  of  memory,  failure  of  will-power  and  of  intel- 
lectual ability,  solely  or  in  part  to  the  effects  of  alcohol.  As  in  other 
morbid  conditions  of  the  hver,  mental  depression  and  hypochondriasis 
are  conunon.  ^Muscular  tremor  is  not  infrequent  and  is  often  largely 
alcoholic  and  due  to  sleeplessness  or  to  nights  disturbed  by  nightmares 
and  bad  dreams. 

Pruritus.— Itch'mg  of  the  skin  is  a  symptom  of  hepatic  inadequacy  and 
depends  on  the  failure  of  the  liver  cells  to  arrest  poisons  manufactured 


CIRRHOSIS    OF   THE    LIVER.  277- 

in  the  alimentaiy  canal.  It  is  more  often  associated  with  jaundice,  but 
may  occur  in  its  absence;  it  is  not  a  common  symptom,  and  when  it 
does  occur  is  usually  seen  late  in  the  course  of  the  disease. 

Hanot  *  speaks  of  a  case  where  it  occurred,  and  was  persistent,  a  year  before 
symptoms  of  cirrhosis  developed,  without  any  jaundice. 

The  more  severe  nervous  symptoms  include  coma,  delirium,  convul- 
sions, paralysis,  and  contractions.  It  has  been  thought  by  some  that 
a  large  cirrhotic  liver  is  more  prone  to  be  associated  with  grave  nervous 
symptoms,  but  there  is  probably  not  enough  to  justify  a  verj^  definite 
statement  as  to  this  relationship. 

Coma. — Cases  of  cirrhosis  which  iim  their  full  course  usually  die  vnXh 
coma,  which  often  comes  on  when  ascites  has  disappeared  (post-ascitic 
stage)  or  is  stationan,-  and  small  in  amount.  Coma  is  due  to  grave 
toxaemia,  which  may  Ije  purely  hepatic  and  depend  on  the  destruction 
of  the  hepatic  cells  being  so  widespread  that  the  liver  fails  to  stop  poisons 
manufactured  in  the  alimentary  canal,  as  a  result  of  which  the  circula- 
tion becomes  flooded  with  them.  If  the  kidneys  are  active,  the  poisons 
may  be  got  rid  of,  but  in  many  cases  coma  is  precipitated  b}^  failure  in 
the  excretory  activit}^  of  the  kidneys.  Though  coma  is  more  commonl}- 
a  terminal  phenomenon,  it  may  be  transitory  and  be  removed  by  treat- 
ment. I  have  several  times  seen  coma  disappear  as  the  result  of  intra- 
venous transfusion;  the  same  result  maj^  follow  bleeding.  A  patient 
in  a  drowsy,  semi-comatose  condition  may  wake  up  sufficiently  to  try 
and  get  out  of  bed  and  then  relapse  into  a  state  of  coma.  Before  coma 
comes  on  there  insiy  be  extreme  irritability  and  restlessness,  clue  to 
toxaemia  and  resembling  that  seen  in  renal  toxaemia  or  uraemia. 

Delirium  may  be  terminal  and  precede  coma,  or  more  rarely  it  may 
temporarily  superv^ene  in  the  course  of  the  disease  and  disappear.  In 
the  case  of  transient  dehrium  it  must  be  borne  in  mind  that  dehrium 
tremens  not  uncommonly  occurs  in  the  course  of  cirrhosis.  I  have  seen 
short  bouts  of  fever  associated  with  delirium  lasting  two  days  or  so, 
recur  in  a  patient  with  cirrhosis  before  ascites  developed.  The  character 
of  the  delirium  varies ;  usually  it  is  of  a  low  wandering  type,  but  occa- 
sionally it  is  very  violent  and  requires  considerable  restraint ;  the  patient 
may  get  out  of  bed  or  attempt  to  do  so.  The  character  of  the  delirium 
may  change,  or  quiet  and  noisy  phases  may  alternate. 

Delirium,  tremens  may  occur  under  different  circumstances  in  the 
course  of  cirrhosis.  It  may  come  on  in  the  usual  wa}-  from  continued 
drinking  in  a  patient  with  latent  cirrhosis,  or  even  when  the  disease  has 
advanced  into  the  stage  of  ascites.  It  may  come  on  after  ha?matemesis, 
and  then  be  more  of  the  nature  of  traumatic  delirium  f  and  comparable 
to  the  dehrium  which  is  precipitated,  so  to  speak,  by  a  fractured  thigh 
or  pneumonia  in  an  alcoholic  subject.  In  other  cases  where  haematemesis 
is  not  very  profuse,  a  mild  form  of  delirium  tremens  may  dcA-elop  and  may 

*  Hanot:  Archiv.  G^n^ral.  de  Med.,  vol.  clxxvii,  p.  67. 
t  Compare  S.  West:  Clinical  Journal,  vol.  vii,  p.  oS. 


278  DISEASES   OF  THE   LIVER. 

possibly  be  due  to  the  treatment — viz.,  deprivation  of  food  by  the  mouth 
for  a  few  days. 

Convulsions  are  sometimes  seen  at  the  close  of  the  disease.  Delirium 
often  passes  into  coma,  and  convulsions  may  be  added  shortly  before 
death. 

Paralysis. — In  addition  to  paraplegia  due  to  peripheral  neuritis 
of  alcoholic  origin,  it  occasionally  happens  that  paralysis  compHcates 
cases  of  cirrhosis.  Cerebral  haemorrhage  or  thrombosis  may  occur  in  a 
patient  Avith  cirrhosis  of  the  hver,  but  usually  when  the  cirrhosis  is 
latent.  In  very  rare  instances  hemiplegia  occurs  in  patients  with  cir- 
rhosis and  no  gross  change  is  forthcoming  to  account  for  it. 

In  an  alcoholic  woman  aged  fifty-three  who  was  under  my  care  in  St.  George's 
Hospital  with  cirrhosis,  right  hemiplegia  and  aphasia  developed  so  as  to  suggest 
cerebral  haemorrhage.  At  the  autopsy  no  naked-eye  morbid  change  could  be  foimd 
in  the  brain.     The  liver  was  markedly  cirrhotic  (weight,  70  ounces). 

Levi  *  fuUy  records  terminal  coma  and  facial  paralysis  in  a  man  aged  seventy 
with  an  alcoholic  history  and  cirrhosis  and  without  any  cerebral  change  except 
oedema. 

It  is  possible  that  cirrhosis  might  dispose  to  cerebral  haemorrhage  by 
producing  a  hsemorrhagic  tendency.  I  have  seen  one  case  of  cirrhosis  in 
a  girl  aged  nine  years  in  whom  there  were  multiple  cerebral  haemorrhages, 
fever,  and  probably  a  terminal  infection.  It  has  been  thought  that 
thrombosis  in  the  cerebral  vessels  may  be  disposed  to  by  hepatic  cirrhosis 
under  cei'tain  conditions. 

In  a  girl  aged  twelve  years  hemiplegia  was  found  to  be  due  to  thrombosis  of  the 
cerebral  veins.  There  was  ascites  due  to  hepatic  cirrhosis  and  it  was  thought  by 
Fisher  f  that  the  tlirombosis  depended  on  absorption  of  organic  bodies  from  the 
peritoneal  cavity. 

In  children  -ndth  multilobular  cirrhosis  there  are  in  exceptional  cases 
marked  nerv^ous  symptoms  suggesting  juvenile  general  paralysis:  very 
possibly  there  are  examples  of  parasyphiHtic  cirrhosis  combined  vnih. 
general  paralysis  of  the  insane. 

Dr.  Ormerod  %  has  given  a  full  description  of  a  case  that  I  often  saw  when  I 
was  house  physician  at  St.  Bartholomew's  Hospital.  Cirrhosis  of  the  liver  was  never 
suspected  during  life,  the  symptoms  being  progressive  paralysis,  loss  of  mental 
power  going  on  to  idiocy,  fever,  and  marked  emaciation.  He  referred  to  three 
cases,  all  in  one  family,  that  had  been  described  by  Gowers  §  as  examples  of  "tetanoid 
chorea,"  and  to  three  cases,  also  in  one  family,  recorded  by  Homen  ||  and  regarded 
as  due  to  inherited  syphilis. 


DURATION. 

Portal  cirrhosis  commonly  lasts  a  considerable  time;  one,  two,  or 
more  j^ears  usually  inters^ene  between  the  appearance  of  symptoms  due 
to  the  liver,  if  indeed  their  first  appearance  can  be  accurately  determined, 

*  Levi:  Archiv.  G^n^ral.  de  M^d.,  vol.  clxxviii,  p.  165. 

t  Fisher,  T.:  Lancet,  1901,  vol.  ii,  p.  845. 

X  Ormerod,  J.  A.:  St.  Bartholomew's  Hosp.  Reports,  vol.  xxvi,  p.  57,  1890. 

§  Gowers:  Diseases  of  Nervous  System,  Ed.  1,  vol.  ii,  p.  656. 

II  Hom^n:  Neurologisches  Centralblatt,  1890,  p.  514. 


CIRRHOSIS    OF   THE    LIVER.  279 

and  the  termination  of  the  case;  while  the  progress  of  the  lesion  in  the 
liver  may  become  arrested,  and  from  compensatory  changes  the  disease 
may  become  latent.  Sometimes,  however,  the  disease  runs  a  veiy  rapid 
course;  in  such  cases  there  are  a  certain  amount  of  fever,  pain  in  the  abdo- 
men on  the  right  side,  enlargement  and  tenderness  of  the  Uver,  oedema 
of  the  legS;  haemorrhages,  and  the  early  development  of  ascites.  These 
cases  are  more  often  seen  in  comparatively  3"oung  subjects,  who  have 
been  drinking  heavily,  and  may  run  their  course  in  two  to  six  months 
(Hanot*).  When  cirrhosis  runs  a  very  rapid  course,  degenerative 
changes  take  place  in  the  liver  cells  and  the  condition  is  complicated  by 
a  process  much  the  same  as  that  underlying  icterus  gravis,  only  less 
acute. 

TERMINATION  AND  METHOD  OF  DEATH. 

As  has  been  pointed  out  (p.  226),  cirrhosis  may  be  latent  o"wing  to 
compensation  having  been  effected.  The  compensatory  anastomosis  of 
the  oesophageal  veins  with  the  gastric  veins  may  be  a  source  of  danger^ 
and  sometimes  very  profuse  and  even  fatal  haematemesis  may  result 
from  ulceration  or  rupture  of  an  oesophageal  varix.  In  such  cases  cir- 
rhosis may  be  quite  unsuspected,  although  the  fatal  issue  is  a  direct 
result  of  hepatic  cirrhosis. 

In  only  6  per  cent,  of  35  cases  of  hsematemesis  from  oesophageal  veins  were 
the  cases  typical  of  cirrhosis  from  a  clinical  point  of  view  (Preble  f)- 

Hsematemesis  is  rarely  directly  fatal,  but  Preble  has  collected  60 
cases  of  fatal  gastro-intestinal  haemorrhage  in  cirrhosis.  In  80  cases 
fatal  from  the  direct  effects  of  cirrhosis  examined  at  St.  George's  Hospital, 
4,  or  5  per  cent.,  only  were  due  to  hsematemesis.  Death  ma}'  occur  after 
a  single  large  haemorrhage  or  after  a  series  of  repeated  haemorrhages.  In 
a  third  of  the  cases  collected  by  Preble  death  followed  a  single  haemor- 
rhage. 

In  patients  with  cirrhosis,  which  has  not  yet  produced  ascites,  death 
may  be  due  to  a  number  of  complications  {vide  p.  281),  which  freciuently 
throw  any  symptoms  due  to  cirrhosis  into  the  shade.  These  complica- 
tions are  in  some  instances  the  results  of  alcoholism;  thus,  there  can  be 
little  doubt  that  the  influence  of  alcoholism  is  responsible  in  great  measure 
for  the  frecpiency  with  which  tuberculosis,  peripheral  neuritis,  and  car- 
diac failure  appear  as  complications  of  hepatic  cirrhosis.  Tuberculosis  is 
extremely  frequent  in  the  course  of  cirrhosis,  and  not  uncommonly  cir- 
rhosis of  the  liver  is  discovered  after  death  in  a  patient  djdng  from 
phthisis.  Generalized  tuberculosis  may  carry  off  a  patient  with  cirrhosis 
long  before  loss  of  flesh  and  impairment  of  general  nutrition  have  ap- 
peared. I  have  several  times  seen  generalised  tuberculosis  in  fat  patients 
with  cirrhosis. 

"Wlien  chronic  renal  disease  is  associate^l  with  cirrhosis  of  the  liver, 
the  clinical  aspect  is  mainly  that  of  kidney  disease,  and  death  usually 

*  Hanot,  V. :  Archiv.  General,  de  M(5d.,  June  and  Juh',  1892. 

t  Preble:  American  Journ.  of  the  Medical  Sciences,  vol.  cxix,  p.  263. 


280  DISEASES   OF  THE   LIVER. 

results  from  urseinia,  which,  it  may  be  noted,  is  very  much  hke  the  late 
toxsemic  stage  of  cirrhosis. 

Acute  infections,  such  as  erysipelas  and  pneumonia,  when  they  occur 
in  the  subjects  of  cirrhosis,  are  extremely  likely  to  lead  to  a  fatal  termina- 
tion. It  has  been  said  that  acute  infections  of  this  kind  are  more  fatal 
in  portal  cirrhosis  than  in  hypertrophic  biliary  cirrhosis,  since  the  liver 
cells  are  in  a  better  state  of  preservation  in  the  latter  disease.  Occa- 
sionally acute  infection  may  fall  on  the  liver  itself  and  set  up  acute 
degenerative  changes  in  the  liver  ceils,  and  so  give  rise  to  symptoms 
resembling  those  of  acute  yellow  atrophy.  But  inasmuch  as  the  liver 
is  not  healthy  previous  to  the  acute  infection,  as  is  the  case  in  acute 
yellow  atrophy,  it  is  perhaps  more  convenient  to  speak  of  the  condition 
as  icterus  gravis.  An  acute  infection  may  attack  the  smaller  bile-ducts 
without  affecting  the  liver  cells  to  such  a  degree  as  to  produce  acute 
yellow  atrophy,  though  the  clinical  resemblance  is  considerable.  In 
this  connexion  the  following  case  is  of  interest : 

An  alcoholic  waiter  at  a  well-known  club,  aged  forty-seven,  had  had  hsematemesis 
seven  weeks  before  death;  ascites,  jaundice,  and  oedema  of  the  feet  subsequently 
developed;  he  was  admitted  into  St.  George's  Hospital  and  was  tapped;  he  re- 
mained jaundiced,  and  for  the  last  three  weeks  of  his  life  was  delirious.  The  liver 
weighed  60  ounces  and  showed  multilobular  and  monolobular  cirrhosis,  with  in- 
flammation of  the  small  bile-ducts,  which  contained  inspissated  masses  of  bile- 
stained  material  or  microscopic  calculi.  The  spleen  weighed  10  ounces  and  was 
soft.  Probably  an  acute  secondary  infection  was  implanted  on  the  top  of  old- 
standing  common  cirrhosis  and  especially  involved  the  bile-ducts. 

When  ascites  has  developed  death  usually  follows  before  the  patient 
requires  tapping  more  than  once,  or  at  the  most  twice.  Indeed,  if 
paracentesis  has  to  be  repeated  several  times,  the  case  is  either  compli- 
cated with  some  degree  of  chronic  peritonitis  or  is  not  one  of  cirrhosis 
at  all.  After  one  or  two  tappings  the  fluid  may  not  reaccumulate  and 
the  patient  may  linger  on  for  a  time  in  a  drowsy  and  very  feeble  condi- 
tion— a  post-ascitic  stage.  Death  is  usually  due  to  increasing  weakness 
and  coma.  There  is  often  low,  muttering  delirium;  active  delirium  is 
rare,  but  I  have  known  it  to  be  maniacal.  More  often  the  patient  be- 
comes more  and  more  insensible  and  passes  into  deep  coma.  Occasion- 
ally while  in  this  toxsemic  state  death  may  be  precipitated  by  profuse 
haemorrhages  from  the  stomach  or  rectum. 

When  ascites  has  developed  death  may  be  due  to  some  complication 
such  as  acute  peritonitis;  in  rare  instances  this  is  due  to  the  introduction 
of  infection  by  the  trocar;  but  it  occurs  independently  of  tapping,  and 
is  then  due  to  infection  from  within,  either  by  the  blood-stream  or  in 
rare  instances  from  some  lesion,  such  as  tuberculous  ulceration  of  the 
intestines,  which  allows  micro-organisms  to  pass  into  the  peritoneal 
cavity.  Acute  infections,  such  as  pneumonia  and  erysipelas,  may  also 
attack  and  cause  the  death  of  a  patient  with  ascites  due  to  cirrhosis. 

From  a  degenerated  and  fatty  condition  of  the  heart  muscle  sudden 
death  may  occur;  this  is  by  no  means  common  in  my  experience,  but 
in  53  fatal  cases  of  cirrhosis  Cheadle  *  found  that  death  occurred  suddenly 
*Cheadle,  W.  B.:  Some  Cirrhoses  of  the  Liver,  p.  51. 


CIRRHOSIS    OF   THE    LIVER.  281 

in  this  way  in  6.     More  often  a  patient  dies  slowly  with  a  faihng  heart 
but  in  a  general  toxsemic  condition. 


COMPLICATIONS. 

Tuberculosis. — ^The  liability  of  patients  suffering  from  cirrhosis  to 
be  affected  with  tuberculosis  of  the  lungs  and  peritoneum  has  been  already 
referred  to  under  the  heading  of  morbid  anatomy,  where  statistics  were 
given. 

In  about  12  to  14  per  cent,  of  cases  with  cirrhosis  death  is  directly 
due  to  pulmonary  tuberculosis:  in  many  of  these  cases  the  cirrhosis  is 
latent  and  is  only  discovered  after  death.  In  other  instances  pulmonary 
tuberculosis  may  escape  detection  or  only  show  itself  by  very  few  signs. 
Tuberculous  peritonitis  may  not  be  suspected,  as  the  ascites  is  very 
naturally  regarded  as  due  to  cirrhosis.  In  tuberculous  peritonitis  super- 
vening in  cirrhosis  there  may  be  more  abdominal  pain  than  in  ordinary 
ascites,  and  if  tapping  be  performed,  the  fluid  is  found  of  a  higher  specific 
gravity  (1020)  than  in  ordinary  cirrhosis  (1010)  and  turbid. 

In  the  following  case  ascites  was  due  to  tuberculous  peritonitis  super- 
vening in  the  course  of  cirrhosis : 

A  fat  woman,  aged  forty-nine,  of  a  marked  alcoholic  aspect,  was  admitted  under 
my  care  at  St.  George's  Hospital  on  January  9,  1902,  with  ascites,  oedema  of  the 
feet,  altered  and  blunted  sensation  in  the  legs,  and  bronchitis.  The  liver  was 
enlarged,  the  breath  very  foul,  and  there  was  morning  sickness.  She  was  treated 
as  a  case  of  cirrhosis,  and  on  January  17  the  abdomen  was  tapped;  the  fluid  was 
turbid  and  of  a  specific  gravity  of  1020;  owing  to  the  thickness  of  the  abdominal 
wall  it  was  difficult  to  get  a  trocar  sufficiently  long  to  reach  the  peritoneal  cavity 
and  only  about  a  pint  of  fluid  was  withdrawn.  Death  occurred  on  January  19. 
At  the  autopsy  the  liver  (68  ounces)  was  markedly  cirrhotic  and  microscopically 
contained  much  fat;  the  spleen  weighed  12^  ounces.  There  were  some  chronic  peri- 
tonitis and  recent  generalized  tuberculous  peritonitis.  There  was  an  old  tubercle  at 
the  apices  and  much  bronchitis  in  the  lower  lobes  of  both  lungs. 

Generalised  Tuberculosis. — In  cirrhosis  the  possibility  of  generalised 
tuberculosis  should  be  thought  of  when  there  is  continued  fever  and 
the  patient  rapidly  goes  down-hill  without  any  appreciable  ascites. 
Generalised  tuberculosis  may  prove  fatal  in  patients  comparatively  fat. 

Bronchitis. — Some  degree  of  bronchitis  is  not  unconnnon  in  cirrhosis 
and  may  be  an  accidental  accompaniment.  On  the  other  hand,  it  may 
be  directly  related  to  the  cirrhosis,  and  may  be  due  to  collapse  of  the 
bases  of  the  lungs  from  upward  displacement  and  im])aired  movement 
of  the  diaphragm  due  to  ascites,  flatulence,  or  an  enlarged  liver.  It 
may  be  part  of  a  general  catarrh  from  alcoholic  excess  or  be  the  result 
of  backward  pressure  from  a  faihng  heart.  Since  what  appears  to  be 
bronchitis  may  be  really  rapid  pulmonary  tuberculosis,  it  is  advisable 
to  test  the  sputum  for  tubercle  bacilli  in  cases  of  bronchitis  in  cirrhosis. 

In  the  following  case  rapid  tuberculosis  gave  rise  to  the  signs  of  gen- 
eral bronchitis. 

A  fat  alcoholic  man,  aged  fifty,  who  had  had  delirium  tremens,  was  under  my 
care  for  a  few  days  in  St.  George's  Hospital  in  March,  1900.     He  had  oedema  of 


282  DISEASES   OF  THE   LIVER. 

the  feet  and  a  hsemorrhagic  eruption  on  the  legs,  a  dilated  heart,  a  large  liver, 
and  general  bronchitis;  the  sputum  contained  a  little  blood.  The  urine  (1020)  was 
free  from  albumin.  He  was  thought  to  have  cirrhosis  of  the  liver  and  backward 
pressure  from  cardiac  dilatation,  with  possibly  a  pulmonary  apoplexy.  After  being 
in  for  three  days,  with  delirium  at  night,  he  quite  suddenly  died.  At  the  autopsy 
the  liver  (108  ounces)  showed  multilobular  cirrhosis  with  much  fatty  change; 
the  left  lobe  overlapped  the  spleen,  which  weighed  28  ounces.  The  kidneys  weighed 
9  ounces  each  and  were  healthy.  There  was  no  ascites.  There  was  a  pint  of  clear 
fluid  in  each  pleural  cavity  and  very  dense  adhesions  at  both  apices.  There  were 
small  cavities  at  both  apices  and  recent  firm  caseous  masses  in  the  lower  lobes 
and  miliary  tubercles  throughout  both  lungs.  There  was  no  pulmonary  apoplexy. 
There  was  bronchitis  and  tuberculous  ulceration  of  the  larynx.  The  heart  (17 
ounces)  showed  fatty  infiltration  and  degeneration  and  was  dilated,  but  was  free 
from  valvular  disease.     Examination  of  the  lungs  showed  tubercle  bacilli. 

Pleurisy  with  Effusion. — Pleurisy  is  not  uncommon  in  the  course 
of  cirrhosis  and  is  often  a  manifestation  of  concomitant  pulmonary 
tuberculosis.  It  is  more  frequent  on  the  right  side,  and  this  is  very 
probably  clue,  as  suggested  by  Villani,*  to  a  spread  of  inflammation  or 
infection  from  the  hver  through  the  diaphragm.  The  pleurisy  may  be 
acute  and  accompanied  by  pain  and  fever,  or  of  an  indolent  and  chronic 
character.  In  the  latter  case  the  condition  is  much  like  a  hydrothorax, 
but,  as  already  mentioned,  it  is  often  tuberculous  in  origin. 

James  f  records  a  curious  case  of  ascites  and  right  pleural  effusion  in  which  a 
commmiication  was  thought  to  exist  between  the  right  pleura  and  the  peritoneal 
cavity,  inasmuch  as  tapping  the  pleura  emptied  the  abdomen,  and,  in  fact,  seemed 
to  be  more  effectual  than  paracentesis  abdominis. 

The  fluid  may  be  serous,  serofibrinous,  or  in  rare  cases  hemorrhagic. 
Hsemorrhagic  pleurisy  is  rare  in  cirrhosis.  It  is  usually  due  to  tubercu- 
losis (Barjon  and  Henry,J  Jean  §),  though  it  is  possible  that  in  some  in- 
stances it  may  be  due  to  hepatic  insufficiency,  and  so  resemble  the 
petechise  and  general  hgemorrhages  seen  in  the  late  stages.  In  some  in- 
stances it  has  been  suggested  that  the  hsemorrhagic  character  of  the  pleural 
effusion  is  due  to  alcohoUsm.  (Fernet.  ||)  A  pleural  effusion,  especially 
on  the  right  side,  is  more  likely  to  be  hsemorrhagic  than  a  concomitant 
ascites.  The  following  case  illustrates  the  relationship  of  tuberculosis 
and  a  hsemorrhagic  pleural  effusion: 

A  man,  aged  forty-nine,  died  in  St.  George's  Hospital  with  cirrhosis  of  the  liver 
and  tuberculosis.  At  the  autopsy  there  was  a  pleural  effusion  on  both  sides — serous 
on  the  right  side,  hsemorrhagic  on  the  left  side;  there  were  numerous  tubercles  in 
the  lung  on  the  side  of  the  hsemorrhagic  effusion. 

In  the  following  case  the  hsemorrhagic  character  of  the  pleural  effusion 
probably  depended  on  traumatism: 

A  billiard  marker,  aged  forty-three,  was  admitted  under  my  care  with  fever,  a 
large  right-sided  pleural  effusion,  enlargement  of  the  liver,  and  ascites.  The  effusion 
was  t^ice  tapped,  and  clear  fluid  was  drawn  off  on  both  occasions,  which  con- 
tained neither  tubercle  baciUi  nor  pneimiococci.  He  passed  into  a  toxsemic  condition, 
and  although  transfused,  died  without  any  improvement.     His  abdomen  never  re- 

*  Villani:  Puf.  Med.,  Rome,  March  9,  1895. 

t  James:  Trans.  Medico-chirurg.  Soc,  Edinburgh,  vol.  xviii,  p.  191,  1898-99. 

t  Barjon  et  Henry:  (Lyon  MMical,  June  19,  1898.) 

§  Jean:  These,  Paris,  1891. 

II  Fernet:  Bull,  de  la  Soc.  Med.  des  Hop.,  June  22,  1900,  p.  781. 


CIRRHOSIS   OF  THE    LIVER.  283 

quired  tapping.  The  right  pleura  contained  much  dark  blood-stained  fluid;  the 
lung  was  collapsed  and  covered  with  lymph,  which  was  hsemorrhagic  in  one  place 
and  suggested  that  the  blood  had  come  from  a  newly  formed  vessel ;  there  was  a 
little  obsolete  tubercle  at  the  apex.  There  was  serous  ascites,  no  chronic  peritonitis, 
a  multilobular  cirrhotic  liver  weighing  65  ounces,  with  small  bilirubin-calcium 
calculi  in  the  gall-bladder.  The  round  ligament  contained  a  big  vein  the  size  of 
the  little  finger.     {Vide  Fig.  32.) 

Taylor*  records  a  case  of  hsemorrhagic  pleural  effusion  which  was 
independent  of  tuberculosis  and  probably  due  to  an  acute  septic  infection. 

The  presence  of  a  right-sided  pleural  effusion- in  a  doubtful  case  is  in 
favour  of  cirrhosis,  as  against  simple  thrombosis  of  the  portal  vein, 
since  it  does  not  occur  in  the  latter  condition  unless  complicated  by 
cirrhosis.  It  should,  however,  be  borne  in  mind  that  some  degree  of 
dulness  on  percussion,  loss  of  vocal  vibrations  and  of  breath  sounds  at 
the  right  base,  may  be  due  to  upward  projection  of  a  large  cirrhotic  liver, 
or  to  a  smaller  cirrhotic  liver  being  pushed  up  by  ascites,  and  not  to  any 
pleural  effusion.  In  the  same  way  friction  at  the  right  base  may  be 
due  to  local  peritonitis  and  not  to  pleurisy. 

Peripheral  Neuritis. — The  early  symptoms  of  peripheral  neuritis 
are  so  often  thrown  into  the  shade  by  the  ascites  or  other  effects  of  cir- 
rhosis on  which  attention  is  focussed  that  the  minor  degrees  of  neuritis 
probably  often  pass  undetected.  Cramps,  muscular  tenderness,  and 
loss  of  knee-jerk  are  not  uncommon  in  cases  of  cirrhosis  admitted  for 
ascites  or  hsematemesis,  and  are,  generally  speaking,  to  be  referred  to 
alcoholism.  Alcoholic  neuritis  is  commoner  in  women  and  is  often 
associated  with  pulmonary  tuberculosis;  in  such  cases  the  liver  is  some- 
times cirrhotic  and  nearly  always  fatty ;  but  the  clinical  picture  is,  in  the 
main,  that  of  neuritis,  not  of  hepatic  disorder. 

The  terminal  stages  of  cirrhosis  are  marked  by  symptoms  due  to 
hepatic  insufficiency,  such  as  epistaxis  and  other  haemorrhages,  delirium, 
and  coma.  The  toxic  coefficient  of  the  urine  will,  if  the  kidneys  be 
healthy,  become  increased  as  a  result  of  the  liver  failing  in  its  antitoxic 
function  of  destroying  or  neutralizing  toxic  bodies  emanating  from  the 
portal  system.  Hence  a  toxsemic  neuritis  may  occur  in  the  late  stages 
of  cirrhosis  as  the  result  of  hepatic  insufficiency.  If  alcohol  has  been 
taken  freely  up  to  the  onset  of  the  neuritis,  it  must  then  be  considered 
to  be  alcoholic  in  origin,  but  when  the  absence  of  this  cause  can  be  estab- 
lished, hepatic  insufficiency  with  resulting  toxaemia  is  a  satisfactory 
explanation. 

In  a  case  of  Gouget'sf  neuritis  came  on  two  weeks  before  death  in  a  woman 
previously  of  alcoholic  habits,  who,  however,  had  not  had  any  stimulant  for 
the  two  months  that  she  had  been  in  hospital.  The  arms  and  legs  were  simul- 
taneously affected,  which  is  unusual  in  the  alcoholic  form.  It  is  interesting  to  note 
that  Hayem  observed  the  same  type  of  neuritis  in  a  case  of  primary  carcinoma  of 
the  liver. 

Delirium  tremens,  another  complication  of  cirrhosis,  has  been  dealt 
with  on  page  277. 

*  Tavlor,  F.:  Guy's  Hospital  Reports,  vol.  lii,  1S96. 
t  Quoted  in  Levi's  Paris  Th^se,  1896. 


284  DISEASES   OF  THE   LIVER. 

The  occurrence  of  chronic  peritonitis  in  the  bodies  of  patients 
dying  with  cirrhosis  of  the  liver  is  referred  to  elsewhere  (p.  222).  The 
importance  of  realising  that  chronic  peritonitis  may  exist  in  cases  of 
cirrhosis  is  that  ascites  thus  produced  may  frequently  recur  and  last 
much  longer  than  in  cases  of  cirrhosis  uncomplicated  by  chronic  periton- 
itis, where  ascites  is  a  close  forerunner  of  death.  As  a  result  of  chronic 
peritonitis  the  omentum  may  become  rolled  up  and  form  a  firm  mass 
running  across  the  abdomen. 

In  a  case,  recorded  by  Benham,*  of  cirrhosis  complicated  by  chronic  peritonitis 
the  omentum  and  mesentery  were  so  thickened  and  matted  together  that  they 
formed  a  pulsating  mass  during  life. 

Renal  Disease. — The  occurrence  of  albuminuria  in  cirrhosis  {vide 
p.  232),  and  the  morbid  lesions  of  the  kidney  {vide  p.  221)  that  may  occur, 
have  been  dealt  with  elsewhere.  Here  the  clinical  aspect  of  cases  where 
the  two  conditions  are  combined  will  be  referred  to.  A  'priori  it 
would  naturally  be  expected  that  death  would  occur  earlier  in  cirrhosis 
complicated  by  renal  disease  than  in  ordinary  cases  of  cirrhosis,  inasmuch 
as  the  toxaemia  depending  on  hepatic  inadequacy  would  not  be  obviated 
by  the  excretion  of  toxic  bodies  by  the  kidneys.  This  hypothesis, 
however,  is  not  supported  by  statistics.  Both  in  Yeld's  f  figures  from 
St.  Bartholomew's  Hospital  and  in  the  cases  at  St.  George's  Hospital 
the  average  age  of  patients  dying  with  the  combined  conditions  was 
higher  than  in  those  patients  who  succumbed  to  uncomplicated  cirrhosis 
of  the  hver.  When  the  two  diseases  are  met  with  in  the  same  person, 
the  clinical  symptoms  are  rather  renal  than  hepatic.  This  is  in  accord 
with  the  hypothesis  that  in  the  combined  condition  the  toxaemia  would 
be  more  marked. 

Gout  not  unnaturally  is  met  with  in  the  past  history  of  some  patients 
who  come  under  observation  with  the  symptoms  of  cirrhosis.  It  is, 
however,  very  rare  to  see  frank  attacks  of  gout  in  patients  with  symp- 
toms of  active  cirrhosis.  A  large  liver,  which  may  in  some  instances 
be  due  to  early  or  latent  cirrhosis,  is  not  infrequent  in  gouty  subjects. 

In  44  cases  of  cirrhosis  tabulated  by  Yeld  %  the  joints  were  healthy  in  34  and  con- 
tained uratic  deposit  in  9,  or  21  per  cent.  In  5  of  the  nine  cases  the  kidneys  were 
granular. 

Secondary  or  Terminal  Infections. — Towards  the  end  of  cases  of 
cirrhosis  secondary  infections  are  far  from  uncommon.  Probably  the 
bactericidal  power  of  the  blood  is  diminished  in  the  same  way  that  it  is 
in  chronic  heart  and  kidney  disease,  and  as  a  result  infection  is  more 
likely  to  occur.  The  peritoneum  is  disposed  to  infection  by  chronic  con- 
gestion, often  by  some  chronic  peritonitis  and  ascites,  while  paracentesis 
may  be  the  immediate  cause  of  infection.  Suppurative  or  fibrinous  peri- 
tonitis is  not  a  very  uncommon  termination  to  a  case;   and,  as  already 

*  Benham,  F,  L.:  Trans.  Clin.  Soc,  vol.  xxviii,  p.  226. 

t  Yeld,  R.  A.:  St.  Bartholomew's  Hospital  Reports,  vol.  xxxiv,  p.  226. 

j  Yeld:  St.  Bartholomew's  Hospital  Reports,  vol.  xxxiv,  p.  215. 


CIRRHOSIS    OF    THE    LIVER.  285 

pointed  out,  tuberculous  peritonitis  may  supervene  in  the  course  of 
cirrhosis. 

Secondary  infection  of  the  hver  itself,  giving  rise  to  acute  degeneration 
of  the  hver  cells  and  to  icterus  gravis,  may  occur.  Cases  have  been  re- 
corded by  Pitt  *  (4),  Weber, t  and  others,  and  are  probably  not  very 
infrequent.  Erysipelas,  pericarditis,  pneumonia,  infective  endocarditis, 
are  also  occasionally  met  with. 

In  65  fatal  cases  of  infective  endocarditis  tabulated  by  Kelynaclc  J  cirrhosis  was 
found  in  4. 

In  a  case  of  cirrhosis  of  the  hver  Councilman  §  found  a  secondary  infection 
with  streptococci  giving  rise  to  purulent  infiltration  of  the  retroperitoneal  glands, 
thrombosis  of  iliac  veins  and  inferior  vena  cava,  with  secondary  embolic  infarcts 
in  the  lungs. 

The  museum  of  St.  Bartholomew's  Hospital  contains  an  interesting  specimen 
(2295  h)  of  a  spleen  containing  a  mass  of  laminated  blood-clot  the  size  of  an  orange 
from  a  man  who  had  cirrhosis  of  the  liver  and  streptococcal  endocarditis  of  the 
aortic  valves. 

Thrombosis. — Thrombosis  is  rare  in  the  course  of  cirrhosis.  Throm- 
bosis of  the  portal  vein  when  it  occurs  is  most  frequently  associated  with 
cirrhosis,  but  it  only  occurred  in  10,  or  3.3  per  cent.,  of  334  cases  of  cir- 
rhosis examined  after  death  at  St.  Bartholomew's  Hospital.  (Langdon 
Brown.  |1)  I  have  seen  severe  phlebitis  of  the  leg  develop  in  the  late  stages 
of  cirrhosis.  A  case  of  multiple  thrombosis  and  haemorrhages  was  re- 
ferred to  on  page  276 . 

DIAGNOSIS. 

The  history  of  dyspepsia,  often  associated  with  evidences  of  alcoholic 
excess  and  of  considerable  duration,  hsematemesis  which  cannot  be 
explained  satisfactorily  on  other  grounds,  and  enlargement  of  the  liver 
and  spleen,  are  the  broad  lines  on  which  the  disease  can  be  diagnosed 
in  the  preascitic  stage.  The  development  of  ascites  in  a  patient  who  has 
manifested  the  above  symptoms  and  is,  in  addition,  more  or  less  cachectic 
leaves  little  room  for  doubt  that  a  late  stage  of  cirrhosis  has  been  reached. 


THE  DIFFERENTIAL  DIAGNOSIS. 

The  diagnosis  of  cirrhosis  from  other  conditions  has  already  been 
partially  dealt  with  under  the  heads  of  ascites  and  hsematemesis.  The 
diseases  which  simulate  cirrhosis,  in  so  far  as  the  production  of  ascites 
and  of  gastro-intestinal  haemorrhage  are  concerned,  such  as  chronic  peri- 
tonitis, in  which  is  included  perihepatitis,  and  gastric  ulcer,  have  thus 
been  dealt  with. 

From  Hypertrophic  Biliary  Cirrhosis  with  Chronic  Jaundice. — 
Portal  and  hypertrophic  biliary  cirrhosis,  though  distinct  types,  may  in 
certain  instances  be  combined,  while  other  cases  show  a  transition  from 

*  Pitt,  G.  N.:  Trans.  Path.  Soc,  vol.  xl,  p.  351. 

t  Weber,  F.  P.:  Trans.  Path.  Soc.,  vol.  1,  p.  136. 

t  Kelynack:  Encyclopaedia  Medica,  vol.  iv,  p.  365. 

§  Councilman,  W.  T. :  Trans.  Assoc.  American  Physicians,  vol.  xi,  p.  213,  1S96. 

II  Langdon  Brown:  St.  Bartholomew's  Hospital  Reports,  vol.  xxxvii,  p.  62. 


286  DISEASES    OF   THE   LIYEE. 

one  to  the  other.  It  may  be  pointed  out  that  exactly  the  same  blending 
of  distinct  t^^pes  is  seen  in  the  case  of  kidney  disease.  Chronic  paren- 
chymatous nephritis,  which  may  be  compared  to  h}-pertrophic  bihan- 
cirrhosis,  and  the  granular  (arteriosclerotic)  kidney,  which  maj^  be  likened 
to  portal  cirrhosis,  may  overlap,  nm  into  each  other,  or  be  combined. 

The  clinical  and  anatomical  features  of  the  diseases  may  both  be 
found  in  the  same  person:  thus,  in  h}-pertrophic  bihaiy  cin'hosis  a  sec- 
ondary poital  ciiThosis  frequently  develops  before  death,  and  the  patient, 
who  has  for  years  presented  the  s^Tnptoms  and  signs  of  bihary  cirrhosis, 
dies  with  ascites  and  perhaps  gastro-intestinal  hsemoiThage.  Cases  of 
portal  cirrhosis  with  a  large  hver  and  rather  persistent,  intercurrent 
jauncUce  occasionally  occur  and  veiy  closely  imitate  h}i3ertrophic  bihar\' 
cirrhosis;  the  distinction  between  the  two  depends  on  the  jaimdice  not 
being  permanent,  in  the  shghter  degree  of  splenic  enlargement,  and  on 
the  occm-rence  of  ascites  or  other  characteristic  evidences  in  portal 
cirrhosis.  In  cases  of  poital  cirrhosis  which  nm  an  acute  com-se,  or 
where  more  acute  inflammatory  changes  supeiwene  on  portal  cin'hosis 
of  some  standing  and  affect  the  bile-ducts,  the  clinical  and  anatomical 
features  may  show  a  combination  of  biliary  and  portal  cirrhosis. 

From  Other  Enlargements  of  the  Liver. — A  patient  may  come 
imder  obseiwation.  say  for  examination  for  life  insurance  or  for  digestive 
distiu-bance.  and  be  found  to  have  an  enlarged  hver  vithout  any  other 
manifestations  of  cinhosis.  The  question  then  arises  whether  there  is 
latent  cirrhosis  or  some  other  morbid  change  in  the  hver.  If  there  is 
proof  or  history  of  alcohohc  excess,  the  enlargement  may  be  due  to 
fatty  change,  to  earh"  or  to  latent  cirrhosis,  or  to  temporary'  engorgement. 
If  the  organ  is  smooth,  free  from  tenderness  and  pain,  and  the  spleen 
is  not  palpably  enlarged,  the  probabihties  are  in  favour  of  fatty  enlarge- 
ment. Tenderness  is  in  faA'Our  of  engorgement  or  of  early  cinhosis; 
enlargement  of  the  spleen  pomts  to  cirrhosis  or  to  malarial  hepatitis  with 
engorgement . 

Malarial  Enlargement. — As  a  restilt  of  chronic  and  severe  malarial 
infection  very  considerable  enlargement  of  the  hver  with  tenderness  on 
palpation  results.  This  is  combined  with  splenic  enlargement  and  usually 
with  irregular  fever.  The  patient  is  much  run  down  in  health  and  weight 
and  the  condition  presented  is  very  like  that  of  early  but  advancing 
cirrhosis.  The  history  that  the  patient,  often  a  young  man  and  not 
specially  alcohohc,  has  been  the  subject  of  continued  malaria  abroad  is 
important.  These  cases  often  improve  verA*  rapidly  under  treatment  in 
England,  and  the  enlargement  of  the  hver  is  much  diminished  or  disap- 
pears entirely. 

Chronic  Venous  Engorgement. — The  enlarged  hver  due  to  the 
backward  pressure  of  obstnictive  heart:  or  lung  disease  may  imitate  a 
cirrhotic  hver;  especially  as  there  is  not  infrequently  a  transient  systohc 
apical  murmur  in  cinhosis.  In  forming  a  diagnosis  the  histor\'  and  ap- 
pearance of  the  patient  and  the  presence  of  other  signs  of  cinhosis  or 
of  heart  disease  are  important.  Thus  alcoholism.  ha?matemesis  and  an 
enlarged  spleen    point  to  cirrhosis,  while  rheumatic  fever  in   the  past, 


CIERHOSIS   OF  THE    LIVER.  287 

haemoptysis,  and  beneficial  results  from  digitalis  and  strophanthus,  are  in 
favour  of  chronic  venous  engorgement. 

In  leukaemia  the  liver  is  often  greatly  enlarged,  and  epistaxis  and 
hsematemesis  may  occur.  In  the  myelogenic  variety  the  spleen  is  very 
greatly  enlarged,  while  in  the  chronic  lymphatic  form  the  superficial 
lymphatic  glands  are  enlarged.  The  diagnosis  is  easily  made  by  examina- 
tion of  the  blood. 

From  Carcinoma  of  the  Liver. — In  the  late  stages  of  cirrhosis  when 
the  patient  is  cachectic  and  ascites  and  jaundice  are  both  present,  the 
resemblance  to  malignant  disease  may  be  very  close.  Enlarged  glands 
above  the  clavicle,  if  present,  are  strongly  in  favour  of  carcinoma.  The 
history  of  the  patient,  revealing  chronic  alcoholism  and  a  considerable 
period  of  ill  health  from  long-continued  dyspepsia,  suggests  cirrhosis.  In 
many  instances  doubt  must  exist  until  the  abdomen  is  tapped  and  the 
liver  can  be  thoroughly  palpated.*  If  it  is  small,  it  is  probably  cirrhotic; 
if  large  and  smooth,  it  might  be  either  cirrhosis  or  massive  cancer  growing 
inside  the  organ,  but  the  former  is  much  more  probable,  both  because 
primary  cancer  is  rarer  and  because  it  need  not  give  rise  to  either  ascites 
or  jaundice.  Enlargement  of  the  liver  with  multiple  umbilicated 
nodules  points  to  malignant  disease. 

A  hydatid  cyst  deeply  embedded  in  the  substance  of  the  liver  expands 
the  affected  lobe,  makes  it  prominent,  firm,  and  enlarged,  usually  in  a 
downward  direction.  In  cirrhosis  the  enlargement  is  more  uniform, 
affecting  both  lobes,  while  the  surface  is  more  or  less  irregular.  It  must, 
however,  be  remembered  that  when  a  large  hydatid  destroys  a  considera- 
ble amount  of  liver  substance,  compensatory  hyperplasia  of  the  other 
lobe  may  occur,  and  that  the  resulting  enlargement  may  appear  uniform, 
as  in  cirrhosis.  A  large  cirrhotic  liver,  unless  displaced  forward  by  a 
flatulent  stomach,  which  is  only  a  temporary  condition,  or  by  some  other 
cause,  an  event  not  often  met  with,  is  not  nearly  so  prominent  as  in 
hydatid  disease.  In  hydatid  the  general  health  is  good,  while  in  cirrhosis 
there  is  usually  some  impairment,  or  signs  of  chronic  alcoholism. 

Syphilitic  Disease  of  the  Liver. — A  past  history  of  syphilitic  infec- 
tion or  manifest  lesions  elsewhere  in  the  body  would  point  to  this  explana- 
tion of  an  enlarged  liver.  In  syphilitic  disease  of  the  liver  the  organ  is 
often  irregularly  enlarged,  whereas  the  two  lobes  of  the  liver  are  generall}^ 
uniformly  affected  in  latent  cirrhosis.  Pain  is  more  frequent  in  syphilitic 
disease,  and  albuminuria,  if  present,  is  of  diagnostic  value  as  pointing  to 
the  probable  existence  of  lardaceous  disease.  Sometimes  all  external 
manifestations  of  syphilis  are  wanting  and  the  only  cHnical  evidence 
forthcoming  is  diminution  of  the  enlarged  liver  under  a  tentative  use  of 
iodides.  The  difficulty  of  distinguishing  between  the  two  conditions  may 
be  so  great  that  a  patient  with  cirrhosis  should  always  be  treated  with 
iodides  for  a  time. 

In  splenic  anaemia,  where  recurrent  attacks  of  hsematemesis  are 
often  met  with,  the  splenic  enlargement  and  the  anaemia  are  more  marked 
than  in  cirrhosis,  and  there  is  usually  a  diminution  in  the  numlier  of 
*  Compare  Landrieux:  Joum.  des  Praticiens,  Nov.  2.5,  1899,  p.  737. 


288  DISEASES   OF  THE   LIVER. 

white  blood-corpuscles,  or  leiicopenia.  The  diagnosis  between  splenic 
anaemia  and  portal  cirrhosis  is  a  rather  dehcate  and  difficult  matter, 
since,  on  the  one  hand,  splenic  anseixda  may  terminate  in  cirrhosis  of  the 
liver  (Banti's  disease),  while,  on  the  other  hand,  both  hamatemesis  and 
ascites  may  occur  in  cases  of  splenic  anaemia  where  fibrosis  of  the  liver 
is  absent,  as  shown  after  death.  Splenic  anaemia  with  periodic  haemat- 
emesis  is  chiefly  distinguished  from  portal  cirrhosis  by  the  greater  degree 
of  anaemia  and  of  splenic  enlargement. 

Intra-hepatic  Suppuration. — In  acute  cases  of  cirrhosis  accompa- 
nied by  fever  and  considerable  enlargement  of  the  liver  the  question  of 
distinguishing  between  it  and  intra-hepatic  suppuration  might  present 
some  difficulties.  Hsematemesis  and  an  alcoholic  history  point  in  favour 
of  cirrhosis,  while  a  hectic  temperature,  locahzed  hepatic  tenderness, 
leucocytosis,  and  a  history  of  residence  abroad  and  dysentery,  or  of  con- 
ditions, such  as  recent  appendicitis,  suppurating  piles,  or  gall-stones, 
which  might  lead  to  pylephlebitis  or  to  suppurative  cholangitis,  are  in 
favour  of  intra-hepatic  suppuration. 

Carrington  *  has  described  the  case  of  a  woman  who  had  an  enlarged  liver  and 
a  temperature  oscillating  between  98.4°  and  104°;  pylephlebitis  was  diagnosed,  but 
after  death  the  liver  weighed  72  ounces  and  showed  rapidly  progressing  cirrhotic 
changes  and  a  fatty  condition  of  the  liver  cells. 

Typhoid  Fever. — In  acute  cases  of  cirrhosis  with  a  raised  temperature 
there  may  be  considerable  resemblance  to  typhoid  fever.  In  patients 
who  have  been  drinking  heavily  and  present  an  enlarged  liver  and  spleen, 
raised  temperature,  and  diarrhoea,  a  rapid  diagnosis  from  typhoid  fever 
is  sometimes  only  possible  by  means  of  the  agglutination  test  (Widal's 
reaction).  In  children  with  a  raised  temperature,  diarrhoea,  and  swollen 
abdomen  the  suspicion  of  a  perforating  typhoid  ulcer  has  even  arisen. 
A  case  in  point  was  referred  to  on  page  219. 

Intestinal  Obstruction.— Strange  though  it  may  seem,  intestinal 
obstruction  has  been  suspected  in  a  patient  with  repeated  vomiting  from 
alcoholic  gastritis  and  abdominal  distension  from  ascites.  Careful  ex- 
amination of  the  patient's  history  and  general  condition  should,  however, 
correct  a  first  impression  of  this  kind  and  lead  to  appropriate  treatment 
for  the  pressing  gastric  symptoms. 

A  man  aged  fifty-two  with  ascites  and  abdominal  distension  was  admitted  under 
me  in  St.  George's  Hospital  on  January  11,  1902.  He  had  been  thought  before 
admission  to  be  suffering  from  acute  intestinal  obstruction,  and  had,  indeed,  been 
seen  in  consultation  by  my  colleague,  Mr.  Sheild,  who  recognised  that  the  condition 
was  cirrhosis  of  the  liver  and  recommended  him  to  the  hospital  for  medical  treat- 
ment. 

It  may  be  pointed  out  that  intestinal  obstruction  might  conceiv- 
ably occur  from  strangulation  by  a  band  of  peritoneal  adhesions  in 
connexion  with  perihepatitis,  and  that,  of  course,  intestinal  obstruc- 
tion may  occur  in  a  patient  with  cirrhosis. 

Treves  t  quotes  Lusseau's  X  case  of  cirrhosis  in  which  the  third  part  of  the 
duodenum  was  compressed  by  a  cicatricial  band. 

*  Carrington:  Guy's  Hospital  Reports,  Series  iii,  vol.  xxvii,  1884. 
t  Treves:  Intestinal  Obstruction,  p.  446,  2d  ed.,  1899. 
t  Lusseau:  Progres  Medical,  1879,  p.  545. 


^  CIRRHOSIS    OF   THP]    LIVER,  289 

PROGNOSIS. 

The  prognosis  depends  in  great  measure  on  the  reparative  power  of 
the  body  and  on  its  abihty  to  compensate  for  the  lesions  of  cirrhosis. 
Some  discussion  on  the  compensatory  mechanism  is  therefore  necessary 
in  order  to  get  a  clear  idea  of  the  problems  involved  in  the  prognosis 
of  cirrhosis. 

The  organism  attempts  to  compensate  for  the  evil  effects  of  cirrhosis 
in  two  ways:  (I)  By  a  further  development  of  the  anastomosis  which 
normally  exists  between  the  tributaries  of  the  portal  vein  and  the  general 
systemic  veins.  (Fide  p.  209.)  (II)  By  compensatory  hyperplasia  of  the 
liver  cells. 

(I)  The  dilatation  of  the  communications  between  the  tributaries  of 
the  portal  vein  and  the  general  systemic  veins  compensates  for  the  me- 
chanical obstruction  to  the  passage  of  portal  blood  through  the  cirrhotic 
liver.  It  thus  relieves  the  engorgement  of  the  portal  area,  and  should 
thereby  tend  to  obviate  hgematemesis,  and  probably  to  delay  the  de- 
velopment of  ascites  and  possibly  to  assist  in  its  removal. 

If  the  effects  of  hepatic  cirrhosis  were  chiefly  mechanical  and  due  to 
venous  engorgement  of  the  portal  area,  the  more  extensively  the  portal 
vein  was  put  into  communication  with  the  inferior  vena  cava,  the  better 
would  be  the  result.  But  a  most  important  element  in  the  pathological 
results  of  cirrhosis  is  the  destruction  of  the  liver  cells  and  the  necessary 
loss  of  their  various  functions,  or  hepatic  insufficiency.  One  of  the  most 
important  of  these  functions  is  the  antitoxic  action,  or  the  power  of  stop- 
ping poisons  absorbed  from  the  alimentary  canal  and  preventing  their 
entry  into  the  general  circulation. 

If,  therefore,  this  collateral  circulation  be  carried  to  its  logical  extreme, 
namely,  by  making  the  portal  vein  open  directly  into  the  inferior  vena 
cava  or  Eck's  fistula,  so  that  the  portal  circulation  is  short-circuited  and 
the  liver  is  virtually  put  outside  the  circulation,  the  results,  as  obtained 
by  Hahn,  Nasse,  Nencki,  and  Pawlow  *  on  dogs,  are  very  striking.  The 
symptoms  were  much  like  those  of  ureemia;  the  urine  contained  carbamic 
acid,  which  is  normally  changed  by  the  liver  into  urea.  Similar  symp- 
toms were  produced  by  carbamic  acid,  and  hence  it  was  regarded  as  the 
cause  of  the  toxic  manifestations  resembling  those  of  uraemia. 

It  is  therefore  probable  that  the  good  effects  of  the  collateral  circula- 
tion in  cirrhosis  are  not  purely  mechanical.  Possibly  diA'ersion  of  some 
of  the  blood  from  the  liver  relieves  congestion  of  that  organ  and  so  enables 
it  to  deal  more  satisfactorily  with  the  remaining  blood  that  still  passes 
to  it.  It  is  also  conceivable  that  the  state  of  nutrition  of  the  organ  is 
improved  by  relieving  the  congestion  of  the  portal  vein,  and  that  it  is 
thus  able  not  only  to  be  more  active  functionally,  but  to  undergo  com- 
pensatory hyperjDlasia  to  greater  effect.  This  sul)ject  was  also  dealt  with 
in  considering  the  way  in  which  the  Talma-Morison  operation  for  the  rehef 
of  ascites  does  good.     (Vide  p.  258.) 

The  second  anatomical  change  ])y  which  an  attempt  is  made  to  com- 

*  Hahn,    Nasse,    Nencki,    and     Pawlow:    Arcliiv    f.    experiment.     Path.    u. 
Pharmak.,  Bd.  xxxii,  p.  161,  1893. 
19 


290  DISEASES    OF   THE    LIYEK.   , 

pensate  for  the  evil  effects  of  cirrhosis  is  compensatory  multipHcation  of 
the  hver  cells.  {Vide  p.  208.)  As  a  result  of  compensatory  hyperplasia 
the  liver  increases  in  size.  This  attempt  at  compensation  in  cirrhosis 
is  very  general,  but  its  success  is  very  variable.  In  many  instances  the 
effort  at  compensation  in  cirrhosis  is  in  vain.  Though  for  a  time  it  staves 
off  the  evil  day  and  the  disease  remains  latent,  there  is  always  the  danger 
that  the  cirrhotic  process  may  spread  to  the  hyperplastic  areas  and  that 
they  may  become  engulfed  like  the  rest  of  the  liver;  further,  the  vigourous 
nodules  of  adenomatous  liver  tissue  may  outgrow  their  nutrition  and 
undergo  necrosis;  or  they  may  undergo  fatty  degeneration  from  some 
general  cause,  as  fever  (action  of  toxines),  for  example,  in  the  nodular 
cirrhosis  sometimes  seen  in  tuberculosis,  or  extensive  hsemorrhage  may 
take  place  into  the  substance  of  the  liver  from  the  dilated  vessels  and 
bring  the  compensation  to  a  premature  end. 

In  some  instances  the  compensation  is  sufficiently  good  to  restore  a 
fair  equilibrium,  and  the  disease  is  latent  so  long  that  it  may  be  thought 
to  be  almost  cured.  Thereis  hardly  a  return  to  perfect  health,  for  there 
is  a  want  of  reserve  power,  and  the  compensation,  if  strained,  may  give 
way.  The  importance  of  this  compensatory  hyperplasia  is  well  expressed 
in  Hanot's  axiom  that  while  the  diagnosis  of  hepatic  cirrhosis  is  made 
from  the  state  of  the  connective  tissues,  the  prognosis  depends  on  the 
condition  of  the  hepatic  cells. 

Period  of  the  Disease. — In  ordinary  cirrhosis  the  prognosis  is,  gener- 
ally speaking,  gloomy,  but  there  are  several  special  points  which  must  be 
taken  into  consideration.  Thus  the  prognosis  is  necessarily  different  at 
an  early  and  at  a  late  period  of  the  disease.  It  is  cpiite  possible  for  the 
earliest  symptom  of  importance — hsematemesis — to  be  succeeded  by  many 
years  of  life,  and  even  for  the  cirrhosis,  which  gave  rise  to  it,  to  remain 
permanently  latent. 

It  should  be  remembered  that  though  the  disease  may  become  latent 
and  remain  so  for  years,  the  condition  is  not  one  of  real  cure.  The  morbid 
change  in  the  liver,  though  compensated  for,  is  still  there,  and  may  be 
restarted,  or  the  compensatory  mechanisms  may  fail.  Thus  fatal  hsemor- 
rhage may  occur  from  dilated  and  varicose  oesophageal  veins,  or,  as  just 
mentioned,  fibrosis  and  fatty  degeneration  may  involve  the  areas  of 
hyperplastic  liver  cells.  It  has  been  pointed  out  several  times  that  the 
prognosis  in  the  late  stages  is  very  bad,  and  that  ascites  due  to  cirrhosis 
imcomplicated  by  chronic  peritonitis  is  usually  followed  by  death  within 
a  short  time.  A  drowsy,  sleepy  condition  points  to  a  general  toxaemia, 
and  though  it  may  be  temporarily  removed  by  treatment,  it  is  prone  to 
recur  and  pass  into  coma,  and  is  therefore  an  extremely  grave  sign. 

The  effect  of  treatment  of  course  has  an  important  bearing  on  the 
prognosis;  not  so  much  in  any  attempt  to  remove  the  fibrous  tissue  in 
the  liver,  for  drugs  such  as  iodide  of  potassium  and  chloride  of  ammonium 
are  useless  in  ordinary  cirrhosis,  but  from  the  point  of  view  of  preventing 
any  further  aggravation  of  the  disease.  Cutting  off  all  alcohol  is  a  most 
important  step,  and  on  the  patient's  power  of  will  to  abstain  his  future 
will  to  a  great  extent  depend. 


CIEEHOSIS   OF   THE    LIVER.  291 

It  may  be  pointed  out  that  very  marked  improvement  under  iodides 
makes  the  prognosis  good  because  it  tends  to  alter  the  diagnosis  of  portal 
cirrhosis  into  that  of  syphilitic  disease  of  the  liver. 

General  Nutrition. — It  is  hardly  necessary  to  insist  on  the  impor- 
tance of  the  patient's  general  state  of  nutrition  as  a  factor  in  the  prog- 
nosis. A  well-nourished  patient  has  naturally  a  much  better  prospect 
than  an  emaciated  subject.  The  appearance  of  the  face,  haggard  and 
sunken  about  the  eyes  and  temporal  fossae  in  cases  which  are  rapidly 
going  down-hill,  is  an  instinctively  recognised  guide  in  forming  a  very 
grave  prognosis,  while  the  nutrition  of  the  skin  elsewhere,  and  of  the 
muscular  development  generally,  is  of  considerable  value.  The  presence 
of  stigmata  on  the  face  has  been  said  to  be  of  bad  prognosis,  but  as  an 
isolated  manifestation  this  has  seemed  to  me  of  little  value;  a  dirty, 
earthy  tint  of  the  skin  is  more  significant  of  a  general  nutritional  change. 

Age  has  some  influence  on  the  prognosis.  Thus,  Cheadle  *  found  that 
the  average  age  of  37  cases  in  which  temporary  or  prolonged  improvement 
occurred  was  thirty-nine  years,  or  nearly  ten  years  less  than  the  aver- 
age age  of  fatal  cases  of  cirrhosis.  It  is  possible  that  in  these  cases  the 
cirrhosis  developed  rapidly  as  the  result  of  heavy  drinking,  and  that  the 
process  was  not  so  far  advanced  as  in  older  subjects  where  the  fibrosis 
has  slowly  developed.  A  comparatively  early  age  is  a  favourable  factor, 
inasmuch  as  the  general  nutrition  is  probably  fairly  preserved,  and  that, 
as  a  result,  reparative  and  compensatory  processes  can  be  carried  out  in 
an  efficient  manner. 

Size  of  the  Liver. — -From  what  has  been  said  about  compensatory 
hyperjDlasia  it  is  theoretically  probable  that  enlargement  of  the  liver 
improves  the  prognosis,  since  it  is  more  likely  to  be  associated  with 
latency  of  the  disease  than  a  small  one.  In  practice  this  is  hardly  reliable 
as  a  hard-and-fast  rule,  since  enlargement  may  be  temporary-  and  due  to 
alcoholic  excess,  to  absorption  of  poisonous  products  from  the  alimentary 
canal,  or  to  complications  such  as  cardiac  failure  and  backward  venous 
pressure.  Further,  in  the  early  stage  when  the  cirrhotic  process  is  ac- 
tively advancing  the  liver  is  considerably  enlarged.  But  in  the  absence 
of  constitutional  symptoms,  complications,  or  other  signs  that  the  disease 
is  active  and  progressive,  the  outlook  is  better  in  a  case  of  cirrhosis  with 
an  enlarged  than  with  a  small  liver. 

This  is  borne  out  by  the  fact  (vide  p.  199)  that  the  liver  is  larger  in 
persons  affected  with  cirrhosis  but  dying  from  accident  or  from  independ- 
ent diseases  than  in  patients  dying  directly  from  the  effects  of  the  disease. 
Most  of  the  cases  of  cirrhosis  reported  as  recoveries  have  enlarged  livers. 
According  to  Hanot  and  Gilbert  t  and  Cheadle,  X  two-thirds  of  the  cases 
conform  to  this  statement.  Cheadle  dealt  with  no  less  than  30  cases  in 
which  recovery,  either  temporary  or  prolonged,  resulted  after  tapping. 

Enlargement  of  the  spleen  is  ])rescnt  in  progressive  cases  and  is 
absent,  as  a  rule,  in  latent  cases  in  which  compensation  has  taken  place. 

*  Cheadle:  Some  Cirrhoses  of  the  Liver,  p.  72. 

t  Hanot  et  Gilbert:  Soc.  M6d.  des  Hop.,  May  27,  1S90. 

j  Cheadle:  Some  ("irrhoses  of  the  Liver,  p.  69. 


292  DISEASES    OF   THE    LIVER. 

Its  size  is,  therefore,  an  indication  of  some  value,  and  in  cases  thought 
to  be  latent,  splenic  enlargement  should  suggest  the  possibility  of  ap- 
proaching hsematemesis,  ascites,  or  toxsemic  manifestations.  It  should 
be  regarded  as  a  danger-signal  and  as  an  indication  for  purgation  by 
which  portal  engorgement  and  intestinal  fermentation  can  be  diminished 
or  ob\dated.  If  the  spleen  remain  enlarged  after  hsematemesis,  the  possi- 
bility of  a  recurrence  or  of  the  near  advent  of  ascites  should  be  borne  in 
mind. 

Haemateinesis  is  usuaUy  an  early  symptom;  often,  indeed,  the  first 
indication  to  the  patient  that  he  has  anything  serious  the  matter  with 
him.  In  such  cases  the  immediate  prognosis  is  usually  good,  for  the 
patient  recovers,  and  may  by  a  careful  life  escape  any  further  manifesta- 
tions of  cirrhosis  for  years,  or  possibly  forever.  Hsematemesis  is  rarely 
fatal,  but  when  it  is  so,  the  first  hsematemesis  is  usually  followed  by  death. 
When  hsemateme&is  is  frequently  repeated  at  shorts  inten^als  it  is  probably 
due  to  an  ulcerated  oesophageal  vein,  and  the  prognosis  is  worse  than  in 
the  ordinary  single  hsematemesis,  as  the  patient  may  die  from  ansemia 
and  exhaustion.  When  hsematemesis  occurs  in  patients  with  ascites,  the 
prognosis  is  even  more  gloomy  than  it  was  before,  as  the  occurrence  of 
hsematemesis  makes  it  probable  that  the  ascites  is  due  to  cirrhosis  of 
the  liver  and  not  to  concomitant  chronic  peritonitis. 

Multiple  or  general  haemorrhages,  from  the  gums,  throat,  nose,  skin, 
etc.,  make  the  prognosis  very  grave,  as  they  point  to  an  advanced  degree 
of  toxsemia,  which  may  be  succeeded  by  coma. 

When  ascites  has  developed,  the  patient's  days  are,  as  a  rule,  already 
numbered.  According  to  Hale  White,*  indeed,  cases  of  uncomplicated 
cirrhosis,  i.  e.,  without  chronic  peritonitis,  never  survive  to  be  tapped 
more  than  once.  Though  this  may  not  be  strictly  in  accord  with  general 
impression,  and  though  recovery  after  paracentesis  has  often  occurred 
in  cases  where  the  existence  of  cirrhosis  has  subsequently  been  established 
after  death  from  other  causes,  the  great  gravity  of  ascites  clue  to  cirrhosis 
can  hardty  be  overestimated. 

While  insisting  on  the  extreme  gravity  of  ascites  due  to  cirrhosis^ 
it  may  be  pointed  out  that  it  is  a  late  phenomenon  in  the  disease,  and 
probably  a  manifestation  of  an  advanced  degree  of  toxsemia.  But  the 
development  of  ascites  in  a  patient  thought  to  have  cirrhosis  must  not 
be  regarded  as  necessarily  the  eciuivalent  of  a  death  warrant.  Man}^ 
eases  have  been  recorded  where  recovery  has  occurred  after  paracentesis 
for  ascites  thought  to  be  due  to  cirrhosis.  (Bristowe,t  Millard, J  and 
Cheadle,§  and  many  others.) 

An  instructive  case  is  mentioned  by  Hawkins  1|  of  a  man  who  had  been  a  hard 
drinker  and  was  under  the  late  Dr.  Murchison  in  St.  Thomas'  Hospital  with  ascites. 
After  this  he  became  a  total  abstainer  and  lived  in  fair  health  for  twelve  years. 
At  his  death  from  pericarditis  and  granular  kidneys  the  liver  was  found  to  weigh 

*  Hale  White:  Guv's  Hospital  Reports,  vol.  xlix,  p.  1,  IS92. 

t  Bristowe:  Trans".  Med.  Soc,  1S92,  p.  271. 

±  Millard:  Bull,  et  mem.  Soc.  Med.  d.  Hop.,  1892,  p.  153. 

§  Cheadle:  Some  Cirrhoses  of  the  Liver,  p.  69. 

II  Hawkins,  H.  P.:  Allbutt's  System,  vol.  iv,  p.  ISO. 


CIRRHOSIS    OF    THE    LIVER.  293 

59  ounces,  its  capsule  was  much  thickened  and  adherent  to  the  diaphragm,  and  on 
section  it  showed  multilobular  cirrhosis.  Ehret  *  reports  the  details  of  a  man  who 
thirty  years  before  his  death,  which  was  due  to  carcinoma  of  the  esophagus  at  the 
age  of  seventy-two,  had  jaundice,  ascites  requiring  several  tappings,  and  pain  over 
the  liver  and  spleen;  he  became  temperate.  The  Hver  was  small  and  cirrhotic,  the 
spleen  large  and  surrounded  by  firm  adhesions. 

When,  as  in  Hawkins'  case,  death  subsequently  occurs  from  some 
other  cause,  and  the  diagnosis  of  cirrhosis  is  confirmed,  "we  must  conclude 
that  the  compensatory  mechanism  is  sufficient  to  explain  the  cure.  This 
event  is  also  well  illustrated  by  cases  of  laparotomy  for  the  cure  of  ascites 
due  to  cirrhosis  by  means  of  the  production  of  artificial  peritoneal  adhe- 
sions. 

It  must  be  remembered  that  ascites  may  be  associated  with  cirrhosis, 
but  due  to  some  concomitant  cause,  such  as  chronic  peritonitis  or  mitral 
disease.  In  such  cases  death  is  less  likely  to  supeiwene  rapidly  than  in 
cases  where  there  is  no  cause  for  ascites  other  than  cirrhosis.  When 
ascites  is  due  to  chronic  peritonitis,  repeated  tappings  may  be  required, 
and  the  outlook  as  regards  prolongation  of  life  is  better  than  when  ascites 
is  solely  due  to  cirrhosis. 

A  point  of  interest  is  how  much  chronic  peritonitis  will  give  rise  to  associated 
ascites  in  cirrhosis;  it  certainly  need  not  be  universal. 

If  in  a  case  thought  to  be  cirrhosis  the  ascitic  effusion  is  loculated 
from  the  presence  of  adhesions,  it  is  probable  that  for  this  reason  the 
prognosis  is  better  than  in  cases  where  there  are  no  grounds  to  suspect 
adhesions.  But,  on  the  other  hand,  it  is  difficult  to  be  certain  that 
cases  of  loculated  or  encysted  ascites  are  not  entirely  due  to  chronic 
peritonitis,  to  the  exclusion  of  cirrhosis. 

(Edema  of  the  legs  in  the  course  of  cirrhosis  is,  apart  from  any  local 
cause,  of  bad  omen,  for  it  either  points  to  a  general  toxcemic  state  or  is 
associated  with  and  is  possibly  due  to  pressure  of  the  ascitic  exudation 
on  the  inferior  vena  cava.  In  either  of  these  conditions  the  outlook  is 
extremely  bad. 

Functional  activity  of  the  kidneys,  or  renal  permeability,  is  an 
important  factor  in  the  prognosis,  and  the  urine  should  always  be  meas- 
ured and  examined,  so  that  any  feature  in  its  amount  and  in  its  solid 
contents  may  be  at  once  detected  and  treated.  So  long  as  the  kidneys 
remove  the  toxic  bodies  which  the  cirrhotic  liver  allows  to  pass  into  the 
general  circulation,  the  patient  is  in  a  fairly  satisfactory  state;  but  failure 
in  the  urinary  excretion  brings  on  a  condition  of  hepatic  toxsemia  which 
resembles  ursemia.  The  presence  of  diacetic  acid,  as  shown  by  the  a]> 
pearance  of  a  port-wine  colom-  on  the  addition  of  ferric  chloride,  in  the 
urine  makes  the  prognosis  very  grave,  as  acid  intoxication  is  imminent 
and  may  lead  to  coma. 

Fever. — A  raised  temperature  is  met  with  in  cases  which  riui  a  com- 
paratively acute  course,  or  when  some  complication  such  as  tubercu- 
losis is  present,  and  is  therefore  of  bad  prognosis. 

Complications,  such  as  pulmonary  tuberculosis,  peripheral  neuritis, 

*  Ehret:  Mimchen.  med.  Wochen.,  1903,  S.  321. 


294  DISEASES    OF   THE    LIVER. 

etc.,  make  the  prognosis  graver.  When  a  granular  kidney  is  found  asso- 
ciated with  cirrhosis,  the  age  at  death  is,  as  shown  by  statistics,  higher 
than  in  cases  fatal  from  uncomplicated  cirrhosis,  and  clinically  the  renal 
symptoms  are  more  prominent.  It  need  hardly  be  added  that  any  of  the 
acute  infections,  such  as  peritonitis,  pericarditis,  erysipelas,  or  pneu- 
monia, necessarily  make  the  outlook  extremely  bad. 

The  integrity  of  the  hepatic  cells  is  of  great  importance  in  recovery  from  ery- 
sipelas (Roger  and  Gamier*).  In  ordinary  cirrhosis  where  the  cells  are  much 
affected  erysipelas  is  usually  fatal.  Ten  cases  of  ordinary  cirrhosis  attacked  with 
erysipelas  all  terminated  fatally  (Bridiers  de  Villemor  f)  ,  whereas  in  hypertrophic 
biliary  cirrhosis,  where  the  liver  cells  may  remain  intact  and  actively  functional, 
recovery  may  be  hoped  for. 

TREATMENT. 

The  important  subject  of  treatment  may  be  considered  under  the 
following  heads : 

1.  To  prevent  any  further  advance  in  the  morbid  change  in  the  liver. 
This  includes  abstinence  from  alcohol,  careful  dieting,  and  special  atten- 
tion to  the  condition  of  the  alimentary  canal  so  as  to  prevent  or  minimise 
fermentation  and  autointoxication.  In  the  early  pre-ascitic  stage  of 
cirrhosis  these  measures  may  be  spoken  of  as  prophylactic. 

2.  The  palliative  or  symptomatic  treatment.  The  treatment  of  con- 
ditions such  as  hsematemesis  and  ascites  will  be  found  under  those 
headings. 

3.  To  promote  the  compensatory  mechanisms  by  means  of  which 
the  disease  becomes  latent. 


I .    TO  PREVENT  AND  REMOVE  FACTORS  WHICH   FAVOUR  THE  MORBID  CHANGE 

IN  THE  LIVER. 

Irritating  or  toxic  substances,  such  as  alcoholic  drinks,  spicy  or  stimu- 
lating food,  must  be  avoided.  Alcohol  must  be  entirely  prohibited 
throughout  the  treatment  of  the  disease,  and  care  should  be  taken  not 
to  give  the  patient  alcohol  in  his  medicines.  Thus,  tinctures,  alcoholic 
extracts,  and  spirituous  solutions,  such  as  spiritus  chloroformi,  should  be 
avoided  and  infusions  or  watery  extracts  substituted.  If  it  is  impossible 
to  prevent  the  patient  taking  some  stimulant,  a  relaxation  of  his  strict 
duty  to  the  patient,  the  medical  attendant  should  see  that  it  is  taken 
after  meals  and  largely  diluted.  On  a  patient's  power  of  will  to  become 
a  rigid  and  total  abstainer  his  future  will  largely  depend.  It  maj^  be 
very  difficult,  from  the  nature  of  their  occupation,  for  some  persons,  such 
as  those  engaged  in  the  liquor  traffic,  commercial  travellers,  etc.,  to 
become  total  abstainers.  In  such  instances  the  advisability  of  change 
of  occupation  or  of  retiring  from  business  must  be  considered,  and  when 
possible  this  step  should  be  taken. 

Most  writers  agree  that  in  the  last  stages  of  the  disease  alcohol  is 
necessary;  Cheadle,  J  indeed,  says  that  total  deprivation  of  alcohol  hastens 

*  Roger  et  Gamier:  Rev.  de  Med.,  Feb.,  1901,  p.  97. 

t  Bridiers  de  Villemor:  These  de  Paris,  1893-4,  No.  428. 

J  Cheadle:  Brit.  Med.  Journal,  1900,  vol.  ii,  p.  693. 


CIRRHOSIS    OF    THE    LIVER.  295 

the  final  collapse.  Personally,  under  such  conditions  I  prefer  to  give 
liquor  strychninje  in  doses  of  two  minims  and  upwards  hypodermicalh' 
twice  a  da5^  The  administration  of  alcohol  in  the  very  last  stage,  when 
death  seems  imininent  in  a  few  days,  is  really  only  a  kindly  act  and 
directed  to  inducing  euthanasia.  Any  attempt  at  curative  treatment  of 
the  disease  is  over,  and  the  passing  of  the  bar  is  made  easier,  possibly 
accelerated,  by  giving  alcohol. 

Diet. — This  is  a  most  important  part  of  the  treatment.  The  object 
is  to  minimise  autointoxication  and  to  prevent  further  progress  of  the 
cirrhotic  process.  Milk  is  the  ideal  diet.  From  the  fact  that  the  fat  in 
it  is  well  emulsified  absorption  takes  place,  even  under  the  difficulties 
presented  by  intestinal  catarrh  and  a  deficient  secretion  of  bile.  The 
proteid  of  milk  is  much  less  harmful  than  the  proteids  of  meat,  since  the 
putrefactive  products  derived  from  it  are  minimised  and  the  liver  is  less 
taxed  in  the  production  of  urea.  Milk  has  some  diuretic  action  on  the 
kidneys  and  leaves  little  residue,  so  that  fermentation  and  gastro- 
intestinal autointoxication  are  much  reduced.  A  patient  should  be  put 
on  milk  diet  and  kept  on  it  till  his  condition  has  very  markedly  im- 
proved. Difficulty  will  often  arise  in  getting  the  patient  to  carry  out 
and  continue  the  strict  diet,  from  its  monotony. 

As  much  as  3  or  4  pints  of  milk  may  be  given  during  the  twenty-four 
hours,  or  even  a  larger  quantity  of  skimmed  milk.  Milk  may  be  diluted 
with  mineral  waters,  such  as  soda,  Apollinaris,  Vichy,  Vals,  etc.  A  little 
bicarbonate  of  soda  may  be  added  with  advantage  and  may  do  good  by 
antagonizing  acid  intoxication.  Milk  may  be  given  as  junket,  in  the 
form  of  milk  jelly,  or  flavoured  with  a  little  tea,  coffee,  or  cocoa,  or  as  a 
soup  with  some  vegetable  flavouring.  Milk  should  be  given  every  two 
or  two  and  a  half  hours  during  the  waking  hours.  When  digestion  seems 
to  be  defective,  milk  should  be  peptonized  or  given  in  the  form  of  Ben- 
ger's  food. 

In  some  persons  milk  gives  rise  to  troublesome  nausea.  Herter  * 
finds  that  this  can  be  obviated  by  reducing  the  amount  of  fat  in  milk, 
by  substituting  skimmed  milk.  The  percentage  of  fat  is  thus  reduced 
from  4  per  cent,  to  1  per  cent.  Koumiss,  or  fermented  mare's  milk,  may 
also  be  given  when  ordinary  milk  upsets  the  stomach,  but  should  not 
be  continued  longer  than  necessary.  It  is  very  readily  absorbed  and 
may  be  given  in  much  larger  c{uantities  than  ordinary  milk.  Whitla  f 
recommends  buttermilk,  or  the  koumiss  made  in  Ireland  by  mixing  half 
a  pint  of  water,  half  a  pint  of  buttermilk,  and  four  pints  of  fresh  milk, 
and  one  ounce  of  loaf  sugar,  leaving  in  a  warm  place  for  thirty-six  hours 
and  occasionally  shaking. 

It  has  been  said,  but  I  do  not  know  Avith  wliat  degree  of  truth,  that 
a  restricted  milk  diet  is  well  borne  hy  French  and  Italian,  but  not  by 
German,  patients.  A  milk  diet  should  be  maintained  until  impro-\'ement 
occurs;  eggs  and  some  easil^y  digested  farinaceous  and  proteid  foods 
should  be  added  to  the  diet,  and  if  these  are  well  borne,  jiounded  fish 

*  Herter,  U.  A. :  Lectures  on  Chemical  Patholog-v,  p.  8S. 

t  Whitla,  W.:  Dictionary  of  Treatment,  p.  502,'3d  ed.,  1896. 


296  disp:ases  of  the  livek. 

should  be  given  after  an  interval.  Beef-tea,  meat  essences,  strong  soups, 
-and  butcher's  meat  are  not  advisable.  As  a  change,  fruit  and  vegetables 
may  be  occasionally  allowed.  All  stimulating  or  spicy  food  should  be 
avoided,  such  as  curries,  pickles,  anchovies,  pickled  fish,  vinegar,  ginger. 
Fatty  food,  inasmuch  as  by  fermentation  it  may  give  rise  to  fatty  acids, 
such  as  acetic,  lactic,  butyric,  valerianic,  should  be  avoided.  Coffee  and 
tea  should  be  taken  in  small  quantities  freely  diluted  with  milk. 

Carbohydrate  Food. — The  glycogenic  function  of  the  liver  is  well 
preserved  in  spite  of  the  marked  histological  changes  in  the  organ, 
and  theoretically  sugar  and  starchy  foods  should  be  readilj^  assimilated. 
In  practice  carbohydrate  food  should  be  given  in  very  small  quantities 
and  only  increased  if  it  is  well  borne.  From  the  frequency  of  gastro- 
intestinal catarrh,  fermentation  is  very  likely  to  take  place  in  sugary- 
food  and  to  give  rise  to  dyspepsia,  flatulence,  and  the  production  of  fatty 
acids,  which  when  absorbed  may  further  degenerative  and  cirrhotic 
changes  in  the  liver. 

Drugs. — Iodide  of  potassium  should  always  be  tried  in  cases  thought 
-to  be  cirrhosis  of  the  liver,  on  the  chance  that  the  condition  is  in  reality 
•syphilitic.  Whether  iodides  do  any  good  in  ordinary  cirrhosis  is  very 
problematical,  and  no  reliance  can  be  placed  on  this  drug  or  on  chloride 
of  ammonium,  though  it  is  well  to  give  them  a  trial.  Cases  of  early 
cirrhosis  often  improve  under  chloride  of  ammonium,  but  the  other 
hygienic  measures  adopted  may  in  reality  have  been  responsible  for  the 
-good  effects  ascribed  to  that  drug.  Iodoform  has  been  employed  inter- 
nally instead  of  iodides,  but  has  no  advantage  over  them  and  may  disturb 
gastric  digestion.  It  is  probable  that  the  potash  and  ammonia  given 
in  these  drugs  are  of  definite  value  in  counteracting  incipient  acid  in- 
toxication— or  acidosis — due  to  the  formation  of  organic  acids  of  the 
fatty  acid  series  which  tend  to  diminish  the  alkalinity  of  the  blood. 
Whenever  the  urine  gives  a  port-wine  colour  with  ferric  chloride  (the 
fallacy  of  the  reaction  with  salicylates  and  other  drugs  being  eliminated), 
due  to  the  presence  of  diacetic  acid  in  the  urine,  bicarbonate  of  soda 
•should  be  given  in  large  doses  so  as  to  counteract  this  acid  intoxication. 

It  is  very  important  to  prevent  or  remove  gastro-intestinal  catarrh, 
which  by  leading  to  the  production  of  toxic  bodies  aggravates  the  changes 
in  the  liver.  This  can  be  most  satisfactorily  obtained  by  keeping  the 
bowels  freely  open  by  salines,  such  as  sulphate  of  soda  and  of  magnesia, 
natural  Carlsbad  or  other  mild  purgative  waters,  and  by  giving  fractional 
doses  (^ijj-  to  yV  grain)  of  calomel,  which  prevent  fermentation  without 
purging  or  interfering  with  the  normal  processes  of  digestion.  Arsenic, 
salicylates,  capsicum,  and  the  tinctures  and  spirituous  solutions  of  drugs 
should  be  avoided. 

Spa  Treatment. — In  the  very  early  stages  of  the  disease  ver}-  con- 
siderable benefit  may  be  obtained  from  a  course  at  some  of  the  numerous 
spas.  The  regulated  life  enjoined  when  taking  the  cure  and  the  effects 
of  mildly  purgative  water  in  reducing  portal  engorgement  and  diminishing 
intestinal  catarrh  and  fermentation  are  factors  for  good  in  the  spa  treat- 
ment of  early  cirrhosis,  but  little  real  benefit  is  likely  to  result  in  the 


CIRRHOSIS    OF    THE    LIVER.  297 

later  stages  of  the  disease,  and  the  fatigue  necessilated  by  the  journey 
is  likely  to  diminish  the  failing  powers  of  the  patient.  The  following 
spas  may  be  mentioned:  Harrogate,  Llandrindod  Wells,  Mchy,  Vals, 
Ems,  Neuenahr,  Hombiirg,  Wiesbaden,  Baden-Baden,  Kissingen,  Carls- 
bad, Marienbad,  Franzensbad,  Tarasp. 


2.    PALLIATIVE  AND  SYMPTOMATIC  TREATMENT. 

Dyspepsia.^The  treatment  of  dyspepsia  must  depend  on  its  nature; 
if  it  is  irritative  and  due  to  gastritis,  bismuth,  dilute  h3'drocyanic  acid, 
bicarbonate  of  soda,  are  indicated.  When  it  is  atonic  and  due  to  inac- 
tivity of  the  gastric  mucous  membrane,  tonics,  such  as  dilute  nitrohy- 
drochloric  acid,  quassia,  liquor  strychninse,  should  be  taken  after  meals, 
and  pepsin  in  various  forms  may  be  given  with  food. 

For  the  relief  of  flatulence  intestinal  antiseptics,  such  as  creasote, 
thymol,  salol,  /5_naphthol,  salicylate  of  bismuth,  are  often  recommended, 
but  it  is  better  to  give  minute  doses  (-^-^  to  -^  grain)  of  calomel  twice 
or  three  times  a  day  or  saline  purges. 

Vomiting  from  gastritis  should  be  treated  by  cutting  off  food  for 
a  time  and  by  drugs,  such  as  bismuth,'  bicarbonate  of  soda,  dilute  hydro- 
cyanic acid,  or  a  little  morjDhin.  Wlien  food  is  resumed,  after  a  few 
hours'  rest,  peptonized  milk  in  small  quantities  should  be  given  cold. 
The  application  of  an  ice-bag  over  the  stomach  has  been  thought  to  act 
as  a  sedative. 

In  the  earlier  stages  constipation  should  be  prevented  by  seeing  that 
the  patient  takes  plenty  of  water,  while  abdominal  massage  and  gentle 
exercise  may  suffice  to  keep  the  bowels  regular.  Mild  purgatives  and 
laxatives  should  be  employed  if  necessary,  but  powerful  drugs,  such  as 
elaterium,  should  be  avoided,  as  they  may  set  up  enteritis  and  exliausting 
diarrhoea.  Salines,  such  as  Epsom  or  Carlsbad  salts;  a  mixture  of  two 
drachms  each  of  sulphate  of  magnesia  and  of  sulphate  of  soda;  tartrate 
of  soda,  or  waters,  such  as  Hunyadi  Janos,  Friedrichshall,  Pullna, 
iEsculap,  Apenta,  Franz  Josef,  may  be  taken  with  advantage  before 
breakfast.  If  these  means  are  not  sufficient,  a  blue  pill  ma}^  be  taken 
overnight  in  addition,  or  recourse  may  be  had  to  small  doses  (-^^  gr.) 
of  calomel,  or  to  cascara,  rhubarb,  scammony,  euonymin,  podophyllin, 
iridin. 

Early  in  the  disease  diarrhoea  or  looseness  of  the  bowels  may  be  part 
of  chronic  alcoholism;  if  this  is  troublesome,  bismuth,  aromatic  chalk 
and  opium  mixture,  dilute  sulphuric  acid,  tannigen,  or,  if  really  necessary-, 
the  enema  opii,  should  be  given.  The  diet  should,  however,  be  super- 
vised in  the  first  instance,  and  alcohol  strictl}'  tabooed.  In  the  late  stage, 
when  toxaemia  has  developed,  diarrhoea  may  set  in  and  kill  the  patient. 
But  when  slight,  it  is  not  always  advisable  to  check  the  diarrhoea,  as 
it  may  serve  a  useful  pui^pose,  like  diarrlioca  in  ath-anced  renal  disease, 
in  diminishing  toxeemia. 

Pain  over  the  liver  or  the  minor  discomfort  of  weight  and  fulness 
may  be  relieved  by  the  application  of  leeches  or  dry  cupping.     Relief  may 


298  DISEASES    OF   THE    LIVER. 

be  experienced  when  the  Hver  is  enlarged  from  the  apphcation  of  a  bandage 
to  support  the  organ.  Hepatic  pain,  discomfort,  etc.,  are  probably  con- 
nected with  active  congestion  of  the  liver,  and  should  be  treated  by  saline 
purges  and  by  a  few  20-grain  doses  of  chloride  of  ammonium. 

The  drowsy,  semi-comatose  condition,  due  to  toxaemia  from  hepatic 
insufficiency,  may  be  relieved  or  even  removed  by  transfusion  of  saline 
solution  into  the  muscles  or  into  the  veins,  the  former  being  the  more 
suitable;  the  transfusion  may  be  repeated  after  twenty-four  hours.  I 
have  seen  a  patient  so  improved  that  he  went  out  of  the  hospital 
well:  six  months  later  he  died  of  lobar  pneumonia;  at  the  autopsy 
the  liver  weighed  88  ounces  and  was  markedly  cirrhotic.  In  another 
case  life  was  prolonged  for  seven  and  a  half  weeks  after  ascites  had 
disappeared.  On  the  other  hand,  transfusion  sometimes  fails  or  gives 
rise  to  very  transient  improvement.  Copious  enemata  of  water  may 
be  given,  but  are  not  very  successful.  When  diacetic  acid  is  pres- 
ent in  the  urine,  bicarbonate  of  soda  (5ij  to  the  pint)  should  be 
added  to  the  water  used  for  transfusion,  so  as  to  counteract  auto- 
intoxication. Hot-air  baths  often  relieve  the  drowsy,  toxsemic  con- 
dition by  making  the  skin  act  and  so  removing  poisonous  products. 
Perspiration  may  be  much  accelerated  by  giving  a  hypodermic  injection 
of  pilocarpine  {^-^  gr.)  before  the  bath;  the  depressing  effect  of  the 
drug  may  be  prevented  by  combining  it  with  two  minims  of  liquor 
strychninse. 

Portal  Engorgement. — The  chronic  venous  engorgement  of  the 
portal  vein  which  shows  itself  by  enlargement  and  tenderness,  ascites, 
dyspepsia,  and  delay  in  the  absorption  of  food  (vide  opsiuria,  p.  230), 
is  treated  by  saline  purges.  The  increased  osmosis  into  the  bowels  dimin- 
ishes the  heightened  pressure  in  the  portal  vein.  Sulphate  of  magnesia 
and  sulphate  of  soda  combined  may  be  given  on  an  empty  stomach 
alone  or  after  a  dose  of  calomel.  The  good  effects  are  often  shown  by 
a  considerable  diminution  in  the  size  of  the  liver. 

Direct  puncture  of  the  liver  has  been  occasionally,  but  usually  unin- 
tentionally, performed.  In  a  case,  mentioned  by  Goodhart,*  where  it 
was  done  accidentally  in  performing  paracentesis,  the  woman,  who  was 
evidently  dying,  was  greatly  improved  by  the  withdrawal  of  blood  from 
the  liver.  It  is,  however,  dangerous  and  should  not  be  countenanced. 
Abstraction  of  blood  from  the  spleen  by  means  of  a  trocar  has  also  been 
described  as  giving  satisfactory  results,t  but  it  is  dangerous  and  cannot 
be  recommended.  Massage  to  the  abdomen,  and  especially  to  the  liver, 
has  been  recommended  as  a  means  of  diminishing  the  portal  congestion 
(Lecerf  t)  which  precedes  hsematemesis. 

Administration  of  Liver  Substance. — On  the  lines  of  the  successful 
treatment  of  myxcedema  by  thyroid  extract,  attempts  have  been  made 
to  compensate  for  the  disturbance  of  hepatic  function  in  cirrhosis  b}' 
giving  liver  substance  by  the  mouth,  or  injecting  an  extract  of  liver 

*  Goodhart:  Guy's  Hosp.  Gaz.,  May  28,  1898. 

t  Remlinger:  Jour,  des  Praticiens,  Oct.  13,  1901,  p.  659. 

t  Lecerf:  These  Paris,  1901. 


CIRRHOSIS    OF    THE    LIVER.  299 

(hepatin)  under  -the  skin.  It  has  been  tried  by  Yidal,*  Gilbert  and 
Carnotjt  and  others  in  Paris.  Mouras  has  collected  14  cases  of  cirrhosis 
treated  in  this  manner,  and  though  none  could  be  regarded  as  cured,  the 
results  were  encouraging;  in  7  ascites  disappeared  and  in  the  others 
improvement  followed.  The  amounts  of  urine  and  of  urea  were  increased, 
and  the  C|uantity  of  urobilin  in  the  urine  was  diminished.  The  liver  of 
the  pig  is  employed;  as  much  as  3^  ounces  of  pulped  liver  were  given 
daily  by  Yidal  with  successful  results.  The  only  bad  effect  appears  to 
be  diarrhoea. 


3.  TO  PROMOTE  THE  COMPENSATORY  MECHANISMS  BY  MEANS  OF  WHICH  THE 
DISEASE  BECOMES  LATENT. 

Since  no  drug  has  the  power  of  producing  absorj^tion  of  the  fibrous 
tissue,  any  attempts  to  cure  the  disease  must  be  directed  to  improving 
the  compensatory  mechanisms  which  enable  the  disease  to  become  latent. 
Nature's  compensatory  efforts  in  cirrhosis  are  (a)  increase  in  the  collateral 
circulation  between  the  branches  of  the  portal  vein  and  the  general 
systemic  veins  (vide  p.  209)  and  (b)  hyperplasia  of  the  liver  cells.  These 
compensatory  mechanisms  have  already  been  discussed  in  the  section  on 
Prognosis,  and  the  operation  of  promoting  vascular  adhesions  around  the 
liver  was  described  in  the  section  on  the  Treatment  of  Ascites. 

Hyperplasia  of  the  Liver  Cells. — There  is  no  drug,  as  far  as  is 
known,  that  can  safely  be  employed  for  this  purpose,  though  one  would 
naturally  turn  to  arsenic  as  hkely,  from  its  power  of  stimulating  growth 
elsewhere,  to  have  this  effect.  Whether  it  has  this  effect  on  the  liver  there 
are,  as  far  as  I  know,  no  experiments  to  show.  A  drawback  to  its  use  in 
patients  with  cirrhosis  is  that  if  given  by  the  mouth  it  might  set  up 
gastro-intestinal  irritation  and  autointoxication  in  the  ahmentary  canal; 
and,  indeed,  there  is  reason  to  believe,  both  from  increased  frequency  of 
ascites  during  the  epidemic  of  arsenical  poisoning  in  the  north  of  England 
in  1899-1900  and  from  experimental  results,  that  arsenic  ma}^  set  up 
cirrhosis.  In  the  present  state  of  our  knowledge  the  administration  of 
arsenic  in  cirrhosis  is  contraindicated.  As  was  pointed  out  elsewhere,  it 
is  theoretically  possible  that  the  surgical  production  of  vascular  adhesions 
around  the  liver  may  so  improve  the  circulatory  conditions  as  to  favour 
hyperplasia  of  the  hepatic  cells.  It  is  hardly  necessary^  to  add  that  the 
general  health  should  be  improved  as  far  as  possible  and  that  fresh 
air,  sun,  and  careful  feeding  are  important  factors  in  the  treatment. 

PIGMENTED  CIRRHOSIS. 
In  the  description  of  the  histological  appearances  of  portal  cirrhosis 
it  was  pointed  out  that  pigmentation  of  the  liver  cells  and  of  the  fibrous 
tissue  may  occur  under  certain  conditions  and  that  some  slight  pigmenta- 
tion of  the  cells  is  not  imcommon,  if  carefully  sought  for,  in  ordinar}^ 
examples  of  that  disease.     Pigmentation  of  a  cirrhotic  liver  may,  in  ex- 

*  Vidal:  Soc.  de  biolog.  Paris,  Nov.  2S,  1S97. 

t  Gilbert  and  Carnot:  Soc.  de  biolog.  Paris,  Nov.  21,  1897. 


300  DISEASES    OF   THE    LIVER. 

ceptional  instances,  be  due  to  foreign  particles  of  carbon,  stone,  or  metals 
reaching  it  by  the  blood-stream  {vide  Cirrhosis  anthracotica).  Some 
degree  of  pigmentation  T\dth  hsemosiderin,  an  iron-containing  derivative 
of  haemoglobin,  may  be  seen  in  cirrhotic  livers  after  local  haemorrhages 
into  the  substance  of  the  organ. 

In  the  foregoing  instances  the  amount  of  pigmentation  is  compara- 
tively small  and  of  Httle  importance.  The  more  important  forms  of  pig- 
mented cirrhosis  are  (i)  that  occurring  in  hsemochromatosis  and  bronzed 
diabetes,  and  (ii)  malarial  pigmentation  of  a  cirrhotic  liver. 

CIRRHOSIS  ANTHRACOTICA. 

This  is  a  very  rare  condition  in  which  cirrhosis  of  the  liver  is  associated 
■with  the  presence  of  small  masses  of  carbon  in  the  organ.  It  is  analogous 
to  anthracosis  of  the  lungs  (coal-miner's  lung).  Welch*  has  described 
such  a  case  and  Adami  t  speaks  of  a  similar  condition  in  relation  to 
silicosis.  The  condition  is  probabh'  not  so  rare  as  the  paucity  of  recorded 
cases  would  suggest,  and  as  it  may  not  be  detected  unless  the  liver  is 
microscopically  examined,  cases  are  probably  not  infrequently  overlooked. 
The  following  case  was  examined  by  me  in  1892. 

A  chimney-sweep  aged  forty-seven  was  admitted  to  St.  George's  Hospital  on 
Jmie  4,  1892,  with  a  transverse  fracture  of  the  left  leg;  a  month  later  he  had  paro- 
titis, and  on  September  8  he  became  jaundiced  and  ascitic;  ten  days  later  the 
abdomen  was  tapped,  and  on  September  25  he  died  from  asthenia.  The  trachea, 
lungs,  and  stomach  were  deeply  pigmented.  The  liver  (59  ounces)  was  cirrhotic, 
but  not  pigmented  to  the  naked  eye.  Microscopically  there  was  old  multilobular 
cirrhosis  with  rather  extensive  pigmentation  of  the  fibrous  tissues.  The  pigment 
was  black  and  amorphous,  quite  different  from  the  j^eUow  pigment  of  hsemochroma- 
tosis, and  was  probably  soot  conveyed  by  the  portal  vein  to  the  hver.  Its  presence 
was  discovered  only  as  the  result  of  microscopic  examination,  and  it  is  quite  possible 
that  such  pigmentation  of  sweeps'  livers  in  some  degree  is  not  uncommon. 

PIGMENTARY   CIRRHOSIS  OF   HAEMOCHROMATOSIS. 
Synonym:  Diabete  Bronze.  J 

History  and  Etiology. — The  condition  of  bronzed  diabetes,  or 
diabete  bronze,  was  first  noticed  by  Troisier  in  1871,  and  was  referred  to 
by  Trousseau  in  his  clinical  lectures.  Hanot  and  Chauffard  in  1882  de- 
scribed two  cases  of  diabetes  with  enlarged  and  pigmented  cirrhotic 
livers.  In  1886  Hanot,  in  collaboration  with  Schachmann,  described  a 
further  case  and  defined  the  condition  as  a  definite  morbid  entit}^  under 
the  name  "diabete  bronze."  They  took  the  ^dew  that  the  diabetes  was 
the  primary  lesion,  and  that  as  a  result  the  hepatic  cell  became  stimulated 
to  an  increased  production  of  pigment.  Further  cases  of  diabete  bronze 
were  described  by  the  French  school:  LetuUe  (1885),  Brault  and  GaUiard, 
Barth,  Mosse,  Marie,  Auscher  and  Lapique,  Meimier,  Rabe,  and  others. 

Letulle  belieA^ed  that  as  a  result  of  h\^erglyc8emia  the  pigment  was 
formed  from  the  haemoglobin  by  the  cells  of  various  organs,  and  that  it 
was  stored  up  in  the  liver  cells,  though  not  produced  there.     In  France, 

*  Welch,  W.  H.:  Johns  Hopkins  Hosp.  Bull.,  1891. 

t  Adami,  J.  G.:  Sajous'  Annual,  1898,  article  "Cirrhosis." 

J  The  bibliographical  references  will  be  found  on  p.  304. 


CIRRHOSIS    OF   THE    LIVER.  301 

where  most  of  the  cases  have  been  described,  the  association  with  diabetes 
has  been  insisted  on,  and  only  five  cases  of  this  variety  of  cirrhosis  without 
glycosuria  have  been  reported  by  French  observers.  In  Germany  more 
attention  has  been  paid  to  general  pathological  pigmentation  without 
glycosuria.  In  1889  v.  Recklinghausen  described  the  condition  of  hsemo- 
chromatosis,  which  consists  in  infiltration  of  the  organs  with  pigment 
derived  from  pathological  destruction  of  the  red  blood-corpuscles. 

It  has  been  suggested  by  Opie  that  there  is  a  toxic  material  which 
both  causes  haemolysis  and  acts  on  the  cells  of  the  liver  and  other  organs 
so  that  they  transform  into  insoluble  hgemosiderin  the  soluble  blood 
pigment  reaching  them.  Meunier,  indeed,  by  repeated  injections  of 
toluylendiamine  into  dogs,  produced  pigmentation  of  the  liver  and  other 
organs  with  an  iron-containing  body,  but  did  not  obtain  results  on  the 
same  dimensions  as  in  hsemochromatosis.  Adami  and  M.  Abbott  regard 
bacterial  activity  as  the  cause  both  of  the  haemolysis  and  of  the  degenera- 
tive changes  in  the  cells  of  the  pigmented  viscera,  and  bring  forward 
facts  to  suggest  that  it  is  a  chronic  intestinal  infection.  Adami  compares 
it  vdih  pernicious  auEemia  and  describes  the  pigment  as  forming  in  and 
around  the  dead  diplococcal  forms  of  the  colon  bacillus. 

The  pigmentation  occurs,  as  was  shown  by  the  French  observ^ers,  in 
the  cells  of  the  liver,  pancreas,  secreting  glands,  in  the  interstitial  tissue 
of  these  organs,  in  the  lymphatic  glands,  and  in  the  heart-muscle,  in- 
testines, and  skin.  In  the  muscular  fibres  of  the  intestines  and  heart  a 
yellow,  iron-free  pigment  called  hsemofuscin  is  found.  The  relation  of 
these  two  pigments  offers  scope  for  discussion,  and  though  it  seems 
probable  that  the  same  conditions  may  lead  to  their  formation,  they  are 
independent.  Goebel  has  found  this  iron-free  pigment  in  the  smooth 
muscular  fibres  of  various  organs  in  persons  of  advanced  years,  so  that 
it  may  be  regarded  as  being  more  or  less  physiological,  though  in  hsemo- 
chromatosis it  is  present  in  large  quantities. 

The  pigmentation  of  the  skin  is  due  to  an  iron-free  pigment,  ap- 
parently the  same  as  the  normal  one.  (Opie.)  The  muscular  fibres  of 
the  heart  contain  both  hsemosiderin  and  hsemofuscin.  In  the  earlier 
stages  of  hsemochromatosis  the  pigment  accumulates  in  the  cells  of  the 
organs,  the  liver  being  the  most  markedly  affected.  As  the  cells  become 
infiltrated  with  pigment,  they  progressively  degenerate,  undergo  necrosis^ 
and  liberate  the  pigment,  which  passes  into  the  interstitial  fibrous  tissue 
of  the  organ.  Interstitial  fibrosis  of  the  liver  and  pancreas  develops  in 
the  wake  of  the  pigmentary  change.  When  the  fibrosis  of  the  pancreas 
reaches  such  a  degree  that  the  islands  of  Langerhans  are  involved,  diabetes 
results.  The  production  of  diabetes  melhtus  is  therefore  a  late  result  of 
the  hsemochromatosis.  (Anschiitz.)  Of  five  cases  described  in  America 
(Osier,  Opie,  Maude  Abbott,  Condon),  there  was  diabetes  in  one  only 
(Condon's  case).  Only  three  cases  have  been  described  in  England,  those 
by  Saundby,  Galloway,  and  G.  Parker,  but  the  condition  is  not  nearly 
so  rare  as  this. 

A  man  aged  fifty-two  died  in  a  drowsy  state  after  paracentesis  for  ascites  in 
1902  under  my  care  in  St.  George's  Hospital.     The  liver  was  cirrhotic  and  of  a 


302  DISEASES    OF   THE    LIVER. 

greenish-blue  colour,  but  did  not  arouse  any  suspicion  of  hsemochromatosis  until 
it  was  microscopically  examined.  Multilobular  cirrhosis  with  very  well-marked 
hsemochromatosis  was  then  found.  During  life  there  had  been  no  glycosuria,  and 
the  skin,  though  somewhat  earthy  in  colour,  was  not  noticeably  pigmented.  The 
pancreas  was  not  kept  for  microscopic  examination,  as  the  body  was  decomposed 
and  no  suspicion  of  hsemochromatosis  arose  until  after  microscopic  examination 
of  the  liver.  I  have  seen  extensive  hsemochromatosis  with  slight  cirrhosis  in  a  Hver 
showing  secondary  endotheliomatous  growths.  There  is  a  piece  of  a  liver  showing 
a  simple  cyst  in  the  museum  of  St.  Bartholomew's  Hospital  which  has  the  charac- 
teristic brick-red  colour  of  the  hver  in  hsemochromatosis. 

Probably  cases  of  pigmentation  of  the  liver  found  after  death  and 
often  assumed  to  be  due  to  past  malaria  are  in  reality  examples  of  hsemo- 
chromatosis. 

Age.— The  condition  of  hsemochromatosis  occurs  chiefly  between 
forty  and  fifty  years  of  age. 

Sex. — In  30  cases  mentioned  by  Letulle  *  the  male  sex  only  was 
affected.  M.  Abbott's  case  is  the  only  one  in  which  a  woman  was  the 
subject  of  the  disease. 

Morbid  Anatomy. — The  liver  is  nearly  always  enlarged,  sometimes 
considerably;  the  left  lobe  may  be  more  enlarged  than  the  right.  The 
organ  has  a  striking  deep-red  or  maroon  colour,  resembhng  that  of  brick 
dust  or  iron  rust,  and  shows  multilobular  cirrhosis.  As  might  naturally 
be  expected,  the  pigmented  liver  is  less  permeable  to  Rontgen  rays  than 
a  normal  one.  (Jeanselme.)  Microscopically  there  is  brownish-yellow 
pigment,  which  gives  the  reaction  for  iron  with  ferrocyanide  of  potassium 
and  hydrochloric  acid  (Perl's  test) ;  it  is  present  in  the  liver  cells,  in  the 
endothehal  cehs  fining  the  vessels,  in  Kupffer's  star-like  connective-tissue 
cells,  and  in  the  fibrous  tissue  between  the  enclosed  lobules.  The  pigment 
collects  first  in  the  liver  cells  in  the  periphery  of  the  lobules;  as  it 
accumulates  the  cell  nucleus  shows  signs  of  degeneration,  and  eventually 
the  cells  necrose  and  break  up.  The  pigment  is  then  carried  along  the 
lymphatics  into  the  fibrous  tissue  of  the  cirrhotic  hver  and  there  forms 
large  masses.  There  is  ordinary  multilobular  cirrhosis.  The  hepatic 
artery  shows  endarteritis  obliterans.  In  the  muscular  coat  and  adven- 
titia  of  the  arteries  and  veins  a  pale-yellow  pigment,  which  contains  no 
iron  and  is  called  hsemofuscin,  is  seen.  It  remains  unchanged  when  ex- 
posed to  ferrocyanide  of  potassium  and  hydrochloric  acid. 

The  spleen  is  enlarged,  firm,  and  pigmented.  The  pancreas  is  en- 
larged and  pigmented,  and  shows  chronic  interstitial  fibrosis.  The  intes- 
tines are  pigmented  from  hsemofuscin  in  the  muscular  fibres  and  hsemo- 
siderin  in  the  epithelial  cells  of  the  glands. 

The  symptoms  may  be  those  of  cirrhosis  or  of  diabetes.  In  the 
latter  event  the  condition  is  spoken  of  as  bronzed  diabetes  (diabete 
bronze).  The  signs  are  generalized  pigmentation  with  enlargement  of 
the  liver  and  spleen.  The  pigmentation  of  the  skin  imitates  that  of 
Addison's  disease;  it  may  be  of  a  slaty  colour  and  might  suggest  the 
rare  condition  of  argyria,  where  the  skin  becomes  permanently  discoloured 
as  the  result  of  the  medicinal  use  of  silver  salts.  Generalized  pigmenta- 
tion is  present  in  most  but  not  in  all  the  cases;  where  it  is  absent  the 
*  Letulle:  Soc.  M^d.  des  Hop.,  1S97. 


CIRRHOSIS    OF   THE    LIVER. 


303 


existence   of  pigmented   cirrhosis   is,    of   course,  onh'   discovered   after 
death. 

The  enlargement  of  the  hver  and  spleen  may  be  considerable.  The 
liver  is  usually,  but  not  always,  bigger  than  in  health.  The  enlargement 
of  the  liver  and  spleen  is  usually  progressive  and  relatively  equal. 
(Osier.*)  In  a  certain  number  of  cases  haemorrhages  may  occur,  and  in 
a  few  instances  there  have  been  recurrent  attacks  of  purpura.  Abbott's 
case  died  of  haemorrhage  from  an  ulcerated  oesophageal  varix.  In  most 
cases  there  is  little  or  no  ascites  and  the  subcutaneous  abdominal  veins 
may  be  dilated.  There  may  be  dyspepsia  and  pain  on  the  right  side  of 
the  abdomen.  Diabetes  is  a  late  phenomenon  and  does  not  always  super- 
vene; when  it  does,  it  usually  appears  a  year  before  death.     The  onset 


Fig.  36. — Shows  Pigmentation  of  the  Liver  Cells  and  Fibrous  Tissue  in  Cirrhosis  op 

h^emochromatosis. 
Some  of  the  pigmented  cells  show  signs  of  degeneration,  and  in  some  instances  the  outlines 
of  the  cells  around  the  collections  of  pigment  have  gone.     (From  case  described  by  Dr.  Maude 
Abbott,  of  Montreal,  who  kindly  provided  me  with  some  of  the  liver.)      X  220. 


may  be  somewhat  abrupt,  with  weakness,  diarrhoea,  oedema  of  the  legs, 
and  lead  to  death  from  coma  or  from  destructive  lung  changes. 

Diagnosis. — Signs  of  cirrhosis  with  glycosuria  and  pigmentation  of 
the  skin  are  the  three  factors  which  justify  a  certain  diagnosis  of  the 
condition.  In  cases  of  cirrhosis  with  marked  cutaneous  pigmentation, 
but  with  no  glycosuria,  the  disease  may  be  suspected,  l3ut  usuall}^  cannot 
be  positively  diagnosed,  since  considerable  pigmentation,  cspecialty  of  a 
dirty  earthy  colour,  may  exist  in  ordinary  cirrhosis,  Avliile  the  effects  of 
past  jaundice  may  discolour  the  skin. 

*  Osier:  American  Journ.  Med.  Sciences,  vol.  cxxiv,  p.  766   Nov.,  1902. 


304  DISEASES    OF   THE    LIVER. 

Differential  Diagnosis. — From  Addison's  disease  the  enlargement  of 
the  hver  and  spleen  and  glycosuria  should  distinguish  it.  In  some  in- 
stances of  hypertrophic  biliary  cirrhosis  the  colour  of  the  skin  may  re- 
semble that  of  hsemochromatosis,  but  the  existence  of  jaundice  as  shown 
by  the  conjunctivae  should  prevent  a  mistake.  In  chronic  splenic  ancemia 
there  is  sometimes  cutaneous  pigmentation,  possibly  from  the  effects  of 
arsenic  given  medicinally,  and  some  resemblance  to  hsemochromatosis 
without  glycosuria  might  occur.  The  spleen  is  greatly  enlarged  in  splenic 
anaemia,  and  only  moderately  in  heemochromatosis,  while  the  course  of 
the  disease  is  usually  prolonged  in  splenic  anaemia. 

In  most  exceptional  cases  alcaptonuria  may  be  associated  with  re- 
markable pigmentation  of  the  face,  ears,  and  internally  of  the  costal 
cartilages  (ochronosis,  Virchow).  In  these  cases  the  reduction  of  copper 
by  the  urine  might  suggest  bronzed  diabetes;  further  examination  of  the 
urine  would,  however,  show  that  there  is  no  sugar  present.* 

Prognosis  is  bad.  Life  may  be  prolonged  for  years  and  death  may 
occur  from  gastro-intestinal  haemorrhage  as  in  cirrhosis.  When  diabetes 
appears,  the  fatal  termination  is  usually  not  delayed  beyond  a  year. 

Treatment. — If  there  is  diabetes,  the  treatment  should  be  directed 
to  that  condition  by  appropriate  dieting,  codeia,  etc.  Since  the  dia- 
betes is  undoubtedly  pancreatic  in  origin,  it  would  be  reasonable  to  try 
the  administration  of  extract  of  pancreas,  but  so  far  the  results  are 
not  encouraging.  Before  the  development  of  glycosuria  the  treatment 
should  be  the  same  as  that  of  early  cirrhosis,  viz.,  a  bland  diet  and 
drugs  directed  to  prevent  intestinal  fermentation  and  putrefaction. 

REFERENCES. 

Troisier:  Bull.  Soc.  Anat.  Paris,  1871. 

Trousseau:  Clinical  Lectures,  vol.  iii,  p.  506.     Transl.  New  Sydenham  Soc. 

Hanot  and  Chauffard:  Rev.  de  Med.,  1882,  p.  385. 

Hanot  and  Schachmann:  Archiv  de  Physiolog.,  1886,  p.  90. 

Hanot:  Brit.  Med.  Journ.,  1896,  vol.  i,  p.  206. 

LetuUe:  La  Semaine  Med.,  1885,  p.  408. 

LetuUe:  Soc.  Med.  des  Hop.,  1897. 

Brault  and  Galliard:  Archiv.  Gener.  de  Med.,  1888,  i,  p.  38. 

Earth:  Bull.  Soc.  Anat.,  1888. 

Mosse:  Congres  Franc  de  Med.,  1894,  p.  777.  . 

Marie:  La  Sem.  Med.,  May  22,  1895,  p.  225. 

Auscher  and  Lapique:  Compt.  Rend.  Soc.  de  biolog.,  1895. 

Hintze:  Virchow's  Archiv,  Bd.  cxxxix. 

v.  Recklinghausen:  Tageblatt  62.    Versammlung  deutsch.  naturforscher  und  Aerzte 

zu  Heidelburg,  1889,  S.  324. 
Adami,  J.  G.:  Journ.  American  Med.  Associat.,  Dec.  23,  1899. 
Rab6:  La  Presse  MMicale,  July  13,  1901;    Feb.  22,  1902.     Bull.  Soc.  Anat.  Paris, 

1900,  p.  854. 
Meunier:  These  de  Paris,  1898. 
Jeanselme:  La  Presse  Medicale,  Feb.  6,  1897. 
Opie:  Journ.  of  Experimental  Med.,  vol.  iv,  p.  279,  1899. 
Goebel:  Virchow's  Archiv,  Bd.  cxxxvi,  S.  482. 
Anschutz:  Deutsch.  Archiv.  f.  klin.  Med.,  Bd.  bcix,  1899. 
Abbott,  Maude:  Trans.  Path.  Soc,  vol.  li,  p.  66;  and  Journ.  Path,  and  Bact.,  vol. 

vii,  p.  55. 

*  For  information  on  this  subject  I  am  indebted  to  Professor  W.  Osier  and  Dr. 
Garrod.  H.  Albrecht's  paper  (Zeitschrift  f.  Heilkunde,  Bd.  xxiii,  S.  366,  1902) 
should  be  referred  to. 


CIRRHOSIS    OF   THE    LIVER.  305 

Osier:    Brit.    Med.    Journ.,   1S99,   vol.   ii,   p.    1595.      Lancet,    1904,   vol.    i,  p.    10. 

(Ochronosis). 
Futcher:  Journ.  American  Med.  Assoc,  Sept.  28,  1901,  p.  S15. 
Condon:  American  Medicine,  Dec,  1900. 

Saundby:  Lectures  on  renal  and  urinary  diseases,  p.  321,  4th  ed.,  1900. 
Galloway:  Brit.  Journ.  of  Dermat.,  vol.  ix,  p.  32,  1897. 
Parker,  G.:  Brit.  Med.  Journ.,  1903,  vol.  ii,  p.  1052. 
Rendu  and  de  Massary:  La  Presse  Medicale,  Feb.  6,  1897. 


MALARIAL  PIGMENTATION  OF  A  CIRRHOTIC  LIVER. 

In  the  past  malaria  was  regarded  as  an  established  cause  of  hepatic 
cirrhosis,  and  several  forms  of  malarial  cirrhosis  were  described.  Frerichs, 
Lancereaux,  and  Kelsch  and  Kiener  *  recognised  malaria  as  a  cause  of 
hepatitis.  Kelsch  and  Kiener  have  described  in  great  detail  the  changes 
induced  in  the  liver  by  chronic  malaria.  In  one  form,  called  ''hypersemia 
phlegmasique/'  the  liver  is  large,  shows  perihepatitis,  cloudy  swelling  of 
the  liver  cells,  and  small-cell  infiltration  of  the  portal  spaces.  In  another 
form,  nodular  parenchymatous  hepatitis,  the  liver  is  larger  and  soft  and 
shows  numbers  of  small  nodules  composed  of  liver  cells  undergoing  hyper- 
plasia. Cirrhosis  may  subsequently  develop.  Kelsch  and  Kiener  be- 
lieved that  the  fibrosis  was  due  to  a  process  of  metaplasia  on  the  part  of 
the  liver  cells,  but  the  view  that  connective  tissue  is  formed  from  epithelial 
cells  is  entirely  opposed  to  modern  pathological  teaching.  The  resulting 
cirrhosis  is  described  as  either  monolobular  or  multilobular.  Both  the 
fibrous  tissue  and  the  liver  cells  are  infiltrated  with  pigment. 

Osler,t  on  the  other  hand,  says  that  during  nine  years'  practice  at  the 
Johns  Hopkins  Hospital  there  was  not  a  single  case  of  advanced  cirrhosis 
due  to  malaria.  Welch  is  quoted  by  Barker  J  as  having  seen  only  one 
case  of  malarial  cirrhosis  in  New  York,  and  that  in  an  Algerian.  Hale 
White  §  regards  malarial  cirrhosis  as  largely  imaginative. 

As  Barker  points  out,  the  degenerative  and  necrotic  changes  in  the 
liver  cells  produced  by  severe  malarial  infection  are  exactly  the  conditions 
favourable  to  the  production  of  chronic  interstitial  fibrosis  of  the  liver. 
Further,  in  malaria  there  may  be  considerable  gastro-intestinal  disturb- 
ance which  might  lead  to  cirrhosis  of  the  liver,  and  it  has  also  been  thought 
that  the  production  of  poisons  in  the  spleen  might  lead  to  secondary 
cirrhosis.  (Chauffard,  ||  vide  p.  189.)  Barker  has  suggested  that  the 
pigmentation  of  the  liver  cells,  which  is  most  marked  in  the  peripheral 
parts  of  the  lobules,  may  act  as  an  irritant  and  set  up  fibrosis  of  the  organ, 
in  the  same  way  that  the  inhalation  of  carbon  particles  induces  chronic 
interstitial  pneumonia. 

Without  denying  the  possibility  that  the  necrotic  changes  in  the  liver 
cells  induced  by  malaria  may  be  succeeded  by  cirrhosis,  this  sequence  of 
counts  is  evidently  so  rare  that  when  cirrhosis  occurs  in  a  malarial  subject 
the  question  must  arise  whether  it  is  cirrhosis  caused  by  malaria  or  merely 

*  Kelsch  and  Kiener:  Archiv  de  Phvsiol.  norm,  et  path.,  1878,  p.  571;  1879, 
p.  354.  t  Osier,  W.:  Practice  of  Med.,  4th  ed.,  1901,  p.  570. 

X  Barker:  Johns  Hopkins  Hospital  Reports,  vol.  v,  p.  241. 
§  Hale  White:  Brit.  Med.  Journ.,  1903,  vol.  i,  p.  533. 
II  Chauffard:  La  Sem.  mM.,  p.  177,  1899. 
20 


306  DISEASES    OF   THE    LIVER. 

cirrhosis  in  a  malarial  patient.  Alcohol  and  intestinal  toxaemia  may  be 
potent  causes  of  hepatic  cirrhosis  in  patients  suffering  from  chronic  mal- 
aria, or  a  patient  vath.  latent  cirrhosis  maybe  attacked T^■ith  malaria.  In 
either  of  these  events  the  liberated  blood  pigment  may  be  deposited  in 
the  liver  and  produce  a  pigmented  cirrhosis.  ClinicaUy  there  is  nothing 
very  special  in  the  signs  of  cirrhosis  in  a  malarial  subject.  The  signs  are 
those  of  ordinary  portal  cirrhosis  terminating  with  ascites.  The  spleen 
is  enlarged,  and  from  the  influence  of  malaria  more  markedly  so  than  in 
ordinary  portal  cirrhosis. 


BILIARY  CIRRHOSIS. 

Biliary  cirrhosis  ^Yill  be  considered  under  two  distinct  heads:  (i) 
Hypertrophic  biliary  cirrhosis,  and  (ii)  obstructive  biliary  cirrhosis. 

HYPERTROPHIC  BILIARY  CIRRHOSIS. 

It  is  sometimes  spoken  of  as  ''hypertrophic  cirrhosis."  This  is  likely 
to  lead  to  confusion,  as  there  are  several  other  kinds  of  large  cirrhotic 
livers;  in  common  or  portal  cirrhosis  the  organ  is  often  much  enlarged, 
a  fatty  cirrhotic  liver  is  of  very  considerable  size,  and  the  pigmented 
cirrhotic  liver  in  hsemochromatosis  is  also  entitled  to  the  adjective  hyper- 
trophic.   The  term  ''hypertrophic  cirrhosis"  should  therefore  be  given  up. 

Definition. — The  disease  is  characterized  by  chronic  jaundice,  peri- 
odic febrile  attacks,  absence  of  ascites,  enlargement  of  the  liver  and  spleen, 
and  by  its  preference  for  young  persons.  There  is  no  gross  obstruction 
to  the  larger  bile-ducts,  and  histologically  the  cirrhosis  is  more  mono- 
lobular  than  in  portal  cirrhosis. 

HISTORY. 

Although  the  condition  was  recognised  by  Requin  *  in  1846,  by  Todd  f 
eleven  years  later  (1857),  and  by  Ha3'em  1  in  1874,  it  attracted  little 
attention  until  Hanot  §  (1876)  sharply  struck  out  the  disease  in  his 
thesis  on  "Hypertrophic  Cirrhosis  T^dth  Chronic  Jaundice." 

Hanot's  thesis  was  based  on  fifteen  cases,  four  of  which  he  had  observed  during 
Ufe;  in  three  of  the  four  a  postmortem  examination  was  obtained. 

In  1893  Kienerll  suggested  that  the  disease  should  be  called  Hanot's 
disease.  Since  then  somewhat  different  though  allied  forms  of  Mq^er- 
trophic  bihary  cirrhosis  have  been  described  in  France  {vide  p.-  307),  and 
discussion  has  arisen  as  to  the  channel  by  which  the  cause  of  the  disease 
reaches  the  liver.  Of  late  years  the  opinion  has  been  growing  that  the 
description  given  by  Hanot  was  too  sharpty  crystallised,  and  that  few 
cases  conform  to  the  rigid  type  he  erected.  It  has  also  been  suggested 
that  the  symptoms  and  signs  do  not  correspond  to   any  one  type  of 

*  Requin:  Pathologic  Medicale,  tome  ii,  p.  748. 

t  Todd:  Med.  Times  and  Gaz.,  Dec.  5,  1857,  p  571. 

t  Havem:  Archiv  de  Phvsiol.  normal  et  path.,  1874. 

§  Hanot:  These  Paris,  1876.  ||  Kiener:  La  Sem.  Mod.,  July  19,  1893. 


BILIARY    CIRRHOSIS.  307 

anatomical  change  in  the  hver,  but  may  be  associated  with  various  forms 
of  cirrhosis.  The  prevalent  view  in  this  country,  as  voiced  by  Hawkins  * 
and  Pye  Smith, t  is  that  no  real  distinction  can  be  drawn  between  portal 
and  hypertrophic  biliary  cirrhosis.  This  depends  on  the  fact  that  the 
clinical  features  of  hypertrophic  bihary  cirrhosis  undoubtedly  occur  in 
cases  which  on  minute  pathological  examination  show  the  changes  of 
portal  cirrhosis.  This  discrepancy  between  the  clinical  picture  and  the 
pathological  changes  is  probably  due  to  the  fact  that  cirrhosis,  wherever 
it  begins,  will  after  a  time  spread  and  lead  to  changes  of  the  nature  of 
a  mixed  cirrhosis.  Thus  there  is  a  special  tendency  for  changes  presuma- 
bly beginning  in  the  small  bile-ducts  to  become  complicated  in  course  of 
time  by  those  of  portal  cirrhosis.  After  much  consideration  of  the  ques- 
tion I  have  come  to  the  conclusion  that  there  is  an  essential  difference, 
both  clinically  and  pathologically,  between  portal  and  hypertrophic 
bihary  cirrhosis,  and  that  Hanot  and  the  French  school  are  fully  justified 
in  their  contention.  No  doubt  transitional  forms  between  the  two  types 
of  cirrhosis  occur,  just  as  they  da  between  the  arteriosclerotic  (granular) 
kidney  and  that  of  chronic  parenchymatous  nephritis  (large  white  kidney) ; 
but  it  would  be  incorrect  to  assume  that  they  are  different  manifestations 
of  one  and  the  same  process.  Although  different  types  exist,  it  is  ad- 
visable to  give  an  inclusive  description  of  the  disease  as  a  whole,  and  to 
draw  attention  to  the  varieties  which  may  occur. 

DIFFERENT  FORMS  OF  HYPERTROPHIC  BILIARY  CIRRHOSIS. 

A  number  of  cumbrous  names  have  been  coined  to  distinguish  varieties 
of  the  disease.  These  varieties  depend  on  differences  in  the  degree  of  the 
splenic  and  hepatic  enlargement,  and  on  the  relationship  between  the 
enlargement  of  the  two  organs,  both  in  size  and  in  the  data  of  appearance. 
These  types,  created  by  Gilbert  and  by  Chauffard,  will  be  referred  to 
again  in  the  description  of  the  physical  signs  of  the  disease,  but  it  may 
be  well  to  give  a  list  of  them  here. 

Ordinary  form  of  hypertrophic  biliary  cirrhosis,  described  by  Hanot, 
in  which  the  liver  and  spleen  are  both  enlarged. 

Splenomegalic  form,  in  which  the  splenic  enlargement  is  the  predomi- 
nant feature. 

Hypersplenomegalic  form,  in  which  the  spleen  is  actually  larger  than 
the  liver. 

Metasplenomegalic  form,  in  which  splenic  enlargement  precedes  any 
manifest  change  in  the  liver. 

Hepatomegalic  or  asplenomegalic  form,  in  which  the  enlargement  of  the 
liver  is  the  prominent  feature. 

Presplenomegalic  form,  in  which  the  enlargement  of  the  liver  precedes 
that  of  the  spleen. 

Atrophic  biliary  cirrhosis,  in  which  the  liver  is  small. 

A  special  juvenile  type  with  great  splenic  enlargement  was  dcscril)e(l 

*  Hawkins:  Allbutt's  System  of  Medicine,  vol.  iv,  p.  185. 

t  Hilton  Fagge  and  Pye  Smith:  Practice  of  Medicine,  vol.  ii,  p.  540,  1902. 


308  DISEASES   OF  THE   LIVER, 

by  Gilbert  and  Fournier,*  and  a  remarkable  form  of  biliary  cirrhosis  has 
been  described  by  Gibbons  and  others  in  native  infants  in  Calcutta. 
(F^dep.  187.) 

In  the  cases  in  which  the  spleen  is  considerably  enlarged  before  the 
liver  is  noticed  to  be  affected — metasplenomegalic  hypertrophic  biliary 
cirrhosis — Chauffard  f  believes  the  hepatic  cirrhosis  to  be  due  to  poisons 
manufactured  in  the  spleen,  and  that  the  disease  is  a  different  one  from 
the  ordinary  type.  There  is  a  gradual  transition  from  the  less  marked 
examples  of  metasplenomegalic  biliary  cirrhosis  to  Banti's  disease  or 
splenic  anaemia  with  a  terminal  cirrhosis.  Cases  without  jaundice, 
"Cirrhoses  biliaires  anicteriques/'  have  also  been  described. 

On  Some  Forms  of  Disease  Possibly  Allied  to  Hypertrophic 
Biliary  Cirrhosis. — As  in  many  other  diseases,  there  are  less  char- 
acteristic cases  ("fruste"  or  larval)  which  present  some  of  the  features 
of  biliary  cirrhosis,  but  are  incomplete  and  wanting  in  others.  Thus, 
as  just  mentioned,  there  may  be  transitional  cases  between  splenic 
anaemia  and  hypertrophic   biliary  cirrhosis. 

Thus  Claude  Wilson  J  described  a  family  in  which  six  individuals  in  three  gen- 
erations had  ansemia,  enlarged  spleens,  and  periodic  attacks  of  jaundice  and  ab- 
dominal pains.  In  one  of  these  cases  a  postmortem  examination  showed  that  the 
liver  was  free  from  cirrhosis.  These  cases  were,  therefore,  more  allied  to  splenic 
ansemia  than  to  biliary  cirrhosis,  though  clinically  the  resemblance  to  metaspleno- 
megalic biliary  cirrhosis  must  have  been  considerable.  Sir  T.  Barlow  and  H.  B. 
Shaw§  have  published  two  cases  of  recurrent  attacks  of  jaundice  and  of  abdominal 
crises  with  hepatosplenomegaly,  occurring  in  a  mother  and  son,  which  seem  to 
form  a  kind  of  connecting  link  between  hypertrophic  bihary  cirrhosis  and  chronic 
splenic  ansemia.  Hayem  1|  in  1898  described  the  clinical  aspect  of  a  condition  which 
he  regarded  as  a  chronic  form  of  Weil's  disease,  and  called  chronic  infectious  jaundice 
with  splenic  enlargement  and  exacerbations.  As  none  of  his  five  cases  was  ex- 
amined after  death,  it  is  impossible  to  say  with  any  exactitude  what  was  the  nature 
of  the  condition;  but  it  is  probable  that  these  cases  and  those  of  Barlow  and  Shaw 
are  closely  allied.  LerebouUet  **  includes  Hayem's  cases  together  with  5  of  his 
own,  3  of  Boinet's,tt  and  one  of  Bettmann's,t  J  and  Minkowski's  §  §  in  a  group  under 
the  name  of  chronic  splenomegalic  jaundice.  Minkowski's  case  was  examined  after 
death  and  the  liver  was  found  to  be  free  from  cirrhosis.  The  title  is  convenient 
in  being  non-committal. 

Incidence. — Genuine  cases  of  hypertrophic  biliary  cirrhosis  are  dis- 
tinctly rare;  this  contrasts  with  the  frequency  with  which  common  or 
portal  cirrhosis  is  met  with.  The  rarity  of  the  disease  is  perhaps  not 
fully  recognised  since  cases  of  ordinary  cirrhosis  with  large  Uvers  but 
without  chronic  jaundice  are  not  infrequently  confused  with  it. 

*  Gilbert  and  Fournier:  Soc.  de  biolog.,  March  26,  1898. 

t  Chauffard:  Semaine  Medicale,  1900,  p.  176. 

J  Claude  Wilson:  Trans.  Chn.  Soc,  vol.  xxiii,  p.  162,  and  (with  D.  Stanley) 
vol.  xxvi,  p.  163. 

§  Barlow  and  Shaw:  Trans.  Clin.  Soc,  vol.  xxxv,  p.  155. 

11  Hayem:  La  Presse  Medicale,  March  9,  1898. 
**  LerebouUet:  Paris  These,  No.  180,  1902,  Les  Cirrhoses  biliaires. 
tt  Boinet:  Archiv.  General,  de  Med.,  1898. 
tt  Bettmann:  Miinchen.  med.  Wochen.,  June  5,  1900,  S.  791. 
§§  Minkowski:  Verhandlungen  Congres.   f.  inn.  Med.,  Wiesbaden,  1900. 


BILIARY    CIERHOSIS.  309 

ETIOLOGY. 

Age. — It  is  commonest  between  the  ages  of  twenty  and  thirty  and 
is  rare  after  forty,  thus  again  contrasting  with  common  cirrhosis,  in  which 
the  average  age  is  about  forty-eight  years.  A  considerable  number  of 
cases  are  met  with  in  young  children  (Gilbert  and  Fournier's  juvenile 
type). 

Sex. — In  children  the  incidence  of  the  disease  falls  equally  on  the  tw^o 
sexes,  but  apart  from  these  juvenile  cases  it  appears  that  males  are  more 
often  attacked.     In  Schachmann's  *  26  cases  only  4  were  females. 

Heredity. — The  disease  is  sometimes  met  with  in  several  members  of 
the  same  family  when  exposed  to  the  same  conditions. 

Finlayson  f  described  three  cases  in  one  family.  Dreschfeld  f  recorded  the 
disease  in  two  brothers,  and  Osier  §  had  a  similar  experience  in  America.  Boix,  || 
Boinet,**  and  Hasenclever  ft  have  also  published  similar  groups  of  cases.  In 
Brahmin  infants  in  India  a  form  of  cirrhosis  described  as  biliary  is  very  common, 
and  is  especially  apt  to  attack  members  of  the  same  family;  thus,  as  many  as  fourteen 
children  of  the  same  parents  have  died  of  it,  one  after  another.  But  it  is  by  no 
means  certain  that  these  cases  are  the  same  as  Hanot's  disease.  Scheube,JJ  in 
fact,  regards  them  as  parasites  and  possibly  due  to  distoma  in  the  bile-ducts,  but 
this  also  seems  unlikely.     The  condition  is  referred  to  elsewhere  (p.  187). 

The  disease  may  be  found  in  more  than  one  generation,  as  sho^^Ti  by 
Boix  and  BoiHet,  but  probably  this  depends  on  the  surroundings  more 
than  on  direct  heredity.  It  is  interesting  to  note  that  in  other  members 
of  the  same  fairdly  who  have  no  symptoms  of  disease  the  spleen  may  be 
found  to  be  enlarged  (Boix,  Boinet) ;  this  is  analogous  to  the  loss  of  knee- 
jerk  in  apparently  healthy  members  of  a  family  containing  some  children 
affected  with  hereditary  ataxia. 

In  one  family  the  father  and  two  children  had  fuUy  developed  hypertrophic 
biliary  cirrhosis,  while  three  other  children  had  big  spleens.     (Boinet.) 

Lereboullet  H  has  described  the  "cholemic  family,"  the  members  of 
which  are  supposed  to  be  specially  susceptible  to  infection  of  the  bile- 
ducts,  much  in  the  same  way  as  other  families  are  rheumatic  or  tubercu- 
lous. Patients  with  this  diathesis  are  probably  more  likely  to  become 
the  subjects  of  hj^ertrophic  bihary  cirrhosis  than  ordinary  persons. 

Alcoholism. — The  antecedents  of  patients  with  hy[:ertrophic  biliar}^ 
cirrhosis  sometimes  include  heavy  drinking,  but  there  is  no  reason  to 
regard  alcoholism  as  related  to  the  disease  in  the  same  way  as  it  is  to 
common  cirrhosis.  It  may  safely  be  said  that  alcoholic  excess  does  not 
protect  against  bihar}^  cirrhosis,  but,  on  the  contrary,  that  it  may  dispose 
to  infection  b}"  reducing  the  resisting  power  of  the  body  as  a  whole  and 
of  the  liver  in  particular.     Of  the  two  brothers  whose  cases  were  recorded 

*  Schachmann:  These  Paris,  18S7. 

t  Finlaj'son:  Glasgow  Hospital  Reports,  vol.  ii,  p.  39,  1899. 

t  Dreschfeld,  J.:  Medical  Chronicle,  April,  1896. 

§  Osier:  Practice  of  Medicine,  p.  574,  4th  edition. 

II  Boix:  La  Presse  Medicale,  March  16,  1898. 
**  Boinet:  Archiv.  General,  de  Med.,  April,  1898,  and  1903,  p.  362. 
ft  Hasenclever:  Berlin,  klin.  Wochen.,  Nov.  7,  1898. 
tt  Scheube:  The  Diseases  of  Warm  Climates,  p.  364. 
§§  Lereboullet:  Les  Cirrhoses  biliaires,  Th^se  Paris,  No.  180,  1902. 


310  DISEASES   OF  THE   LIVER. 

by  Dreschfeld,  one  was  a  hard  drinker  while  the  other  was  temperate. 
Boix  has  recently  put  forward  the  view  that  the  infection  is  introduced 
into  the  body  in  water,  and  it  has  been  thought  that  cold  and  damp 
houses  favour  the  occurrence  of  the  disease. 

Malaria,  etc. — In  some  instances  malarial  infection  has  preceded  the 
development  of  the  disease,  but  in  the  majority  of  instances  this  can  be 
ruled  out  of  court. 

Geraudel  *  has  revived  Lancereaux's  view  of  1871 — that  the  signs  and  symptoms 
ascribed  to  the  disease  are  malarial  in  origin. 

There  is  no  reason  to  believe  that  syphilis  or  tuberculosis  plays  any 
special  part  in  the  causation  of  the  disease.  It  has  been  noticed  to  de- 
velop after  typhoid  fever  in  a  few  isolated  cases.     (Boinet.) 

Infective  Origin. — Hanot  originally  regarded  the  initial  lesion  as  a 
catarrhal  inflammation  of  the  small  bile-ducts.  Such  a  lesion  irdght 
originate  in  the  minute  ducts  and  be  due  to  a  poison  reaching  them  by 
the  blood,  as  in  experimental  poisoning  by  toluylendiamine;  in  other 
words,  a  descending  cholangitis.  The  condition  of  the  liver  would  then 
be  a  local  manifestation  of  a  general  toxsemic  or  infective  process.  In 
favour  of  an  infective  origin  for  hypertrophic  biliary  cirrhosis  the  following 
points  may  be  urged : 

1.  The  frequency  of  fever. 

2.  The  considerable  splenic  enlargement,  which  indeed  may  precede 
or  be  more  marked  than  that  of  the  liver. 

3.  Glandular  enlargement,  not  only  in  the  portal  fissure,  but  occa- 
sionally in  more  distant  parts  of  the  body. 

The  enlargement  of  the  spleen,  which  may  precede  and  be  more  promi- 
nent than  the  hepatic  enlargement,  may  be  explained  as  due  to  an  in- 
fective agent  in  the  blood,  which  at  the  same  time  as  it  leads  to  changes 
in  the  liver,  settles  down  in  the  spleen  and  there  multiplies  and  produces 
toxic  bodies.  It  is  not  improbable  that  the  poison  thus  manufactured 
passes  into  the  portal  vein  and  sets  up  a  secondary  portal  cirrhosis  (vide 
Cirrhosis  of  Splenic  Origin,  p.  189)  on  the  top  of  the  already  existing 
bihary  cirrhosis,  and  thus  accounts  for  the  confused  and  mixed  tj'pe  of 
cirrhosis  so  often  found  in  the  livers  of  long-standing  cases  of  bihary 
cirrhosis.  In  cases  where  the  spleen  becomes  manifestly  enlarged  before 
the  liver  (metasplenomegahc  form  of  bihary  cirrhosis)  is  affected,  the 
liver  is  probably  more  resistant  to  infective  or  toxic  influences  than  in  the 
ordinary  cases  of  biliary  cirrhosis. 

The  alternative  view  is  that  hypertrophic  bihary  cirrhosis  is  due  to 
a  local  infection  of  the  bile-ducts  from  the  duodenum — an  ascending 
cholangitis.  According  to  this  theory,  it  would  be  analogous  to  broncho- 
pneumonia following  bronchitis  of  the  larger  tubes.  Gilbert  and  Four- 
nier  f  regard  it  as  an  ascending  infection  from  the  intestine  and  due  to 
the  prolonged  action  of  bacilli  belonging  to  the  colon  group.     Potain  % 

*  Geraudel:  Thfese  Paris,  1902. 

t  Gilbert  and  Fournier:  See.  de  biolog.,  July  10,  1897. 

t  Potain:  Semaine  Medical,  1896,  p.  101. 


BILIARY    CIRRHOSIS.  311 

and  other  French  obsen-ers  held  the  same  view.  The  enlargement  of  the 
spleen  is  regarded  as  secondary  to  the  local  and  primary  infection  of  the 
liver  and  due  to  micro-organisms  or  their  poisons  absorbed  from  the 
infected  bile-ducts.  In  favour  of  this  view  is  the  fact  that  in  some  cases, 
which  have  been  operated  upon  during  life  and  the  gall-bladder  drained, 
micro-organisms  such  as  the  Bacillus  coli  and  Diplococcus  pneumoniae 
have  been  found  in  the  biliary  tract.  The  operative  treatment  of  hyper- 
trophic biliary  cirrhosis  is  referred  to  below  {vide  p.  326);  there  may  be 
some  question  whether  all  the  cases  included  in  Greenough's  *  list  of 
seventeen  operations  were  genuine  examples  of  hypertrophic  l^iliary 
cirrhosis,  but  the  marked  success  in  13  of  the  cases  must  be  regarded  as 
weighty  evidence  in  favour  of  an  ascending  infection. 

Against  the  view  that  it  is  an  ascending  infection  might  be  urged 
the  comparative  infrequency  of  dyspepsia  as  an  antecedent  symptom  and 
the  fact  that  a  catarrhal  condition  of  the  duodenum  is  not  found  at  the 
autopsy.  The  fact  that  the  spleen  may  be  enlarged  before  the  liver, 
and  before  there  is  any  jaundice  which  may  be  regarded  as  evidence  of 
infection  of  the  bile-ducts,  is  against  the  theory  of  an  ascending  infection 
and  in  favour  of  the  primary  factor  being  a  general  hsemic  infection.  If 
the  condition  were  due  to  an  ascending  infection  from  the  duodenum, 
the  pancreatic  duct  should  also  become  infected,  and  as  a  result  chronic 
interstitial  pancreatitis  with  increase  in  the  size  of  the  head  of  the  pan- 
creas should  occur. 

Guillain  f  has  described  such  a  condition,  under  the  name  of  "Sclerose  hepato- 
pancreatique  hypertrophique  avec  hypersplenomegalie,"  in  a  temperate  woman 
aged  fifty-two  years;  there  were  hypertrophic  biliary  cirrhosis  and  enlargement  of 
the  pancreas  to  double  its  normal  size.  He  regarded  the  condition  as  due  to  an 
ascending  infection. 

In  biliaiy  cirrhosis,  however,  the  pancreas  is  not  enlarged,  as  is  shown 
by  Lefas'  J  statistical  observations,  so  no  support  to  the  theory  that 
biliary  cirrhosis  is  due  to  an  ascending  infection  is  forthcoining  on  these 
grounds.  On  the  whole,  it  seems  more  probable  that  hypertrophic  biliary 
cirrhosis  is  due  to  a  hsemic  infection  of  a  chronic  nature  leading  to  in- 
flammatory changes  in  the  liver,  than  that  it  is  an  ascending  infection  of 
the  bile-ducts  from  the  duodenum. 

Congeilital  obliteration  of  the  bile-ducts  which  is  associated  with 
a  mixed  (multilobular  and  monolobular)  cirrhosis  of  the  liver,  can  be 
regarded  as  in  part  due  to  a  poison  circulating  in  the  blood,  which 
when  excreted  into  the  small  bile-ducts  sets  up  a  descending  cholangitis. 
This  cholangitis  leads  to  union  of  the  inflamed  surfaces  of  the  larger  ducts, 
analogous  to  obliteration  of  the  vermiform  appendix  after  catarrhal 
appendicitis. 

Possibly  among  the  different  forn\s  of  hy])ertrophic  biliary  cirrhosis 
there  are  some  cases,  like  Guillain's  type,  due  to  an  ascending  infection, 
though  the  majority  are,  like  scarlatinal  nephritis,  due  to  a  poison  reach- 

*  Greenough:  American  Journ.  of  Mod.  Sciences,  vol.  cxxiv,  p.  979. 

t  Guillain:   Rev.  de  Mrd..  Sept.,  1900,  p.  701. 

X  Lefas:  Archives  Generales  de  M(5decine,  May,  1900,  p.  539 


312  DISEASES    OF   THE    LIVER. 

ing  the  liver  by  the  general  circulation.  A  Cjiiestion  which  cannot  at 
present  be  answered  is  whether  poisons  reaching  the  liA'er  by  the  portal 
vein  ever  set  up  the  lesions  of  hypertrophic  biUary  cirrhosis.  As  shown 
by  experiments  with  toluylendianiine,  poisons  in  the  general  circulation 
are  excreted  into  the  small  bile-ducts  and  set  up  inflammation  of  the 
smaller  ducts;  this  is  analogous  to  hypertrophic  biliaiy  cirrhosis.  As  far 
as  we  know,  poisons  arriving  by  the  portal  vein  tend  to  produce  common 
(portal)  cirrhosis.  An  exception,  however,  must  be  made  for  congenital 
syphilis,  where  the  fibrosis  is  intercellular. 

Bacterial  Origin. — Although  a  specific  origin  for  the  disease  has  been 
anticipated,  no  microbic  cause  has  yet  been  satisfactorily  established. 
The  colon  bacillus  has  been  found  in  blood  -^dthdrawn  by  puncture  from 
the  liver  during  hfe  and  subsequently  in  the  liver  and  spleen  in  the 
same  case  (Gilbert  and  Fournier*).  But  further  evidence  must  be 
brought  foi^"ard  before  the  colon  bacillus  can  be  regarded  as  the  siDecific 
cause.  Hayem,t  in  his  cases  of  chronic  infective  jaundice  vdth  splenic 
enlargement  and  exacerbations,  which  is  very  closely  aUied  to,  if  not  the 
same  disease  as,  hypertrophic  biliary  cirrhosis,  found  the  Diplococcus 
pneumonise  in  blood  aspirated  from  the  spleen  during  hfe.  A  diplococcus 
has  also  been  described  by  Kirckow  i  as  the  cause  of  the  disease. 

MORBID  ANATOMY. 

The  liver  is  uniformly  enlarged  and  usually  weighs  from  SO  ounces 
upwards;  it  may  reach  a  weight  of  eight  pounds  or  even  more. 

In  very  exceptional  cases  the  liver  is  described  as  smaller  than  natural — "atrophic 
biliary  cirrhosis."  It  does  not  seem  clear  that  Weber's  §  case,  sometimes  quoted 
as  an  example  of  atrophic  biliary  cirrhosis,  in  -u'hich  the  liver  of  a  girl  aged  fourteen 
years  was  hobnailed  and  weighed  265  ounces,  was  not  one  of  ordinary  portal  cirrhosis. 

Perihepatitic  adhesions  uniting  the  liver  to  the  diaphragm  are  not 
uncommon,  but  otherwise  the  surface  is  fairly  smooth,  and  is  at  most 
finely  granular.  It  does  not  present  the  gnarled  and  hobnailed  appear- 
ance of  common  cirrhosis.  In  long-standing  cases  secondary  portal 
(multilobular)  cirrhosis  supen'enes  and  the  surface  may  be  irregular. 
It  is  of  a  dark-green  colour  and  on  section  is  firmer  than  natural  and  has 
an  aspect  hke  granite,  due  to  the  fine  mesh  of  the  fibrosis. 

The  portal  vein  and  the  hepatic  artery  show  no  signs  of  inflammation. 
The  gall-bladder  contains  bile  and  is  usuaUy  healthy,  though  its  walls 
are  sometimes  thickened.  The  larger  bile-ducts  appear  normal.  It  is 
remarkable,  inasmuch  as  there  is  cholangitis,  that  bilirubin-calcium  cal- 
culi are  not  more  often  present  in  the  ducts.  Gall-stones  have  been 
found  in  cases  of  hypertrophic  biliary  cirrhosis,  and  can  be  quite  well 
explained  as  a  secondary  formation;  it  it  not  necessary  to  assume  that 
they  are  j^rimarv^  and  the  cause  of  the  cirrhosis. 

*  Gilbert  and  Fournier:  Compt.  Rend.  Soc.  de  biolog.,  July  10,  1S97. 
t  Hayem:  La  Presse  ]kledicale,  March  9,  1898. 

j  Kirckow:  Bobiichnaja  Gazeta  Botkina,  1900.  Quoted  in  Rev.  de  Med.,  July, 
1901,  p.  727. 

§  Weber,  F.  P.:  Trans.  Path.  Soc,  vol.  xlvi,  p.  71,  1896. 


BILIARY    CIRRHOSIS. 


313 


Microscopic  Appearances. — ^The  liver  shows  fibrosis,  which  in  the 
earUer  stages  is  monolobular  and  tends  to  surround  each  lobule,  much 
in  the  same  way,  though  not  so  diagrammatically,  as  in  a  normal  pig's 
liver.  In  looking  at  a  section  in  the  early  stages  the  monolobular  ar- 
rangement is  well  seen  and  forms  a  contrast  to  multilobular  cirrhosis. 
But  in  long-standing  cases  the  fibrosis  is  often  irregular  and  there  is 
usually  multilobular  cirrhosis  as  well.  This  is  confusing,  and  no  doubt 
accounts  for  the  difficulty  experienced  by  many  writers  in  accepting 
h5^ertrophic  biliary  cirrhosis  as  a  distinct  pathological  tyi^e.  This  multi- 
lobular cirrhosis  is,  I  beheve,  a  secondary  and  superadded  change,  and 
may  very  plausibly,  on  Chauffard's  theory  of  splenogenous  cirrhosis,  be 
referred  to  the  action  of  poisons  manufactured  in  the  enlarged  spleen 


Fig.    37.— Drawing   of    Monolobular   Cirrhosis  with    some  Invasion  of    the    Lobules   by 

Delicate  Connective  Tissue. 

The  liver  cells  are  shrunken  from  the  effects  of  the  hardening  agent  (absolute  alcohol).     X  25. 


and  conveyed  to  the  liver  by  the  portal  vein.  In  cases  that  die  from 
accident  or  from  some  intercurrent  disease  the  monolobular  cirrhosis, 
described  by  Hanot,  may  be  seen  unobscured  by  the  secondary  multi- 
lobular cirrhosis  which  develops  in  long-standing  cases. 

The  connective  tissue  of  the  monolobular  cirrhosis  is  delicate  and 
fibrillar,  somewhat  like  neuroglia,  and  has  an  open  structure.  In  some 
parts  it  invades  the  lobules  and  becomes  pericellular.  As  compared  •udth 
the  fibrosis  of  multilobular  cirrhosis  it  is  much  less  dense,  but  is  more 
intimately  related  to  the  lobules  and  cells  of  the  liver.  The  delicate 
connective  tissue  contains  branching  anastomosing  elastic  fibres,  which 
invade  the  lobules  and  form  a  fine  network  between  the  cells.     The 


314  DISEASES   OF  THE   LIVER. 

elastic  tissue  is  derived  from  the  sheaths  of  the  hepatic  arterj^,  portal 
vein,  and  bile-ducts,  and  may  also  spread  in  from  the  capsule,  where  it 
is  normally  present.  There  is  less  newly  fonned  elastic  tissue  in  bihary 
cirrhosis  than  in  portal  cirrhosis.     (Flexner.*) 

The  existing  small  bile-ducts  show  prohferation  of  their  lining  epithe- 
lium which  may  block  up  the  lumen  and  so  lead  to  biliary  obstruction; 
as  a  result,  the  bile  capillaries  often  contain  plugs  of  inspissated  bile. 
Around  the  inflamed  bile-ducts  there  is  fibrosis. 

Pseiidobile  CanaUculi. — ^Around  the  margins  of  the  lobules  and  in  the 
fibrillar  interlobular  connective  tissue  there  are  columns  of  small,  deeply 
staining  cells.  The  cells,  which  surround  a  potential  lumen,  are  either 
cubical  or  elongated  so  as  to  he  paraUel  to  the  long  axis  of  the  coluimi. 
Occasionally  the  lumen  is  dilated,  and  though  ordinarily  empty,  may 
contain  minute  biliarj^  calculi.  The  columns  of  cells  tvdst  and  branch 
in  the  neighbourhood  of  the  lobules.  Though  they  are  particularly  well 
marked  in  h}'pertrophic  bihary  cirrhosis,  and  are  only  exceptionally 
absent  in  that  disease,  their  presence  cannot  in  any  way  be  considered 
diagnostic  of  it,  for  they  are  met  with  in  a  large  number  of  other  morbid 
conditions  of  the  fiver,  such  as  portal  cirrhosis,  abscess,  acute  yeUow 
atrophy,  gumma,  tuberculosis,  etc.,  which  tend  to  destroy  the  liver  ceUs 
or  interfere  with  their  functional  activity.  The  histological  appearances 
of  the  so-called  new  bile-ducts  are  the  same  in  all  these  various  conditions 
and  differ  from  normal  bile-ducts  in  that  there  is  either  a  complete  absence 
of  a  covering  of  elastic  fibres  or  a  very  imperfect  development  of  this 
tissue  aroimd  them.     (Flexner.t) 

A  great  deal  of  discussion  has  taken  place  as  to  their  nature  and 
origin.  (Vide  Portal  Cirrhosis,  p.  205.)  They  have  been  thought  to  be 
the  pre-existing  bile-ducts  brought  into  greater  prominence,  to  be  new 
bile-ducts  derived  from  the  ducts  normally  present,  compressed  liver  cells 
surrounded  by  fibrous  tissue,  or,  lastly,  3^oung  fiver  cells — ^the  result  of 
compensatory"  h}qDei*[3lasia  of  the  hepatic  cells  at  the  peripheiy  of  the 
lobules.  The  Cjuestion  is  discussed  on  page  206,  and  the  most  probable 
conclusion  is  that  they  are  the  result  of  comi^ensatory^  hyperplasia  of  the 
liver  cells. 

Hanot  and  Gastou  1  regard  these  so-called  new  bile-ducts  as  the  first  results  of 
irritation  on  the  liver  cells,  and  explain  their  frequency  in  hypertrophic  biliary 
cirrhosis  as  a  direct  consequence  of  the  exacerbations  in  the  course  of  the  disease. 

The  fiver  ceUs  are  for  a  long  period  extremely  weU  preser^-ed,  and 
when  the  patient  dies  from  some  other  cause,  do  not  show  the  fatty  and 
degenerative  changes  seen  in  portal  cirrhosis.  In  many  cases  acute  de- 
generative or  toxic  changes  occur  shortly  before  death. 

Relation  of  Bcmti's  Disease  to  Hypertrophic  Biliary  Cirrhosis. — In 
chronic  splenic  anaemia  a  terminal  multilobular  cirrhosis  may  supervene, 
probably  as  the  result  of  poisons  manufactured  in  the  spleen;   this  is 

*  Flexner:  University  Medical  Magazine,  Philadelphia,  Nov.,  1900,  p.  614. 
t  Flexner:  University  Med.  Magazine,  Philadelphia,  1900,  p.  617. 
±  Hanot  et  Gastou:  Soc.  de  biolog.,  July  15,  1S93,  p.  741. 


BILIARY    CIRRHOSIS.  315 

called  Banti's  disease.  H3'pertrophic  biliary  cirrhosis  is  essentially  mono- 
lobular,  but  in  the  late  stages  a  secondary  multilobular  cirrhosis,  probably 
of  splenic  origin  and  like  that  of  Banti's  disease,  maj^  supen'ene. 

The  Spleen. — The  spleen  is  enlarged  to  a  much  greater  degree  than 
in  portal  cirrhosis;  its  weight  commonly  varies  between  15  and  40  ounces, 
but  may  scale  considerably  more.  The  organ  may  thus  weigh  twice  to 
six  times  its  normal  weight,  while  the  liver  is  seldom  more  than  twice 
or  three  times  its  ordinary  weight.  The  spleen  is  therefore  relatively 
more  increased  in  weight  than  the  liver.  In  some  rare  cases  the  spleen 
is  absolutely  bigger  and  heavier  than  the  liver;  this  is  more  likely  to  be 
met  with  in  children  than  in  adults.  To  this  condition  Gilbert  *  has 
applied  the  somewhat  cumbrous  term  hypersplenomegalic  hypertrophic 
biliary  cirrhosis. 

In  F.  Taylor's  f  case  the  spleen  weighed  87J  ounces  and  the  liver  40  ounces, 
and  in  a  case  recorded  by  Milian  and  Landrieux  J  the  spleen  weighed  94^  ounces 
and  the  liver  665  ounces. 

In  a  case  of  hypertrophic  biliary  cirrhosis  of  very  chronic  nature,  in  which 
jaundice,  enlargement  of  the  spleen  dowTi  to  the  umlDiUcus,  and  clubbing  of  the 
fingers  were  noticed  seven  years  before  death,  the  liver  weighed  65  ounces  and 
the  spleen  77  ounces.     (H.  Roger  Smith.  §) 

There  are  frecpiently  perisplenic  adhesions  from  local  peritonitis  and 
thickening  of  the  capsule  with  local  exaggerations  of  this  change  or 
lamellar  fibromata.  In  uncomplicated  cases,  i.  e.,  where  death  is  not 
the  result  of  a  secondary  and  acute  infection,  the  spleen  is  firmer  than 
natural. 

Microscopically  there  is  fibrosis  with  distension  of  the  sinuses  with 
blood.  The  Malpighian  bodies  in  an  early  stage  are  hypersemic,  while 
later  they  may  undergo  fibrotic  atrophy,  a  process  which  occurs  in  other 
chronic  toxsemic  processes,  and  has  been  obtained  experimentally  by 
Pilliet  II  as  a  result  of  poisoning  by  metatoluylendiamine,  paraphenylene, 
and  nitrate  of  soda.  There  is  also  some  endothelial  h}q3erplasia  in  the 
splenic  pulp. 

The  lymphatic  glands  in  the  portal  fissure  are  sometimes  enlarged, 
but  are  so  soft  that  they  do  not  exert  pressure  on  the  bile-ducts.  They 
are  dark  in  colour  and  oedematous;  microscopically  there  are  fibrosis  and 
pigmentation.  The  pigment  is  probably  derived  from  destruction  of  the 
red  blood  coi-puscles  (hemolysis),  but  differs  from  the  pigmentation  of 
general  hsemochromatosis  in  not  involving  the  liver  and  spleen.  The 
lymphatic  glands  around  the  pancreas  may  also  be  affected  in  a  similar 
manner,  and  in  exceptional  instances  glandular  enlargement  has  l)een 
detected  in  distant  parts  of  the  body,  such  as  the  groin,  axilla,  medias- 
tinum, and  neck.     (Popoff.**) 

The  alimentary  canal  is  usually  free  from  signs  of  past  inflamma- 

*  Gilbert:  La  Semaine  M^dicale,  1900,  p.  124. 
i  Taylor,  F.:  Guy's  Hosp.  Reports,  vol.  liv,  p.  .5. 
%  Milian  et  Landrieux:  La  Semaine  Medicalo,  1900,  p.  124. 
§  Smith,  H.  Roger:  Trans.  Clin.  Soc,  vol.  xxxi,  p.  264. 
II  Pilliet:  Compt.  rend.  soc.  de  biolog.,  Paris,  1894,  p.  331. 
**  Popoff:  Sovrem  klin.,  1895,  .St.  Petersburg. 


316  DISEASES    OF   THE    LIVER. 

tion.  Hanot  noted  that  the  duodenum  ui  the  region  of  the  bihary 
papiUa  was  not  affected  by  catarrh;  Debove's  experience,  however,  is 
rather  in  the  opposite  direction. 

The  pancreas,  as  a  rule,  is  not  increased  in  size  or  weight,  but  it 
is  far  from  normal.  It  is  indurated  and  may  be  imited  by  adhesions  to 
neighbouring  organs.  There  is  an  intimate  fibrosis  of  an  embr>^onic  type 
spreading  from  the  ducts.  In  addition  to  this  periductular  fibrosis 
there  is  some  proliferation  of  the  cells  lining  the  ducts  and  fatty  degenera- 
tion of  the  cells  of  the  acini.  (Lefas.*)  In  exceptional  cases,  as  in 
Guillain's  t  hypertrophic  cirrhosis  of  the  hver  and  pancreas  with  extreme 
splenic  enlargement,  the  pancreas  may  be  enlarged. 

The  kidneys,  except  for  bile-staining,  are  healthy  and  may  show 
hypertrophy.     (^lilian.i)     All  the  organs  are  bile-stained. 

CLINICAL  PICTURE. 

The  onset  may  be  gradual,  and  before  jaundice  sets  in  malaise,  loss 
of  strength,  and,  in  some  cases,  dyspepsia  and  abdominal  pain  may  be 
noticed.  OccasionaUy  pain  is  first  noticed  in  the  left  h}"pochondrium, 
and  physical  examination  shows  that  there  is  considerable  enlargement 
of  the  spleen.  Usually,  however,  the  patient  first  seeks  medical  advice 
and  thinks  seriously  of  his  condition  after  the  appearance  of  jaundice. 
The  onset  of  jaundice  may  be  almost  imperceptible;  in  other  cases  it 
may  be  sudden  and  be  accompanied  by  gastro-intestinal  disturbance, 
thus  resembhng  catarrhal  jaundice,  or  be  accompanied  by  abdominal 
pain  and  some  fever,  so  as  to  imitate  an  attack  of  intermittent  hepatic 
fever  due  to  a  calculus  in  the  common  bile-duct. 

Gilbert  §  has  described  three  modes  of  onset:  (i)  The  hepatic,  with  jaundice  and 
pain  over  tlie  liver;  (ii)  the  gastro-intestinal,  -n-itli  loss  of  appetite,  sickness,  diarrhoea, 
and  abdominal  pain,  and  (iii)  the  splenic,  vnth  pain  in  the  left  hypochondrium  and 
enlargement  of  the  organ. 

The  course  of  the  disease  is  characteristically  slow.  For  a  consider- 
able time — often  for  years — the  general  health  is  fairly  maintained  in 
spite  of  persistent  jaundice.  From  time  to  time  attacks  of  abdominal 
pain  with  fever  and  increase  in  the  degree  of  jaundice  occur;  these  ex- 
acerbations, like  those  in  pernicious  ansemia  and  in  Addison's  disease, 
leave  the  patient  in  a  deteriorated  condition  of  general  health  and  nutri- 
tion. As  time  goes  on  the  periodic  exacerbations  become  more  frequent 
and  the  disease  makes  steady  though  slow  progress;  wasting  and  loss  of 
strength  appear  and  the  patient's  general  condition  becomes  very  un- 
satisfactory. Death  may  occur  from  intercurrent  disease,  from  the 
gradual  development  of  complete  hepatic  insufficiency  and  the  resulting 
toxaemia,  or  during  one  of  the  exacerbations  acute  degenerative  changes 
in  the  hver  cells  may  lead  to  the  phenomena  of  icterus  gravis.  In  the 
last  event  jaundice  deepens,  delirium  and  neiwous  symptoms  appear, 
and  a  "t5^hoid"  or  comatose  condition  ushers  in  death. 

*  Lefas:  Archives  Generales  de  Medecine,  Mav,  1900,  p.  539. 
t  Guillain:  Revue  de  Medecine,  Sept.,  1900.  p.  701. 
j  Milian:  Bull.  Soc.  Anat.  Paris,  1901,  p.  .323. 
§  Gilbert:  La  Semaine  Medicale.  1900,  p.  1S6. 


BILIARY    CIRRHOSIS.  317 

Symptoms. — The  tongue  is  often  furred,  but  may  be  clean  for  long 
periods.  The  appetite  is  sometimes  poor,  but  is  frequently  normal  and 
in  some  instances  has  been  very  excessive.  There  is  not  the  same  marked 
distaste  for  fatty  food  met  with  in  ordinary  obstructive  jaundice.  Dys- 
pepsia is  much  less  frequent  than  in  portal  cirrhosis.  Hayem  stated  that 
h3^eracidity  is  constant,  but  Ilirikow  *  examined  a  number  of  cases 
without  being  able  to  confirm  this.  Nausea  and  vomiting  are  occasionally 
present.  Hsematemesis  is  very  seldom  met  with.  It  may  occur  late  in 
the  course  of  the  disease  as  the  result  of  secondary  portal  cirrhosis  and 
even  prove  fatal. 

Milian  f  has  recorded  fatal  hsematemesis  from  an  CESophageal  varix. 

Attacks  of  diarrhoea  on  shght  provocation  are  not  uncommon.  The 
motions  contain  bile;  this  is  a  point  of  distinction  between  the  disease 
and  obstructive  jaundice  with  hepatic  enlargement. 

In  26  cases  collected  by  SchachmannJ  bile  was  absent  from  the  fseces  in  only 
two.  From  attacks  of  intercurrent  catarrhal  jaundice  the  stools  may  be  temporarily 
devoid  of  bile. 

The  abdomen  is  prominent  and  distended,  especially  in  the  upper 
quadrants,  from  the  large  size  of  the  fiver  and  spleen.  Some  of  tfie  dis- 
tension is  due  to  tympanites  and  a  weakened  condition  of  the  abdominal 
waUs.  L'ntil  late  in  the  course  of  the  disease  ascites  is  absent  or  only 
present  in  slight  amount,  being  then  due  to  intercurrent  attacks  of  peri- 
hepatitis and  perisplenitis.  Towards  the  tennination  of  the  disease 
ascites  may  be  considerable  from  the  development  of  secondary  portal 
cirrhosis  and  concomitant  toxaemia.  The  abdominal  distension,  which 
is  present  more  or  less  throughout  the  disease,  is  independent  of  ascites. 

There  is  a  sense  of  weight  in  the  right  hypochondrium  and  periodic 
attacks  of  pain  with  tenderness  over  the  fiver  and  spleen.  These  attacks 
may  even  suggest  bifiary  colic.  There  may  be  fittle  or  no  enlargement 
of  the  subcutaneous  veins  around  the  umbilicus,  but  it  cannot  be  said 
that  this  feature  of  portal  cirrhosis  is  completely  absent  in  hj^^ertrophic 
bifiary  cirrhosis.  It  may  develop  as  the  result  of  superadded  portal 
cirrhosis  in  the  later  stages  of  the  disease. 

Physical  Signs. — The  liver  is  much  and  uniformly  enlarged,  and 
smooth  and  firm  to  the  touch,  as  a  rule,  but  occasionally  slightly  irregular 
from  the  presence  of  perihepatitic  adhesions.  Its  dulness  often  extends 
upwards  to  the  fourth  rib  in  the  right  nipple  line,  and  downwards  to  the 
umbilicus  or  even  below  that  point,  and  as  far  as  the  crest  of  the  ilium. 
The  pressure  of  the  enlarged  organ  pushes  the  costal  arch  out.  On  pal- 
pation there  is  slight  general  but  not  any  localized  tenderness.  There  is 
no  enlargement  of  the  gall-bladder.  The  enlargement  of  the  liver  is, 
generally  speaking,  progressive;  it  may  vary  from  time  to  time,  and 
increase  in  size  during  the  periodic  exacerbations  of  the  disease.     Late 

*  Kirikow:  St.  Petersburg  med.  Wochen.,  Bd.  xxvii,  S.  357,  1902. 
t  Milian :  La  progres  Medical,  April  14,  1900. 
%  Schachmann:  These  de  Paris,  1889. 


318  DISEASES    OF   THE    LIVER. 

in  the  disease  it  sometimes  diminishes  in  iDiilk  from  some  degree  of  con- 
traction of  the  fibrous  tissue,  probably  of  that  constituting  the  multi- 
lobular cirrhosis. 

A  rare  and  special  form  of  the  disease — atropine  biliary  cirrhosis — 
has  been  described  *  in  which  the  hver  is  small,  and  the  symptoms  are 
those  of  biliary  cirrhosis  in  general,  but  develop  rapidh\ 

The  spleen  is  very  considerably  enlarged — much  more  so  than  in  com- 
mon cirrhosis.  It  is  more  marked  in  children,  in  accordance  with  the 
fact  that  its  capsule  is  more  distensible  than  in  adults.  A  special  form 
of  hypertrophic  biliary  cirrhosis  has  been  described  bj^  Gilbert  and 
Fournier  as  the  juvenile  t}^3e,  or  "cirrhose  bihare  splenomegahque." 
The  spleen  may,  indeed,  be  not  only  relati^'ely  but  absolutely  hea^der  than 
the  liA'er. 

Three  forms  of  the  disease  have  been  described  by  Gilbert  and  Cas- 
taigne  f  according  to  the  amount  and  degree  of  splenic  enlargement: 

(I)  The  ordinar}'  or  hepatic  type,  in  which  the  liver  and  spleen  are 
both  considerably  enlarged. 

(II)  The  splenomegahc  type,  in  which  the  splenic  enlargement  is  the 
predominant  feature.  For  cases  where  the  spleen  is  actually  larger  than 
the  hver  Gilbert  %  has  more  recently  employed  the  title  'Ti}73erspleno- 
megalic  biliary  cirrhosis." 

(III)  The  heiDatomegalic  type,  where  the  enlargement  of  the  hver 
is  the  predominating  feature.  Gilbert  more  recently  speaks  of  this  as 
the  microsplenic  or  asplenomegalic  form  of  biliar\"  cirrhosis.  The  spleen 
may  not  be  enlarged. 

The  splenic  enlargement  may  precede  any  enlargement  of  the  liver; 
Boix  §  and  Popoff  1|  insist  that  it  always  does.  Chauffard  **  lays  great 
importance  on  the  time  relations  between  the  hepatic  and  splenic  en- 
largement and  diA'ides  the  cases  into  three  groujDs: 

(I)  Where  the  spleen  and  liver  are  simultaneously  and  ec[ually  affected. 

(II)  "WTiere  the  spleen  is  affected  first  and  in  a  greater  degree — 
met  asplenomegalic  hypertrophic  biliarj^  cirrhosis;  the  cirrhosis  he  believes 
to  be  secondarj^  to  poisons  manufactured  in  the  spleen. 

(III)  AVhere  the  liver  enlarges  first  and  probably  determines  the 
splenic  enlargement — ^presplenomegalic  hypertrophic  biliary  cirrhosis. 

The  spleen  is  firm,  smooth  on  the  surface,  but  not  so  hard  as  in 
myelogenous  leukaemia.  WTien  attacks  of  inflanmiation  of  the  capsule 
supervene,  friction  may  be  heard  with  the  stethoscope,  and  in  some  in- 
stances a  soft  blowing  murmur  may  be  audible  over  the  spleen. 

Jaundice  is  slight  at  first  and  becomes  more  marked  as  the  disease 
progresses;  it  is  permanent,  but  varies  in  degree,  being  intensified  at 
intervals  when  exacerbations  in  the  disease  occur.  After  these  crises  it 
recedes  a  little,  but,  on  the  whole,  slowty  jDrogresses.     The  jaundice  may 

*  Lereboullet:  Les  Cirrhoses  Biliares,  These  Paris,  1902,  Xo.  ISO. 
t  Gilbert  and  Castaigne:  Soc.  de  biolog..  May  20,  1899,  p.  403. 
X  Gilbert:  La  Semaine  Medicale,  1900,  p.  1.54. 
§  Boix;  Soc.  de  biolog.,  March  12,  1S9S,  p.  297. 
II  Popoff:  Legons  CUnique,  St.  Petersburg,  1S96.     Quoted  bv  Boix. 
**  Chauffard:  La  Semaine  Medicale,  1900,  p.  176. 


BILIARY   CIRRHOSIS.  319 

eventually  become  very  dark  or  green.  There  may  be  considerable 
bro^Ti  discolouration  of  the  skin,  reseml)hng  that  of  Addison's  disease. 
This  melanoderma  may  occur  early,  before  icterus  has  made  its  appear- 
ance (Roger  Smith),  but  usually  it  is  combined  with  the  icteric  staining 
of  the  skin.  There  may  be  troublesome  itching,  and  from  scratching 
the  skin  may  become  covered  by  an  eczematous  or  lichenous  eruption. 
Long-continued  jaundice  may  lead  to  the  striking  lesion  of  the  skin — 
xanthelasma.  I  have  seen  it  in  a  case  where  moderate  jaundice  had 
existed  for  nine  months.  It  is  said  that  in  some  cases  of  otherwise 
typical  hypertrophic  biliary  cirrhosis  jaundice  is  absent. 

Hceinorrhages.— Ill  the  later  stages  of  the  disease  there  may  be  a 
haemorrhagic  tendency,  shown  by  cutaneous  petechise,  epistaxis,  bleeding 
from  the  gums  and  throat,  and  in  exceptional  instances  haemoptysis  and 
hfematuria;  hsematemesis  is  rare. 

Physical  Development. — The  patients  are  thin,  badly  nourished,  and 
when  not  adults,  frequently  small  for  their  age.  As  in  a  number  of  other 
conditions,  such  as  cretinism,  hereditary  syphilis,  and  congenital  morbus 
cordis,  growi;h  and  bodily  development  may  be  greatly  interfered  yaih. 
and  the  onset  of  puberty  and  in  girls  menstruation  postponed.  To  this 
condition  the  term  "infantihsm"  is  apphed.*  The  skin  is  dry;  some- 
times there  is  dark-brown  pigmentation,  suggesting  that  some  other 
cause  than  jaundice  is  at  work.  (Edema  of  the  feet  may  occur  in  the 
kte  stages. 

Clubbing  of  the  Fingers. — In  some  cases  of  long  standing  a  peculiar 
change,  consisting  in  clubbing  of  the  terminal  phalanges  of  the  fingers 
and  toes,  has  been  obser^^ed.  The  terminal  phalanges  may  be  expanded 
and  broadened  so  that  the  finger  resembles  a  spoon  or  even  a  pendulum. 
The  nails  ma}^  be  overcurved  at  the  same  time  and  may  be  longitudinally 
striated;  in  extreme  instances  the  nails  have  been  compared  to  a  parrot's 
beak.  This  change  is  much  the  same  as  that  seen  in  congenital  morbus 
cordis  and  chronic  lung  disease,  and  sometimes  spoken  of  as  "Hippocratic 
fingers."  Its  occurrence  in  biliary  cirrhosis  is  rare,  though  Gilbert  and 
Lereboullet  f  were  able  to  refer  to  40  cases  in  1901.  It  is  met  with  more 
often  in  children,  in  whom  it  was  first  described  by  Gilbert  and  Fournier,| 
than  in  adults.  ExaiTiination  with  the  a:-rays  shows  that  there  is  no 
bony  enlargement  of  the  terminal  phalanges  (F.  Taylor,§  Boutron  ||). 
The  clubbing  is  due  to  thickening  of  the  soft  tissues,  and  on  the  analogy 
of  its  occurrence  in  bronchiectasis  and  empyema  the  change  is  probably 
due  to  the  action  of  toxines.  But  although  the  change  resembles  Marie's 
hypertrophic  pulmonary  osteo-arthropathy  in  a  minor  degree,  it  is  not 
associated  with  intra-thoracic  disease,  and  there  is  no  reason  to  think 
that  it  is  due  to  embarrassment  of  the  right  lung  by  the  upward  pressure 
of  the  enlarged  liver.     Neither  is  it  confined  to  this  form  of  hepatic  dis- 

*  For  references  on  the  subject  of  infantilism  see    Hutinel:   Gaz.  hebdom.  de 
Md'd.  et  de  chirurg.,  1902,  p.  37;   H.  Meige:  Gaz.  des  HAp.  Paris,  1002,  p.  207. 
t  Gilbert  and  Lereboullet:  Gaz.  hebd.  de  M6d.  et  de  chirurg.,  1902,  p.  1. 
t  Gilbert  and  Fournier:  Rev.  Mens,  de  Malad.  de  I'enfance,  July,  189.5,  p.  .309. 
§  Taylor,  F.:  Guy's  Hospital  Reports,  vol.  liv,  p.  13. 
II  Boutron:  Thdse  de  Paris,  1899,  No.  513. 


320  DISEASES   OF  THE   LIVER. 

ease,  for  it  was  well  marked  in  a  boy  aged  seventeen,  under  the  care  of 
my  colleague,  Dr.  Ewart,  with  syphilitic  stricture  of  the  bile-ducts  (vide 
Fig.  38),  and  in  very  rare  instances  it  has  occurred  in  portal  cirrhosis. 
In  a  few  cases  the  bulbous  or  "Hippocratic"  fingers  have  been  found 
associated  with  perforating  ulcer  of  the  foot,  and  neuritis,  in  hyper- 
trophic biliary  cirrhosis. 


Fig.  38.— Photograph  showing  Bulbous  Fingers  Resembling  those  seen  in  Hypertrophic 
Biliary  Cirrhosis.  From  a  Case  op  Tardive  Hereditary  Syphilis  with  Stricture 
OF  the  Hee'atic  Ducts.     (Photograph  by  Dr.  H.  G.  Drake-Brockman.) 

Reference  for  the  subject  of  clubbed  fingers  in  biliary  cirrhosis  may  also  be 
made  to  the  following  sources:  Roger-Smith:  Trans.  CHnic.  Soc,  vol.  xxxi,  p.  258; 
F.Taylor:  Guy's  Hospital  Reports,  vol.  hv;  Parmentier  and  Castaigne:  La  Sem. 
med./l901,  p.  94;  Rhorassandri :  These  Paris,  1900,  No.  160. 

Arthritis,  etc. — Enlargement  of  the  ends  of  the  bones,  synovitis,  and 
pain  in  the  joints,  so-called  biliary  rheumatism,  has  been  described  by 
Gilbert  and  Fournier.  The  enlargement  of  the  ends  of  the  bones  is  an 
osteopathy  analogous  to  Marie's  pulmonary  form. 

In  a  man  aged  twenty-three  years,  who  rapidly  developed  the  clinical  picture 
of  hypertrophic  bihary  cirrhosis,  a  remarlvable  attitude  of  the  body  appeared.  The 
right  shoulder,  pelvis,  and  hip  were  depressed  without  any  spinal  curvature  to 
account  for  it.  The  patient  himself  was  unconscious  of  the  condition  and  could 
by  an  effort  temporarily  correct  it.  Sicard  and  Remlinger  *  thought  that  the  en- 
larged liver  might  possibly  have  some  part  in  bringing  about  this  curious  attitude, 
though  it  had  not  been  noticed  in  cases  with  much  bigger  hvers. 

Nervous  System. — As  a  rule,  there  is  nothing  special  to  note  with 
regard  to  the  nervous  system.  As  the  result  of  jaundice  there  may  be 
some  mental  depression  and  some  failure  of  memory,  while  occasionally 
there  may  be  emotional  disturbance.  Marked  drowsiness  is  not  a  very 
rare  symptom.  In  the  terminal  stages  toxsemic  symptoms,  such  as  de- 
lirium, coma,  and  convulsions,  are  seen.  I  have  seen  definite  peripheral 
neuritis  with  numbness  of  the  fingers,  but  this  appears  to  be  quite  un- 
usual. 

The  heart  tends  to  dilate,  and  a  systohc  mitral  murmur  or  heemic 
murmurs  may  be  heard  at  some  time  during  the  course  of  the  disease. 
The  pulse  is  regular  and  of  fair  tension.     There  is  no  slowing. 

*  Sicard  and  Remhnger:  Rev.  de  Med.,  Sept.,  1S97,  p.  693. 


BILIARY   CIRRHOSIS.  321 

Blood. — There  is  anaemia  of  a  secondary  character,  the  red  coipuscles 
being  usually  reduced  to  between  4,500,000  and  2,200,000  and  the 
haemoglobin  value  being  below  1. 

Observations  by  Hayem  and  by  Cabot*  have  shown  that  in  exceptional  in- 
stances the  amount  of  haemoglobin  may  be  relatively  excessive.  Thus  in  Hay  em's 
case  there  were  1,884,000  red  corpuscles  with  50  per  cent,  of  haemoglobin;  the  diag- 
nosis was  confirmed  by  an  autopsy.  It  must  be  borne  in  mind,  as  pointed  out  by 
Cabot,  that  the  presence  of  bile  in  the  blood  renders  the  estimation  of  haemoglobin 
unsatisfactory. 

There  is  no  poikilocytosis  (Milian  f) ;  the  blood  is  less  coagulable  than 
in  health.  The  question  as  to  the  presence  or  absence  of  leucocytosis  is 
not  settled.  Hanot  stated  that  leucocytosis  was  present,  but  this  state- 
ment has  not  been  universally  confirmed.  It  appears  that  leucocytosis 
is  not  constant,  and  may  be  absent.  When  present,  it  is  not  very  marked, 
var3'ing  between  9000  and  15,000,  and  is  due  to  an  increase  in  the  poly- 
moriDhonuclears  (Milian  |). 

Hanot  and  Meunier  §  found  leucocytosis  in  5  cases  and  Cabot  ||  in  4  out  of  6 
cases;  DaCosta  **  in  2  out  of  6.  It  was  absent  in  cases  reported  by  Taylor,  and 
Milian  and  Kirikow  ff  found  that  leucocytosis  was  only  present  when  there  were 
complications,  and  that  a  normal  count  or  leucopenia  was  the  rule.  Bigart's  J  J 
observation  of  increase  in  the  number  of  mast  cells  appears  to  be  quite  unique  and 
may  have  been  due  to  some  independent  factor. 

Respiratory  Systein. — ^There  may  be  shortness  of  breath,  due  to  the 
upward  displacement  of  the  diaphragm,  anemia,  and  cardiac  dilatation. 
Occasionally,  as  part  of  the  general  hsemorrhagic  tendency,  hsemoptysis 
may  occur.  Cough  is  sometimes  persistent,  and  suggestive  of  tubercu- 
losis, but  tubercle  bacilli  are  very  rarely  found  in  the  sputum. 

Urine. — ^The  quantity  passed  is  subject  to  considerable  variations; 
usually  it  is  increased  in  amount,  but  during  the  exacerbations  it  may  be 
diminished.  Milian  §§  lays  stress  on  polyuria  as  a  characteristic  feature. 
It  is  high-coloured  and  rich  in  urinary  pigments.  Urobilin  and  indican 
are  both  occasionally  present.  Bile  pigment  is  practically  alwa^'s  present. 
Unlike  the  concentrated  urine  of  portal  cirrhosis,  there  is  little  tendency 
to  deposit  urates. 

There  is  usually  no  albuminuria;  when  present,  it  has  been  noticed 
to  be  intermittent.  Casts,  if  carefully  looked  for,  are  nearly  always 
found;  their  presence  appears  to  depend  on  the  jaundice.  The  amount 
of  urea  varies;  it  may  be  normal  or  may  at  times  be  diminished.  Glyco- 
suria does  not  occur.  Owing  to  the  fact  that  the  liver  cells  preserve 
their  nutrition  for  a  considerable  period,  alimentary  glycosuria,  induced 

*  Cabot:  Examination  of  the  Blood,  p.  250. 

t  Milian:  Bull.  Soc.  Anat.  Paris,  1903,  p.  13. 

t  Mihan:  Bull.  Soc.  Anat.  Paris,  1903.  p.  13. 

§  Hanot  and  Meunier:  Compt.  Rend.  Soc.  biolog.,  1895,  tome  ii,  p.  49. 

II  Cabot:  Examination  of  the  Blood,  p.  250. 
**  DaCosta:  Clinical  Hoimatology,  p.  352. 

ft  Kirikow:     Zeitschrift    f.    klin.   Med.,      Bd.    xxxvi,    S.    444.     Kirikow  and 
Korobkow:  Russ.  Archiv  f.  Path.,  klin.  Med.,  u.  Bakt.,  St.  Petersburg,  1902. 
tt  Bigart:  Soc.  de  Biolog.,  Dec.  27,  1902. 
§§  Milian:  Bull.  Soc.  Anat.  Paris,  1901,  p.  32.3. 
21 


322  DISEASES    OF    THE    LIYEE. 

by  giving  three  ounces  of  sugar  on  an  empty  stomach,  cannot  be  produced 
in  most  cases. 

The  toxicity  of  the  urine  is  said  to  be  feeble,  and  this  has  been  used  as  an  argu- 
ment against  the  view  that  hypertrophic  bihary  cirrhosis  is  primarily  due  to  a 
general  hsemic  infection.  The  freezing-point  of  the  urine,  or  its  cryoscopic  value, 
has  been  found  to  be  high  (Ferrannini*) . 

TERMINATION. 

In  uncomphcated  cases  the  cUsease  slowly  progresses  until  a  fatal 
toxsemic  condition  results  from  destruction  of  the  liver  cells.  The 
''typhoid"  state  develops  and  the  patient  becomes  more  jaundiced, 
drowsy,  and  passes  into  coma.  During  this  stage  ascites  may  develop, 
or  in  rare  instances  death  may  be  precipitated  by  fatal  gastro-intestinal 
haemorrhage,  as,  for  example,  in  the  following  case : 

A  married,  childless  woman,  aged  thirty-two,  who  had  had  one  miscarriage,  was 
admitted  under  my  colleague,  Dr.  Penrose,  at  St.  George's  Hospital  vdth  jaundice 
of  four  months'  duration,  a  greatly  enlarged  and  tender  hver,  enlarged  spleen  and 
no  ascites,  but  a  history  of  several  attacks  of  hsematemesis.  The  urine  was  bile- 
stained  and  contained  a  trace  of  albumin.  There  were  no  distended  abdominal  veins. 
There  was  a  systoUc  murmur  over  the  pulmonary  artery.  There  was  no  definite 
history  of  alcoholism,  but  it  was  suspected.  A  few  days  after  admission  hsemate- 
mesis  recurred  and  was  often  repeated;  the  patient  became  delirious  and  finally 
comatose,  and  in  spite  of  being  bled  from  one  arm  to  about  a  pint  and  transfused 
to  two  pints  in  the  other  arm,  she  died.  At  the  autopsy  there  was  no  ascites. 
The  liver,  weight  7  pounds  9  ounces,  was  slightly  irregular  on  the  surface  and  on 
section  showed  fine  cirrhosis;  it  was  deeply  bile-stained.  The  bile-ducts  were  per- 
\'ious  and  the  gall-bladder  contained  dark  bile  but  no  calculi.  Portal  vein  healthy. 
Microscopically,  cirrhosis  was  comparatively  slight;  liver  cells  very  fatty,  no  signs 
of  acute  atrophy,  numerous  so-called  new  bile-ducts.     Ciirhosis  ahnost  unilobular. 

As  in  most  chronic  diseases  death  may  be  due  to  some  acute  infection; 
thus,  pneumonia,  erysipelas,  or  peritonitis  may  carry  the  patient  off. 
Erysipelas  is  very  prone  to  attack  patients  with  chronic  jaundice,  and, 
from  their  want  of  resistance,  to  prove  fatal;  but  in  hypertrophic  biliary 
cirrhosis  erysipelas,  though  a  severe  complication,  is  not  necessarily  fatal. 
If  acute  infection  falls  on  the  liver  itself,  the  symptoms  of  icterus  gravis 
develop. 

DIAGNOSIS. 

Chronic  jaundice  without  complete  bihary  obstruction,  as  shown  by 
the  colour  of  the  faeces;  the  occurrence  of  periodic  exacerbations,  and 
considerable  enlargement  of  the  liver  and  spleen,  v^ithout  any  evidence 
of  cholelithiasis,  in  a  young  person,  are  the  essential  points  o.n  which 
to  base  a  diagnosis  of  hypertrophic  biliary  cirrhosis. 

Differential  Diagnosis. — ^In  cases  of  -portal  cirrhosis  with  big  livers 
and  intercurrent  jaundice  the  diagnosis  depends  on  the  jaundice  being 
transitory  and  not  permanent,  on  the  comparatively  slight  degree  of 
splenic  enlargement,  and  on  the  history  and  presence  of  signs  of  common 
cirrhosis.  It  cannot,  however,  be  maintained  that  the  tAvo  diseases 
(portal  and  biliary  cirrhosis)  are  always  distinct,  either  anatomically  or 
clinically.     Sometimes  they  are  combined,  and  not  infrequently  the  two 

*  Ferrannini:  Centralblatt  f.  inn.  Med.,  March  14,  190-3. 


BILIARY   CIRRHOSIS.  323 

diseases  overlap  in  the  same  way  as  the  parenchymatous  and  interstitial 
forms  of  nephritis. 

The  follo'uing  case  presented  features  of  both  diseases,  but  it  might 
also  be  interpreted  as  a  case  of  portal  cirrhosis  vnth  acute  and  recent 
inflammation  of  the  intra-hepatic  bile-ducts: 

A  man  aged  fortj'-seven  died  in  St.  George's  Hospital;  he  had  had  hsematemesis 
and  ascites  which  required  tapping;  for  the  last  three  weeks  of  his  hfe  he  was  de- 
lirious and  jaundiced.  His  hver  weighed  50  ounces  and  was  typically  hobnailed; 
microscopically  it  showed  multilobular  and  monolobular  cirrhosis,  a  large  number  of 
pseudobile  canaliculi,  and  microscopic  calculi  in  the  bile  capillaries.  The  spleen 
weighed  IS  ounces. 

In  licemochromatosis,  a  condition  in  which  there  is  widespread  ing- 
mentation  of  the  body  with  secondary  cirrhosis  of  the  liver  and  pancreas, 
the  liver  is  enlarged  and  some  of  the  symptoms  resemble  those  of  hyper- 
trophic biliary  cirrhosis.  The  skin,  however,  though  pigmented,  is  not 
jaundiced,  and  in  five-sixths  of  the  cases  there  is  glycosuria  (bronzed 
diabetes). 

In  cases  of  obstructive  jaundice  the  Kver  may  be  enlarged  and  swollen 
from  retained  bile;  but  this  condition  differs  from  hypertrophic  biliary 
cirrhosis  in  the  absence  of  bile  from  the  faeces,  in  the  fact  that  there  is 
no  splenic  enlargement,  while  in  many  cases  the  presence  of  an  enlarged 
gall-bladder  can  be  made  out  when  the  common  bile-duct  is  obstructed. 

Chronic  jaunidce  due  to  a  calculus  in  the  common  duct  may  imitate 
hj'pertrophic  bihary  cirrhosis  in  the  periodic  attacks  of  intermittent 
hepatic  fever,  and  in  the  fact  that  the  stools  are  not  necessarily  devoid 
of  bile.  Calcuh  usually  occur  later  in  life  than  bihary  cirrhosis,  the 
periodic  attacks  of  pain  are  more  severe  than  in  hj^ertrophic  biliarj^ 
cirrhosis,  and  the  spleen  is  either  not  enlarged  at  all  or  only  in  a  slight 
degree. 

In  some  cases  of  hydatid  cysts  in  the  liver  with  jaundice  the  resemblance 
to  bihary  cirrhosis  is  considerable.  In  ordinarj^  hydatid  disease  the 
spleen  is  not  enlarged,  the  periodic  attacks  of  fever  and  pain  are  absent, 
and  jaundice  when  present  is  either  due  to  rupture  of  a  cyst  into  the 
duct,  in  which  case  there  is  usually  continued  fever,  or  due  to  pressure 
on  the  larger  ducts  yviih  complete  exclusion  of  bile  from  the  intestines. 

In  prolonged  catarrhal  jaundice  the  spleen  is  either  not  enlarged  or 
very  slightly,  and  bile  is  absent  from  the  faeces.  In  cases  of  chronic 
infectious  jaundice  the  condition  is  indistinguishable  from  that  of  hyper- 
trophic biliary  cirrhosis,  except  when  recovery  occurs;  in  other  words, 
the  symptoms  of  the  two  diseases  are  practically  identical,  though  their 
results  and  course  are  different. 

In  WeiVs  disease  the  clinical  course  is  rapid  and  acute,  whereas  in 
hypertrophic  biliary  cirrhosis  it  is  a  matter  of  years,  not  of  days. 

Malaria,  which  has  in  the  past  been  erroneously  regarded  as  the 
cause  of  hypertrophic  biliary  cirrhosis,  can  be  eliminated  by  examination 
of  the  blood  and  by  the  failure  of  quinine  to  affect  the  course  of  the 
disease. 

Some  rather  exceptional  cases  of  syphilitic  disease  of  the  liver  with 


324  DISEASES   OF  THE   LIVER. 

chronic  jaundice  and  very  considerable  enlargement  of  the  liver  and 
spleen  may  imitate  hypertrophic  biliary  cirrhosis.  Syphilitic  lesions 
elsewhere,  albuminuria  as  pointing  to  lardaceous  disease  as  the  cause 
of  splenic  enlargement,  irregularity  of  the  surface  of  the  liver  from 
gummata,  the  presence  of  enlarged  veins  near  the  umbilicus,  and  the 
beneficial  effects  of  antisyphilitic  treatment  point  to  syphilis.  Another 
point,  which,  however,  is  of  rather  doubtful  value,  is  the  absence  of  leuco- 
cytosis  in  syphilis  and  its  presence  in  hypertrophic  biliary  cirrhosis. 

In  the  following  case  the  presence  of  gummata  on  the  limbs  pointed 
to  syphilis,  but  in  other  respects  the  features  closely  resembled  those  of 
Gilbert  and  Fournier's  splenomegalic  type  of  hy]3ertrophic  biliary 
cirrhosis : 

A  boy  aged  seventeen  years  was  frequently  under  the  care  of  my  colleague. 
Dr.  Ewart,  with  chronic  jaundice,  no  ascites,  great  enlargement  of  the  liver  and 
spleen,  both  of  which  were  smooth,  clubbing  of  the  fingers,  and  gummata  on  the 
limbs  and  head.*  He  died  of  erysipelas:  the  liver,  which  weighed  5  pounds,  was 
jaundiced  and  consisted  almost  entirely  of  an  hypertrophied  left  lobe;  the  right 
lobe  showed  numerous  cicatrices  and  was  atrophied.  The  left  hepatic  duct  was 
obliterated  by  scar  tissue  while  bile  entered  the  gall-bladder  and  intestines  by  the 
right  hepatic  duct.  There  was  no  cirrhosis  of  the  left  lobe.  The  spleen  weighed 
2  pounds  13  ounces.  There  was  no  lardaceous  change  in  any  of  the  organs  of  the 
body. 

From  Banti's  Disease. — As  already  mentioned,  there  is  a  gradual 
transition  between  (a)  cases  of  so-called  metasplenomegalic  biliary 
cirrhosis,  in  which  the  splenic  enlargement  jDrecedes  any  manifest  change 
in  the  liver,  and  (6)  cases  of  chronic  splenic  anaemia  which  eventually 
develop  a  terminal  cirrhosis  of  the  liver  and  jaundice — so-called  Banti's 
disease.  To  distinguish  between  the  two  a  reliable  history  is  necessary. 
In  chronic  splenic  anaemia  there  is  marked  anaemia  of  the  chlorotic  type, 
an  absence  of  any  leucocytosis  or  even  a  diminution  in  their  number 
(leucopenia),  and  recurrent  gastro-intestinal  haemorrhages  before  the  de- 
velopment of  jaundice,  while  in  metasplenomegalic  biliary  cirrhosis  there 
would  be  practically  an  absence  of  symptoms  during  the  period  in  which 
splenic  enlargement  (splenomegaly)  was  the  only  physical  sign. 

DURATION. 

Though  the  disease  must  be  regarded  as  incurable,  it  is  essentially 
chronic,  and  jaundice  may  exist  for  ten  years  or  even  longer.  The 
average  duration  is  about  five  years.  In  a  few  instances  the  disease 
runs  an  acute  course,  and  then  proves  fatal  within  two  3'ears.     ■ 

PROGNOSIS. 

The  prognosis  is  bad,  since  the  disease  is  incurable.  But  it  is  often 
extremely  slow  in  its  progress  and  patients  may  retain  fair  strength  for 
years.  Careful  treatment  and  supervision  may  be  followed  b}-  improve- 
ment, and  the  outlook  depends  on  the  surroundings  of  the  patient.  An 
easy  life  in  a  healthy  locality  will  prolong  life,  while  o^'erwork,  exposure 

*  The  case  was  described  bv  W.  S.  Lazarus  Barlow:  Trans.  Path.  Soc,  vol.  1, 
p.  15.8. 


BILIARY    CIRRHOSIS.  325 

to  cold  and  wet,  and  unsanitary  conditions  vnll  surely  lead  to  deteriora- 
tion. 

The  patient's  general  nutrition  has,  of  course,  an  important  bearing 
on  the  prognosis.  Wasting  and  the  recurrence  of  exacerbations  and 
haemorrhages  at  more  frequent  inten^als  show  that  the  disease  is  ad- 
vancing towards  its  termination.  The  incidence  of  compHcations,  such 
as  pneumonia,  peritonitis,  or  erysipelas,  at  once  makes  the  outlook  very 
serious.  Erysipelas  may  be  recovered  from  in  cases  where  the  urinary- 
secretion  is  well  maintained.  Clubbing  of  the  fingers,  though  a  rare 
condition,  is  only  met. with  in  long-standing  cases,  and  is  an  indication 
that  the  course  of  the  disease  has  been  slow. 

TREATMENT. 

The  general  lines  of  treatment  are  the  same  as  those  in  portal  cirrhosis. 
In  certain  points  there  are  differences:  thus,  a  more  generous  diet  may 
be  allowed  in  this  diseasQ  than  in  portal  cirrhosis,  while  itching  of  the 
skin  due  to  jaundice  is  more,  and  ascites  and  hsematemesis  less,  hkely  to 
require  treatment  than  in  ordinary  cirrhosis.  In  the  early  stages  an 
attempt  may  be  made  to  put  the  patient  in  more  healthy  surroundings 
and  to  remove  him  from  the  conditions,  among  which  the  water-supply 
may  plaj^  a  part,  that  favoured  the  onset  of  the  disease.  Fresh  air  is 
important,  but  exposure  to  chills,  and  especially  to  cold  and  damp 
weather,  should  be  avoided  and  the  patient  should  be  warmly  clad.  A 
course  at  Homburg,  Ems,  Neuenahr,  Kissingen,  Vichy,  Vals,  Harro- 
gate, may  be  tried.  If  the  patient  goes  to  Carlsbad,  the  course  must  be 
comparatively  mild. 

Diet. — It  is  important  that  the  diet  should  be  simple  and  nourishing. 
Irritating  and  unduly  stimulating  articles  of  food  should  be  carefully 
excluded.  Milk  should  be  given  freely,  eggs,  bread  and  butter,  simple 
puddings,  fish,  and  occasionally  meat  may  all  be  taken.  Alcohol  must 
be  avoided;  and  if  taken  at  all,  must  be  in  small  quantities  and  weU 
diluted.  Water  should  be  taken  freely,  but  it  will  be  advisable  to  have 
it  boiled  when  the  patient  is  still  living  in  the  house  where  the  disease 
developed. 

Intestinal  fermentation  and  putrefaction  should  be  prevented  by 
careful  dieting,  correction  of  constipation,  and  by  minute  doses  of  calo- 
mel (to~21t  of  a  grain)  three  times  a  day;  rather  larger  doses  (|-^  grain) 
may  be  employed  in  single  doses  to  combine  its  antiseptic  and  purgative 
properties.  Calomel  is  preferable  to  salol,  /9-naphthol,  betol,  and  the 
synthetic  intestinal  antiseptics.  Saline  purgatives,  such  as  sulphate  of 
magnesium  and  sulphate  of  soda  in  combination,  are  also  useful  in  pre- 
venting intestinal  fermentation,  while  mineral  waters  may  be  employed 
with  the  same  object.  It  has  been  suggested  by  Parkes  Weber  *  that 
an  attempt  should  be  made  to  treat  the  catarrhal  condition  of  the  small 
bile-ducts  by  drugs  which,  when  excreted  into  the  intra-hepatic  ducts, 
should  disinfect  the  ducts  in  the  same  way  that  urotropin  and  salol 

*  Weber,  F.  Parkes:  Edinburgh  Med.  Joum.,  new  series,  vol.  xiv,  p.  14,  Aug., 
1903. 


326  DISEASES    OF   THE    LIVER. 

disinfect  the  urinary  tract.  Possibly  salicylates  or  some  similar  drug 
may  do  good  in  this  way. 

Itching  of  the  skin  may  be  treated  externally  by  warm  baths  or 
fomentations  wdth  carbolic  acid  lotions;  while  internally  chloride  of 
calcium  in  20-gr.  doses  or  antipyrin,  grs.  v-x,  may  be  employed.  Small 
hypodermic  injections  of  pilocarpine  have  also  been  recommended. 

Surgical  Treatment. — ^Terrier  *  and  Delageniere  j  have  drained  the 
gall-bladder  in  a  number  of  cases  and  with  very  good  results.  Thus,  in 
13  cases  tabulated  by  Maurice  Guillot  J  10  were  cured;  Greenough  § 
adds  4  cases,  making  up  a  total  of  17  cases,  of  which  13  were  relieved. 
It  is  not  certain  that  all  the  cases  were  of  the  same  type;  some  of  them 
may  possibly  have  been  examples  of  chronic  infective  cholecystitis  and 
cholangitis  and  not  genuine  cases  of  biliary  cirrhosis  {tide  Michaux  |1), 
but  it  appears  that  many  of  them  were  examples  of  hypertrophic  biliary 
cirrhosis.  The  drainage  of  the  gaU-bladder  was  continued  for  periods 
varying  from  ten  days  to  three  months,  and  in  some  instances  the  bile, 
which  was  at  first  infected,  became  aseptic. 


OBSTRUCTIVE   BILIARY   CIRRHOSIS. 

By  obstructive  biliary  cirrhosis  is  meant  a  fibrosis  spreading  from  the 
bile-ducts  around  the  lobules  of  the  liver  and  clue  to  obstruction  of  the 
large  bile-ducts. 

History. — -The  conception  of  cirrhosis  due  to  biliary  obstruction  was 
first  prominently  brought  forward  by  Charcot  and  Gombault  **  in  1876, 
though  two  years  previously  Wickham  Legg  tt  in  England  had  de- 
scribed a  clinical  case  with  full  pathological  details.  In  1882  Mangels- 
dorf  Jt  collected  184  cases,  and  in  1901  W.  W.  Ford  §§  and  in  1903 
Weber  ||  ||  argued  in  favour  of  the  truth  of  this  sequence  of  pathological 
events. 

EXPERIMENTAL  LIGATURE  OF  THE  BILE-DUCTS. 

As  bearing  on  the  production  of  obstructive  biliary  cirrhosis,  numerous 
experiments  have  been  performed  in  which  the  bile-ducts  have  been 
ligatured  and  the  liver  subsequently  examined  for  any  fibrosis.  The 
conclusions  arrived  at,  as  will  be  seen,  are  by  no  means  uniform. 

Meyer  ***  in  1872  ligatured  the  common  bile-duct  of  cats  and  produced  dilata- 
tion  of  the  bile-ducts   with   intralobular  and  extralobular  fibrosis.     Charcot  and 

*  Terrier:  Rev.  de  chirurg.,  tome  xii,  p.  553,  1S92. 
t  Delageniere:  Archiv  provinc  de  Chirurg.,  1897. 

I  Guillot,  M.:  Gaz.  hebdom.  de  Med.  et  de  chirurg.,  Jan.  16,  1902,  p.  69. 

§  Greenough:  American  Journ.  of  Med.  Sciences,  vol.  cxxiv,  p.  979,  Dec, 
1902. 

II  Michaux:  Rev.  de  chirurg.,  tome  xxiii,  p.  126. 

**  Charcot  and  Gombault:  Archiv  de  Phvsiol.  norm.  et.  path.,  1876,  2d  series, 
t.  iii,  p.  272. 

ft  Wickham  Legg:  f3t.  Bartholomew's  Hosp.  Reports,  1873. 
it  Mangelsdorf:  Deutsch.  Archiv  f.  klin.  Med.,  Bd.  xxxi,  S.  522,  1882. 
§§  Ford,  W.  W. :  American  Journ.  Med.  Sciences,  vol.  cxxi,  p.  60. 
nil  Weber,  F.  P.:  Trans.  Path.  Soc,  vol.  liv,  p.  103.  1903. 
***  Meyer:  Med.  Jahrb.,  Vienna,  1872. 


BILIARY    CIRRHOSIS.  327 

Gombault's  *  (1S76)  results  are  well  known  and,  like  the  earlier  experiments  of 
Wickham  Legg  f  (1S7S),  showed  that  ligature  of  the  duct  led  to  dilatation  of  the 
intra-hepatic  ducts  with  fibrosis  which  surrounded  the  individual  hepatic  lobules 
(insular  cirrhosis)  and  spread  into  their  substance  (intralobular  cirrhosis).  The 
lobules  tended  to  undergo  atrophy,  Avhile  numerous  newly  formed  bile-ducts  in  the 
perilobular  tissue  passed  by  a  gradual  transition  into  the  liver  cells  at  the  margin  of 
the  lobule.  Somewhat  similar  results  were  obtained  by  Chambard,  and  by  Foa  and 
Salvioli.  Charcot  and  GomI:)ault  referred  these  changes  to  the  irritating  properties 
of  the  retained  bile,  and,  indeed,  incidentally  mention  that  the  bile  contained 
"vibrios."  Maffucci  J  also  induced  cirrhosis  as  the  result  of  hgature  of  the  bile- 
duct. 

These  results  were  obtained  before  the  days  of  antiseptics,  and  it  has  often  been 
urged  that  the  cirrhosis  was  due,  not  to  mechanical  pressure  and  irritation  exerted 
by  the  retained  bile,  but  to  accidental  infection.  Thus  Steinhaus  §  found  that 
after  ligature  of  the  bile-ducts  in  guinea-pigs,  who  were  killed  at  periods  varying 
from  six  hours  to  ten  days,  no  interstitial  hepatitis  was  produced  unless  septic  in- 
fection occurred.  The  interval  of  ten  days  is  very  short,  but  as  most  of  the  animals 
died  within  a  fortnight  after  ligature  of  the  common  duct,  this  was  unavoidable. 
In  order  to  keep  animals  alive  longer  Josselin  de  Jong  ||  Ugatured  individual  branches 
of  the  hepatic  duct  instead  of  the  common  bile-duct  and  obtained  much  the  same 
results  as  Steinhaus.  Similar  experiments  in  the  hands  of  Nasse,**  and  of  Vaughan 
Harley  and  Barratt.ft  showed  that  intralobular  fibrosis  resulted.  The  latter  ob- 
servers ligatured  the  left  hepatic  duct  in  cats  and  kept  them  aUve  for  four  to  sixteen 
months,  and  in  dogs  without  any  jaundice  resulting;  microscopic  sections  of  the  left 
and  of  the  healthy  right  lobe  could  then  be  compared.  The  changes  observed  were  not 
absolutely  constant,  but  in  many  instances  well-marked  interlobular  fibrosis,  hyper- 
plasia of  the  interlobular  bile-ducts,  and  atrophy  of  the  hepatic  lobules,  beginning 
at  the  periphery,  were  present  in  the  area  of  the  liver  corresponding  to  the  ligatured 
bile-duct.  It  is  interesting  to  note  that  Hanot  and  Gastou  tj  in  1893  explained 
the  appearance  of  so-called  new  bile-ducts  after  aseptic  ligature  of  the  bile-duct 
as  an  irritative  lesion  of  the  liver  cells  in  response  to  poisonous  bodies  absorbed  from 
the  bowel,  where  excessive  fermentation  depending  on  the  absence  of  bile  had  taken 
place. 

Ligature  of  the  common  duct  in  frogs,  guinea-pigs,  and  rabbits  (Lahousse  §§) 
under  antiseptic  precautions  gave  rise  to  some  fibrosis ;  other  observers  (Beloussow ,  ||  || 
Gerhardt  ***)  have  obtained  similar  results.  There  is  thus  very  considerable  differ- 
ence of  opinion  as  to  whether  fibrosis  is  produced  or  not.  In  some  cases  where  the 
ligature  is  applied  to  the  duct  near  the  duodenum  the  part  of  the  duct  above  the 
ligature  may  contain  micro-organisms,  so  that  although  the  ligature  itself  is 
aseptic,  the  conditions  are  complicated.  Lamacq  ttt  points  out  that  in  dogs  the 
liver  may  normally  show  infective  nodules.  Ris  results  show  that  when  sepsis  is 
avoided  ligature  leads  to  necrosis  of  the  liver  cells  in  rabbits  when  the  bile  pressure 
is  relatively  high,  but  that  in  dogs  necrosis  is  rare  and  when  present  not  marked. 
No  leucocytic  infiltration  or  fibrosis  occurred  around  the  areas  of  necrosis  and  no 
proliferation  of  bile-ducts.  The  same  results  were  obtained  by  Ribadeau-Dumas 
and  Lucene  JJI  in  guinea-pigs. 

To  sum  up  the  effects  of  ligature  of  the  bile-ducts:  fibrosis  may  be 
abi?ent,  it  may  be  present  and  be  due  to  infection,  or  may,  even  where 

*  Charcot  and  Gombault:  Archiv  de  Physiol,  norm,  et  path.,  2d  series,  t.  iii, 
p.  272, 1876. 

t  Legg,  W.:  St.  Bart.'s  Hosp.  Reports,  vol.  ix,  p.  161,  1873. 
X  Maffucci:  Giornal.  Internaz.  della  Scien.  Med..  1SS2,  p.  889. 
§  Steinhaus:  Archiv  f.  exper.  Path.  u.  Pharm.,  Hd.  xxviii,  S.  432,  1891. 
II  JosseUn  de  Jong:    Inaug.  Diss.,  Leyden,  189-4.      Quoted  by  Harley  and 
Barratt. 

**  Nasse:  La  Semaine  Medicale,  1894,  p.  202. 

ft  V.  Harley  and  Barratt:  Brit.  Med.  Journ.,  1898,  vol.  ii,  p.  14,  1743.     Journ. 
Path,  and  Bact.,Vol.  vii,  p.  203,  1901. 

tt  Hanot  et  Gastou:  Soc.  de  biolog.,  July  15,  1893,  p.  741. 
§§  Lahou.sse:  Archiv  de  biolog.,  vii,  p.  187. 
II  jl  Beloussow:  Archiv  f.  experiment.  Path.  u.  Pharmak.,  1881. 
***  Gerhardt:  Archiv  f.  experiment.  Path.  U.  Pharmak.,  1892. 
ttt  Lamacq:  Archiv  de  Med.  experiment,  et  d'anat.  path.,  Nov.,  1897. 
Jtt  Archiv  de  Med.  experiment,  et  d'anat.  path.,  tome  xvi,  p.  191,  1904. 


328 


DISEASES    OF   THE    LIVEE. 


infection  is  absent,  be  found  in  varying  degrees.  This  fibrosis  following 
aseptic  ligature  ma}"  be  explained  in  several  ways:  it  may  be  regarded 
merely  as  a  fibrosis  replacement,  perhaps  more  apparent  than  real.  In 
cases  such  as  Nasse's  and  Harley's  and  Barratt's,  where  one  hepatic  duct 
is  Hgatured  and  where  the  fibrosis  is  limited  to  the  correspondiijg  part 

of  the  liver,  this  may  be 
the  explanation.  Harley 
and  Barratt,  however, 
referred  the  fibrosis  to 
the  continued  slight  irri- 
tation of  the  bile.  In 
other  instances  the  cirr- 
hosis may  be  due  to  toxic 
influences  which  are 
brought  into  existence 
by  failure  of  the  lireT 
properly  to  jDerform  its 
antitoxic  function  of 
stopping  and  destrojdng 
poisons  brought  to  it  by 
the  blood,  especially  that 
of  the  portal  vein;  in 
such  an  event  the  poisons 
would  reach  the  liver  a 
second  time  by  the  he- 
patic artery.  Or,  again, 
in  cases  where  the  com- 
mon bile-duct  is  tied  the 
cirrhosis  may  be  due  to 
poisons  absorbed  from  the  alimentary  canal,  where,  as  the  result  of 
interference  with  the  flow  of  bile,  fermentation  and  putrefaction  have 
been  excessive.  Lastly,  the  fibrosis  may  be  entirely  independent  of 
ligature  of  the  bile-ducts  and  due  to  extrinsic  causes  developing  after 
the  duct  has  been  ligatured. 


Pig.  39. — Focal  Necrosis  due  to  Biliary  Obstructiox. 

From  a  Guixea-pig  whose  Bile-duct  was  Compressed 

BY  A  Cyst 

The  pale  areas  show  complete  necrosis  of  the  liver  cells ; 
there  is  some  small-cell  infiltration  around  the  portal  space. 
The  bile-ducts  contained  inspissated  bile.  (From  a  speci- 
men kindly  lent  by  Dr.  J.  H.  Drysdale.) 


INCIDENCE. 

The  statistics  of  Mangelsdorf  *  showed  that  up  to  1882  the  published 
cases  of  cirrhosis  which  could  be  ascribed  to  biliary  obstruction  numbered 
184;  between  1882  and  1900  W.  W.  Ford  f  collected  21  more  and  added 
3  fresh  examples.  From  his  21  cases  collected  from  literature  10  may 
be  deducted,  since  9  belong  to  the  group  of  congenital  obliteration  of  the 
ducts  and  one  was  an  example  of  congenital  cystic  disease  of  the  liver. 
Cases  of  cirrhosis  due  to  bihary  obstruction  are  therefore  not  often  de- 
scribed.   The  general  opinion  as  voiced  by  Osler,±  Sharkey,?  and  Hale 

*  Mangelsdorf:  Deut.  AichW  f.  klin.  Med.,  Bd.  xxxi,  S.  522. 
t  Ford,  W.  "VY. :  American  Journ.  Med.  Sciences,  vol.  cxxi,  p.  60. 
j  Osier,  W.:  Practice  of  Medicine,  p.  570,  ed.  iv. 
§  Sharkey:  St.  Thomas'  Hospital  Reports,  vol.  xviii,  p.  245. 


BILIARY    CIRRHOSIS.  329 

White  *  is  that  mechanical  bihary  obstruction  seldom  or  never  causes 
genuine  cirrhosis,  and  that  although  fibrosis  may  be  detected  on  micro- 
scopic examination,  it  is  not  of  any  clinical  or  practical  significance. 

EFFECTS  OF  BILIARY  OBSTRUCTION  ON   THE  HUMAN  LIVER. 

The  facts  observed  in  the  human  subject,  like  those  obtained  by 
experimental  work  on  animals,  are  not  uniform,  but  there  is  very  httle 
evidence  to  support  the  view  that  biliary  obstruction  'per  se  causes  cirrho- 
sis. When  the  common  bile-duct  is  completely  occluded  from  without, 
for  example,  by  malignant  disease  of  the  head  of  the  pancreas,  there  is 
dilatation  of  the  ducts,  but  as  a  rule  little  or  no  fibrosis,  while  the  liver 
cells  are  degenerated,  atrophied,  and  occupied  by  bile  pigment.  The 
liver  substance  is  atrophied  and  the  organ  is  in  a  condition  comparable 
to  that  of  hydronephrosis.  It  is  somewhat  remarkable  that  manifest 
microbic  infection  does  not  more  often  occur,  since  the  biliary  stagnation 
must  dispose  to  infection  by  micro-organisms  reaching  the  liver  by  the 
blood-stream. 

Malignant  disease  of  the  pancreas  with  complete  biliary  obstruction 
is  not  a  rare  disease,  but  it  is  remarkable  how  it  is  hardly  ever  associated 
with  cirrhosis  of  the  liver.  If  biliary  obstruction  per  se  produced  fibrosis 
of  the  liver,  the  association  should  be  often  seen.  The  cases  are  so  few 
that  it  seems  possible  that  when  hepatic  cirrhosis  and  malignant  disease 
of  the  pancreas  are  found  in  the  same  person,  the  cirrhosis  was  the  older 
lesion  and  was  latent,  and  that  the  growth  in  the  pancreas  developed 
subsequently. 

Maffucci  t  and  Legrand  X  have  recorded  cases  where  these  two  conditions  were 
associated. 

In  addition  to  the  possibility  that  bacterial  infection  of  the  dilated 
bile-ducts,  when  obstructed  by  the  pressure  of  a  tumor  from  without, 
may  occur  from  the  blood-stream,  it  must  be  remembered  that  complete 
obstruction  prevents  bile  entering  the  duodenum.  In  the  absence  of 
bile  from  the  intestine  putrefactive  and  fermentative  processes  in  the 
bowel  would  tend  to  become  excessive  and  might  lead  to  the  produc- 
tion of  poisons,  which,  when  carried  to  the  liver,  might  be  expected  to 
set  up  the  ordinary  portal  or  multilobular  cirrhosis.  This  change  would, 
indeed,  in  all  probability  more  often  be  met  with,  were,  it  not  that 
the  liver,  being  flooded  with  bile,  which  has  acquired  toxic  properties, 
as  shown  by  the  focal  necroses  of  the  liver  cells,  is  incapable  of  any 
reaction. 

The  cirrhosis  of  the  liver  found  in  association  with  congenital  obliteration  of  the 
bile-ducts  has  been  regarded  by  Ford  as  secondary  to  the  biliary  obstruction  and 
as  a  good  example  of  obstructive  biliary  cirrhosis.  It  is,  however,  quite  as  reasona- 
ble to  believe  that  the  process  starts  in  the  smaller  ducts,  where  it  sets  up  peri- 
cholangitic  fibrosis  and  then  spreads  to  the  larger  ducts  and  gall-bladder,  where  it 
sets  up  obliterative  cholangitis  and  cholecystitis. 

*Hale  White:  Guy's  Hospital  Gaz.,  May  28,  1898.  Brit.  Med.  Journ.,  1903, 
vol.  i,  p.  534. 

t  Maffucci:  Quoted  by  Ford,  American  Journ.  Med.  Sciences,  Jan.,  1901. 
t  Legrand:  Rev.  de  M<5d.,  1SS9.  p.  165. 


330  DISEASES    OF   THE    LIVER. 

On  the  other  hand,  when  a  gall-stone  is  lodged  in  the  common  bile- 
duct,  the  results  are  not  so  constant ;  sometimes  the  changes  are  the  same 
as  in  aseptic  closure  of  the  common  duct,  but  in  other  instances  there 
are  cholangitis  and  pericholangitis,  which,  if  the  process  is  chronic,  result 
in  fibrosis  around  the  ducts.  Litten  thought  that  rough  and  angular 
calculi  were  much  more  likely  than  smooth  round  stones  to  set  up  cholan- 
gitis and  fibrosis.  In  long-standing  cases  the  liver  cells  undergo  wide- 
spread degeneration  and  atrophy  and  the  amount  of  fibrosis  may  be  very 
considerable. 

Mangelsdorf  tabulated  54  cases  of  hepatic  cirrhosis  associated  with  gall-stones,  in 
16  of  which  calculi  WQre  found  in  the  ducts.  Parkes  Weber  *  has  recently  collected 
12  cases  of  biliary  cirrhosis  from  obstruction  of  the  larger  ducts  by  gaU-stones. 

Hypertrophic  biliary  cirrhosis  has  sometimes  been  found  in  association 
with  gaU-stones,  but  it  is  quite  reasonable  to  think  that  the  gall-stones 
are  secondary  to  cholangitis  and  not  the  primary  morbid  factor.f  The 
association  of  impacted  gall-stones  and  hypertrophic  biliary  cirrhosis 
must  be  extremely  rare,  since  Naunyn  J  has  not  met  with  it.  There 
seems  to  be  very  little  doubt  that  the  factor  which  determines  fibrosis 
around  the  intra-hepatic  ducts  in  gall-stone  obstruction  is  bacterial 
infection.  As  the  result  of  biliary  stasis,  icteric  necrosis  of  the  liver  cells 
occurs  and  fibrosis  of  a  diffuse  character  may  thus  be  favoured. 

MORBID  ANATOMY. 

The  liver  in  mechanical  obstruction  of  the  bile-ducts,  though  en- 
larged in  the  early  stages,  is  small  when  seen  at  the  autopsy,  unless 
occupied  by  secondary  growths  or  by  a  hydatid  cyst.  The  surface  is 
irregular,  shows  dilated  and  varicose  bile-ducts  filled  with  mucus,  and 
is  of  a  dark  green  colour.  Occasionally  there  are  perihepatitic  adhesions. 
On  section  of  the  organ  the  dilated  ducts  are  prominent  objects  and  give 
the  liver  a  sponge-like,  honeycombed  appearance,  the  substance  of  which 
is  usually  somewhat  flabby  from  atrophy  of  the  secreting  cells,  and  cuts 
very  differently  from  an  ordinary  cirrhotic  liver.  There  is  atrophy  and 
condensation  of  the  liver  parenchyma  around  the  dilated  bile-ducts,  and 
a  certain  amount  of  pericholangitic  fibrosis.  In  cases  where  acute  in- 
fection has  been  superadded  there  may  be  suppuration  in  or  around  the 
bile-ducts,  and  the  formation  of  minute  abscesses.  The  naked-eye 
appearances  are  therefore  very  different  from  those  of  hypertrophic  biliary 
cirrhosis.. 

Further,  the  histological  changes  are  not  the  same  as  those  of  hyper- 
trophic biliary  cirrhosis.  In  calculous  obstruction  the  ducts  are  dilated 
and  tend  to  become  progressively  more  so  in  proportion  to  the  duration  of 
the  obstruction,  while  in  hyj^ertrophic  cirrhosis  this  does  not  occur.  In 
biliary  obstruction  the  larger  ducts  are  chiefl}^  affected  and  may  show 
cholangitis  and  pericholangitis,  while  in  h}T[3ertrophic  biliary  cirrhosis  the 

*  Weber,  F.  P.:  Trans.  Path.  Soc,  vol.  liv,  p.  105. 

t Compare  Sharkey:  St.  Thomas  Hospital  Reports,  vol.  xviii,  p.  245. 

t  Naunyn :  Cholelithiasis,  p.   163,  Transl.  New  Sydenham  Soc. 


BILIARY    CIRRHOSIS.  331 

smallest  intra-hepatic  ducts  are  inflamed.  Rapid  degeneration  of  the 
liver  cells  with  focal  necroses  are  marked  features  in  mechanical  obstruc- 
tion of  the  larger  ducts,  whereas  in  h}^oert,rophic  biliary  cirrhosis  the  hver 
cells  maintain  their  nutrition  for  long  periods.  The  small  bile-ducts  are 
not  prominent;  in  one  case  Weber  *  found  their  nmnber  diminished. 

The  columns  of  small  cubical  liver  cells,  known  as  ''pseudobile  canal- 
icuh,"  are  described  in  man}'  cases,  but  are  certainly  not  always  present. 
Ford  has  laid  stress  on  a  wreathe-hke  arrangement  of  these  pseudobile 
canaliculi.  \^Tien  fibrosis  occurs  it  spreads  out  from  the  larger  bile-ducts 
and  may  give  rise  to  multilobular  cirrhosis  or  to  a  more  diffuse  form 
of  cirrhosis  which  not  only  tends  to  surround  the  individual  lobules,  but 
invades  their  substances  and  passes  between  the  hepatic  cells.  From 
his  study  of  184  cases  of  cirrhosis,  thought  to  be  due  to  biliary  obstruction, 
Mangelsdorf  came  to  the  conclusion  that  no  particular  form  of  cirrhosis 
could  be  said  to  depend  on  biliary  obstruction. 

The  spleen  is  sometimes  small  or  of  normal  size,  but  in  cases  where 
considerable  fibrosis  of  the  liver  coexists  with  obstruction  of  the  larger 
ducts,  as  in  Weber's  f  cases,  there  may  be  very  considerable  enlargement, 
though  not  to  the  same  degree  as  in  hypertrophic  biliary  cirrhosis. 

The  pancreas  in  cases  where  a  calculus  occupies  the  lower  end  of 
the  bile-duct  or  the  ampulla  of  Vater  may,  from  obstruction  combined 
with  infection  of  its  duct,  show  dilatation  of  the  duct  and  fibrosis  with 
atrophy  of  the  ordinary  secreting  tissues  of  the  organ.  This  chronic 
interstitial  pancreatitis  is  perilobular  and  of  a  somewhat  coarse  form; 
only  in  very  late  stages  does  it  become  interacinous  and  lead  to  changes 
in  the  islands  of  Langerhans.  As  a  rule,  therefore,  the  islands  of  Langer- 
hans,  which  provide  the  internal  secretion  of  the  pancreas,  being  pre- 
serv'ed,  diabetes  mellitus  is  not  produced. 

CLINICAL    FEATURES. 

When  cirrhosis  of  the  liver,  whether  it  be  pericholangitic  or  portal, 
occurs  in  a  patient  with  biliary  obstruction,  it  does  not,  as  a  rule,  reveal 
itself  by  any  special  signs  or  symptoms,  the  features  being  those  of 
biliary  obstruction.  (Vide  p.  532.)  Complete  aseptic  obstruction  of  the 
common  bile-duct  leads  to  dilatation  of  the  intra-hepatic  ducts  and  to 
focal  necrosis  of  the  liver  cells.  The  functional  activity  of  the  liver  is 
thus  very  gravel}^  interfered  with,  and  as  a  result  of  this  hepatic  inade- 
ciuacy,  cholsemia  or  biliary  toxsemia  results,  a  condition  which  is  much 
more  rapidly  fatal  than  cirrhosis.  The  symptoms  are  those  of  complete 
obstructive  jaundice  and  cholsemia;  the  gall-bladder  is  usually  dilated; 
this  and  the  history  should  distinguish  it  from  impacted  gall-stone. 

Cases  of  long-standing  gall-stone  obstruction  of  the  common  bile-duct 
associated  with  ordinary  portal  cirrhosis  undoubted!}^  occur.  As  a  rule, 
symptoms  of  portal  cirrhosis  are  absent  or  cast  into  the  shade  by  those 
of  biliary  obstruction.  But  in  some  instances  the  manifestations  of  cirr- 
hosis, such  as  ascites  and  dilated  veins  over  the  abdomen,  are  present. 

*  Weber:  Ti-ans.  Path.  Soc,  vol.  liv,  p.  1 10. 

t  Weber,  F.  P.:  Trans.  Path.  Soc,  vol.  liv,  p.  118. 


332  DISEASES    OF   THE    LIVER. 

In  some  instances  the  clinical  features  of  ordinary  portal  cirrhosis  may 
develop  after  obstruction  due  to  gall-stones  or  other  causes  has  been 
estabUshed;  the  cirrhosis  is  then  reasonably  explained  as  the  result  of 
poisons  manufactured  in  the  intestines  and  carried  to  the  Uver  by  the 
portal  vein. 

Ford  has  collected  10  cases  in  which  ascites  and  other  sj^mptoms  of  portal 
cirrhosis  were  associated  -n-ith  obstruction  of  the  common  bile-duct.  In  six  of  these 
the  obstruction  was  by  gall-stones,  and  in  four  by  tumors,  glands,  or  a  cicatrix  press- 
ing on  the  duct  from  without. 

Finalh",  biliar\'  obstruction  does  not  give  rise  to  any  fixed  t^'pe, 
either  pathological  or  clinical,  of  cirrhosis. 

In  instances  where  a  gall-stone  becomes  lodged  in  the  conmion  bile- 
duct  Tvithout  any  liistor}^  of  colic  being  obtained  the  question  of  diag- 
nosis may  be  one  of  considerable  difficulty.  As  time  progresses  bile 
may  escape  by  the  side  of  the  stone  into  the  duodenum  and  the  fseces 
are  no  longer  pale;  they  then  contain  bile;  just  as  they  do  in  hyper- 
trophic biliary  cirrhosis.  In  differentiating  these  two  conditions,  the 
size  of  the  spleen  is  unportant;  it  is  much  enlarged  in  M'pertrophic 
bihary  cirrhosis,  while  in  gall-stone  obstruction  the  sjDleen,  if  at  aU 
increased  in  size,  is  relatively  insignificant.  In  hypertrophic  bihary 
cirrhosis  the  Uver  is  greatly  increased  in  size;  in  bihaiy  obstruction  it 
may  be  swollen  from  retention  of  bile,  but  in  the  late  stages  it  becomes 
smaller. 

TREATMENT. 

The  treatment  is  that  of  obstructive  jaundice  by  operative  measures 
and  by  symptomatic  remedies.  (Vide  p.  555.)  In  the  rare  cases  where 
there  are  ascites  and  symptoms  pointing  to  ordinary  cirrhosis  the  treat- 
ment should  be  on  the  lines  of  that  disease. 


HEPATIC   CIRRHOSIS   IN   CHILDREN. 

Cirrhosis  is  far  from  conunon  in  children,  though  probably  not  C|uite 
so  rare  as  might  be  concluded  from  the  late  Dr.  C.  West's  *  experience 
of  only  4  examples  of  cirrhosis  in  70,000  cases  of  children's  diseases.  In 
1889  Hatfield  t  "^'as  able  to  refer  to  156  cases  of  cirrhosis  in  children. 
Since  then  a  very  considerable  number  are  to  be  found,  scattered  about 
in  medical  Hterature,  as  shoTMi  by  the  fact  that  in  1899  ]\Iusser  %  col- 
lected 529  additional  cases.  Children  are  affected  by  the  forms  of 
cirrhosis  seen  in  adults,  and  in  the  main  react  in  very  much  the  same 
manner.  In  the  following  summary  dealing  with  cirrhosis  in  children 
reference  will  only  be  made  to  points  deserving  special  attention. 

The  various  forms  of  cirrhosis  of  the  liver  that  occur  in  children 
have  a  distinct  tendency  to  attack  more  than  one  member  of  the  family; 
this  depends  on  hereditary  influences,  of  which  syphilis  is  preeminent, 
and  on  the  fact  that  exposure  to  influences  favouring  cirrhosis,  such 
as  alcohol  and  improper  food,  etc.,  form  part  of  the  family  environment. 

*  West,  C:  Lectures  on  Diseases  of  Infancy  and  Childhood,  p.  654,  1884. 

t  Hatfield:  Cyclopsedia  of  Children's  Diseases,  vol.  iii,  p.  488. 

J  Musser,  J.  H.:  Supplement  to  Cyclop£Echa  of  Children's  Diseases,  1899,  p.  798. 


BILIARY    CIRRHOSIS.  333 

The  pericellular  cirrhosis  of  hereditary  syphilis  and  the  lesions  of 
tardive  hereditary  syphihs  wiU  be  fully  dealt  with  elsewhere  (p.  375), 
and  it  will  then  be  pointed  out  that  after  recovery  from  pericellular 
cirrhosis  the  liver  is  probably  left  with  its  resistance  so  diminished  that 
it  may  readily  become  affected  by  ordinary  portal  cirrhosis,  the  resulting 
change  being  neither  due  to  syphilis  nor  curable  by  anti-syphilitic  treat- 
ment, but  disposed  to  by  the  influence  of  former  syphilis,  and  therefore 
parasyphilitic  and  comparable  to  locomotor  ataxia  and  general  paralysis 
of  the  insane.  Some  cases  of  marked  portal  cirrhosis  in  early  life  may 
thus  be  distantly  related,  though  not  directly  due  to  syphilis. 

There  are  other  forms  of  intra-uterine  or  congenital  cirrhosis.  It 
occurs  in  a  marked  form  in  congenital  obliteration  of  the  bile-ducts,  and 
is  seen  in  cases  which  clinically  resemble  that  group,  but  anatomically 
do  not  present  obliteration  of  the  ducts.  It  is  reasonable  to  believe  that 
the  change  is  due  to  poisons  conveyed  from  the  mother  to  the  foetus. 
For  a  discussion  on  this  point  the  reader  is  referred  to  the  section  on 
Congenital  Obliteration  of  the  Bile-ducts. 

Vanverts  and  Ramond  *  record  an  interesting  case  of  congenital  ascites  and 
hepatic  cirrhosis  in  which  the  foetus'  abdomen  had  to  be  tapped  before  it  conld  be 
delivered.  The  liver  was  enlarged  and  cirrhotic.  There  was  no  evidence  of  syphilis, 
alcoholism,  or  tuberculosis  in  the  parents. 

Portal  Cirrhosis. — ^As  in  adults,  the  liver  may  be  larger  than  normal, 
or  may  be  small  and  markedly  hobnailed.  In  cases  where  nodular  hyper- 
plasia is  well  marked  the  liver  may  look  as  if  occupied  by  multiple  new- 
growth.  In  some  cases  the  cirrhosis  can  be  traced  to  precocious  alco- 
holism, or  to  some  specially  irritating  kind  of  food,  such  as  fish,  etc., 
soaked  in  vinegar.  It  is,  therefore,  not  surprising  that  occasional^  two 
or  more  children  in  the  same  family  suffer  from  portal  cirrhosis.  (Vide 
p.  181.)  In  many  cases  alcoholism  can  be  excluded  and  some  other  cause 
must  be  sought  for,  such  as  gastro-enteritis  or  the  specific  fevers.  Proba- 
bly some  of  the  cirrhotic  livers  of  early  life  are,  like  granular  kidneys  in 
childhood,  in  reality  parasyphilitic;  it  is  interesting  in  this  connexion 
to  note  that  cirrhosis  has  been  observed  in  juvenile  general  parah'sis  of 
the  insane  due  to  hereditary  syphilis. 

BIBLIOGRAPHY. 

Brown:  Archiv  of  Pediatrics,  1890,  p.  49. 

Dickinson,  W.  H.:  Illustrated  Medical  News,  April  20,  1889. 

Edwards:  Archiv  of  Pediatrics,  vol.  vii,  vol.  xii. 

Hall:  St.  Bartholomew's  Hospital  Reports,  vol.  xxviii,  p.  167. 

Henoch:  Diseases  of  (  hildren,  Transl.  New  Sydenham  Soc,  vol.  ii,  p.  113. 

Jollye:  Brit.  Med.  Journ.,  1S92,  vol.  i,  p.  858! 

Morse:  Boston  Medical  and  Surgical  Journ.,  vol.  cxlvii,  p.  299,  Sept.  11,  1902. 

Targett:  Trans.  Path.  Soc,  vol.  xl,  p.  136. 

Tidv;  Brit.  Med.  Journ.,  1892,  vol.  ii,  p.  125. 

Willis:  Trans.  Path.  Soc,  vol.  xiv,  p.  175. 

Clinical  Features  of  Portal  Cirrhosis  in  the  Young. — Hirmateme- 

sis  seems  loss  frcriueiil  llian  in  adiihs, possibly  Ix'cause  the  spleen  is  more 

*  Vanverts  and  Ramond:  Bull.  Soc.  Anat.  Paris,  1896,  p.  153. 


334  DISEASES    OF   THE    LIVER. 

distensible  and  therefore  accommodates  relatively  more  portal  blood 
than  in  the  adult.  Saunal,*  however,  records  a  case  of  fatal  haemorrhage 
from  an  oesophageal  varix  in  a  girl  aged  twelve  years.  Haemorrhages 
elsewhere,  from  the  nose  and  into  the  skin,  and  depending  on  severe 
toxaemia,  are  quite  as  frequent  proportionately  as  in  adults.  The  enlarge- 
ment of  the  liver  and  spleen  is  more  prominent  than  in  adults.  This 
may  in  part  depend  on  the  liver  being  relatively  larger  in  children  and 
on  greater  power  of  repair  and  hyperplasia  of  the  liver  in  early  life. 
The  spleen  is  more  readily  distended  in  early  life.  In  children  mixed 
cases  of  portal  and  biliary  cirrhosis  are  not  infrequent;  this,  again,  bears 
on  the  more  marked  enlargement  of  the  liver  and  spleen. 

A  raised  temperature  is  more  frequent  in  children  than  in  adults. 
The  fever  may  be  so  marked  as  to  suggest  typhoid  fever  or  generalised 
tuberculosis. 

Tn  a  case  of  Dr.  Wickham  Legg's  f  a  boy  aged  twelve  years  was  first  thought 
to  have  typhoid  fever  and  later  acute  tuberculosis.  Another  case  regarded  as 
typhoid  fever  occurred  at  St.  George's  Hospital.     {Vide  p.  219.) 

Ascites  is  not  uncommon,  and  is  very  likely  to  be  regarded  as  evidence 
of  tuberculous  peritonitis.  Pulmonary  tuberculosis  is  very  rarely  seen  as 
a  complication,  but  infection  of  the  peritoneum  may  occur.  In  some 
cases  a  terminal  suppurative  peritonitis  is  met  with.  A  curious  symptom 
sometimes  observed  is  ravenous  appetite.  Jaundice,  often  quite  slight, 
and  diarrhoea  are  more  often  found  in  association  with  cirrhosis  in  children 
than  in  adults. 

In  an  interesting  group  of  cases  described  by  Ormerod  t  and  Homen  § 
the  symptoms  are  entirely  nervous  and  cirrhosis  is  not  suspected  during 
Ijfe.  These  cases  show  loss  of  power,  muscular  contractures,  mental 
weakness  progressing  to  idiocy,  fever,  and  great  emaciation.  The  con- 
dition may  occur  in  several  members  of  the  same  family.  (Gowers,  |1  Ho- 
men.) Cirrhosis  of  the  liver  and  inflammatory  softening  in  the  len- 
ticular nuclei  are  found  after  death.  Hom6n  regarded  his  cases  as  due 
to  hereditary  syphilis,  and  it  is  quite  conceivable  that  they  were  examples 
of  juvenile  general  paralysis  of  the  insane  in  which  parasyphilitic  cir- 
rhosis of  the  liver  was  also  present. 

Hypertrophic  biliary  cirrhosis  is  relatively  a  commoner  form  of 
cirrhosis  in  children  than  in  adults;  it  presents  some  special  features 
which  Gilbert  and  Fournier  **  have  described  as  the  juvenile  type  of 
the  disease.  Development  is  arrested  and  the  condition  termed  '-'infan- 
tihsm"  results.  The  cases  may  run  an  extremely  protracted  course,  and 
the  type  of  the  disease  may  change,  and  eventually  present  the  features 
of  ordinary  or  portal  cirrhosis.  The  latter  morbid  condition  supervenes 
in  biliary  cirrhosis  just  in  the  same  way  that  interstitial  fibrosis  may 

*  Saunal:  These  Paris,  1892. 

t  Legg,  Wickham:  St.  Bartholomew's  Hospital  Reports.  a'oI.  xiii,  p.  14S,  1877. 
j  Ormerod,  J.  A.:  St.  Bartholomew's  Hospital  Reports,  vol.  xxvi,  p.  57,  1890. 
§  Homen:  Neurologisches  Centralblatt,  S.  514,  1890.     Quoted  by  Ormerod. 
II  Gowers:  Diseases  of  Nervous  System,  vol.  ii,  p.  656,  1886. 
**  Gilbert  and  Fournier:  Soc.  de  biolog.,  1895,  419. 


BILIARY    CIRRHOSIS.  335 

occur  in  protracted  cases  of  chronic  parenchymatous  nejjhritis  and  lead 
to  a  contracting  white  kidney  with  a  corresponding  change  in  the  clinical 
aspect  of  the  case.  For  the  account  of  the  disease  the  reader  is  referred 
to  page  306. 

Cirrhosis  in  Young  Children  in  India. — -A  peculiar  form  of  cirrhosis 
among  young  nati^•e  children  in  India,  attacking  cliiefly  Hindus,  has 
been  described  by  Gibbons,*  Ghose^f  and  others. J  It  occurs  especially 
around  Calcutta,  but  is  by  no  means  limited  to  that  part  of  India.  It 
is  common — Ghose  had  seen  as  many  as  400  cases  personally — and  ex- 
tremely fatal,  often  killing  off  one  child  after  another  in  the  same  family; 
about  95  per  cent,  of  those  attacked  die  from  the  disease  before  the  end 
of  the  second  year  of  life.  In  1891-93  there  were  1748  deaths  in  Calcutta; 
only  six  of  Ghose's  400  cases  recovered.  It  is  not  due  to  syphilis,  alcohol, 
or  malaria.  It  has  been  thought  to  depend  on  irritating  bodies  in  the 
food  (vide  Etiology,  p.  187) .  The  change  begins  as  a  pericellular  cirrhosis, 
and  then  becomes  interlobular;  the  amount  of  fibrous  tissue  may  be  very 
large,  there  is  great  destruction  of  the  liver  cells,  and  extensive  formation 
of  new  bile-ducts.  Kundrat  and  Paltauf  of  Vienna,  to  whom  Gibbons 
showed  his  specimens,  regarded  the  change  as  a  hitherto  undescribed 
form  of  biliary  cirrhosis.  The  spleen  is  usually  enlarged.  The  disease 
is  not  congenital,  but  generally  begins  about  seven  months  of  age  with 
fever  and  enlargement  of  the  liver  and  spleen.  There  is  constipation, 
nausea,  and  jaundice  which  eventually  becomes  intense.  A  terminal 
ascites  may  develop. 

In  rickets  the  liver  is  enlarged,  in  addition  to  being  somewhat  dis- 
placed downwards  by  deformity  of  the  chest.  As  the  result  of  absorj^tion 
of  toxic  products  from  the  alimentary  canal  there  is  some  fatty  change 
in  the  liver  cells  and  fibrous  hyperplasia  in  the  portal  spaces. §  Hogben  || 
seems  alone  in  describing  the  change  as  a  biliary  cirrhosis.  The  change 
seems  to  be  temporary  and  of  no  importance;  it  does  not  appear  to  be 
the  precursor  or  first  stage  of  cirrhosis.  The  changes  in  the  liver  sec- 
ondary to  morbus  cordis  and  spoken  of  as  cardiac  cirrhosis,  pericarditic 
hepatic  pseudo-cirrhosis,  and  cardiotuberculous  cirrhosis  (vide  p.  101) 
are  chiefly  met  with  in  children. 

*  Gibbons,  J.  B.:  Scientific  Memoirs  by  Medical  Officers  of  the  Army  of  India, 
part  vi,  1891,  and  the  Indian  Lancet,  May  i,  1896,  p.  426. 

t  Ghose:  Lancet,  1895,  vol.  i,  p.  321. 

J  Nil  Ratan  Sircar:  Indian  Lancet,  July  1,  1896.  Mackenzie:  Lancet,  1895, 
vol.  i. 

§  Vide  W.  H.  Dickinson:  Enlargement  of  the  Viscera  in  Rickets,  Trans.  Royal 
Medical  and  Chirurg.  Soc,  1869. 

II  Hogben:  Birmingham  Med.  Review,  vol.  xxiv,  p.  65,  1888. 


TUBERCULOSIS   OF   THE   LIVER  AND  BILE-DUCTS. 

SYNOPSIS. 

Introduction. 

Paths  by  which  tubercle  bacilli  reach  the  liver. 

By  the  umbilical  vein  (congenital  tuberculosis);  hepatic  artery;  portal  vein; 
lymphatics;   bile-duct. 
Forms  of  hepatic  tuberculosis. 

(I)  Miliary  tuberculosis. 

(II)  Local  tuberculosis. 

(a)   Involving  the  bile-ducts. 

(6)  Solitary  tubercle.     Abscess. 
Other  changes  in  the  liver  associated  with  tuberculosis. 
Focal  necrosis.     Fatty,  lardaceous  change. 
Tuberculosis  and  cirrhosis. 

INTRODUCTION. 

Tuberculosis  of  the  liver  has  little  clinical  importance,  can  seldom 
be  diagnosed  with  certainty  during  hfe,  and  when  found  after  death  is 
usually  part  of  generalised  tuberculosis.  Larger  tuberculous  masses  are 
more  often  seen  in  children  and  young  subjects  than  in  adults,  but  seldom 
give  rise  to  clinical  manifestations.  In  the  exceptional  instances  where 
a  tuberculous  mass  or  abscess  has  produced  enlargement  of  the  liver, 
some  commoner  result  of  tuberculosis,  such  as  fatty  or  lardaceous  change, 
would  probably  be  diagnosed.  The  comparative  infrequency  of  ad- 
vanced tuberculous  changes  in  the  liver  niight  suggest  that,  like  the 
thyroid  gland,  the  liver  is  inimical  to  the  growth  of  the  tubercle  bacillus. 
This  is  probably  not  the  case,  for  in  lower  animals,  especially  in  birds, 
hepatic  tuberculosis  is  common,  and  Sergent  *  has  shown  experimentally 
that  the  bile  is  not  more  antagonistic  to  the  growth  of  tubercle  bacilli 
than  of  other  micro-organisms.  It  is  probable  that  the  reason  why  ad- 
vanced tuberculous  changes  are  rare  in  the  liver  is  that  the  liver  does 
not,  like  the  mesenteric  glands,  lie  in  the  direct  line  of  the  lymphatic 
vessels  conveying  lymph  from  the  intestines.  The  lymphatic  glands  in 
the  portal  fissure  receive  the  efferent  lymphatic  vessels  conveying  lymph 
away  from  the  liver.  In  order  that  tuberculous  infection  should  pass 
into  the  liver  along  the  lymphatics  of  the  portal  fissure  the  bacilli  would 
have  to  work  their  way  against  the  flow  of  lymph.  Possibly  this  does 
occur,  but  in  most  cases  where  the  intestines,  the  liver,  and  the  lymphatic 
glands  in  the  portal  fissure  are  tuberculous,  the  tubercle  bacilli  have 
probably  travelled  from  the  intestine  to  the  liver  by  the  portal  vein, 
set  up  tuberculous  foci  in  the  portal  canals,  and  so  infected  the  lymphatic 
glands  in  the  portal  fissure. 

Marmorekjt  however,  finds  from  experiment  that  there  is  a  certain  amount  of 
immunity  to  tuberculous  infection  on  the  part  of  the  liver  which  cannot  be  satis- 
factorily explained  on  the  anatomical  grounds  mentioned  above.  He  believes  that 
chemical  factors  inhibit  the  development  of  tubercle  bacilli  in  the  liver. 

*  Sergent:  These  Paris,  1S95-6,  No.  92. 
t  Archiv.  Gdn^ral.  de  Med.,  Nov.  24,  1903. 
336 


TUBERCULOSIS   OF   THE   LIVER  AND    BILE-DUCTS.  337 


PATHS   BY   WHICH  TUBERCLE   BACILLI  CAN    REACH   THE   LIVER. 

Tubercle  bacilli  may  reach  the  liver  from  various  sources. 

By  the  Umbilical  Vein. — During  foetal  life,  if  there  were  tuberculous  disease  of 
the  placenta  the  bacilli  would  reach  the, liver  by  the  umbilical  vein.  This  is  so  very 
rare  and  exceptional  that  it  can  only  be  regarded  as  a  pathological  curiosity.  It 
is  chiefly  interesting  from  Baumgarten's  theory  that  tubercle  bacilli  are  retained 
in  the  liver  from  early  foetal  life  in  the  form  of  spores.  Experimentally  tuberculosis 
of  the  liver  in  the  foetus  has  followed  local  tuberculous  infection  of  the  genital  organs 
in  guinea-pigs.  (D'Arrigo.*)  Cases  of  hepatic  tuberculosis  in  children  within  the 
first  fortnight  of  life  have  been  described  by  Sabouraud  f  and  by  Horl,  and  are 
undoubtedly  due  to  infection  during  foetal  life.  Fcetal  tuberculosis  in  calves  appears 
to  be  equally  rare,  but  its  existence  has  been  established  by  Nocard,t  MacFadyean,§ 
and  Johne. 

By  the  Hepatic  Artery. — In  generalised  tuberculosis  tubercle  bacilli  reach  the  Ywev 
by  the  hepatic  artery.  It  is  probable  that  tubercle  bacilli  often  reach  the  liver 
when,  although  a  number  of  bacilli  have  gained  entrance  to  the  general  circulation, 
generalised  tuberculosis  does  not  result.  Thus,  in  chronic  puhnonary  tuberculosis 
tubercles  in  the  liver  may  be  due  to  bacilli  which  have  strayed  into  the  blood- 
stream. The  miliary  tubercles  are  scattered  through  the  liver  both  inside  the 
lobules  and  in  the  portal  spaces.  It  is  possible  that  when  a  number  of  tubercles 
thus  arise  in  the  portal  spaces  they  may  increase  in  size  and  form  a  caseous  mass 
which  bursts  into  the  bile-ducts  and  thus  gives  rise  to  the  condition  described  as 
tuberculous  cholangitis.  But  death  usually  occurs  from  tuberculous  lesions  else- 
where, e.  g.,  meningitis,  long  before  this  sequence  of  events  can  complete  itself  in 
generalised  tuberculosis,  and  it  is  only  exceptionally  that  tuberculous  cholangitis  or 
abscess  is  due  to  bacilli  reaching  the  liver  by  the  arterial  blood. 

By  the  Portal  Vein. — Tubercle  bacilli  "from  the  bowel  in  cases  of  tuberculous 
ulceration  readily  pass  by  the  portal  vein  to  the  liver,  and  there  set  up  either  miliary 
tubercles,  or  the  larger  and  more  chronic  tuberculous  changes  in  connexion  with 
the  bile-ducts.  Tubercle  bacilli  can  pass  through  the  mucous  membrane  of  the 
intestine  without  any  gross  lesion  of  the  mucous  membrane.  Sergent  ||  insists  that 
tubercle  bacilli  first  set  up  inflammation  and  thrombosis  of  the  terminal  intrahepatic 
branches  of  the  portal  vein  before  tuberculous  changes  occur  in  the  immediate 
neighbourhood  of  the  bile-ducts,  but  I  have  not  been  able  to  convince  myself  of  this. 

By  the  Lymphatics. — In  cases  of  tuberculous  peritonitis  bacilli  may  possibly 
work  their  way  in  through  the  lymphatic  vessels  of  the  capsule  and  gain  a  footing 
in  the  substance  of  the  liver,  but  as  a  matter  of  fact  there  is  very  little  evidence  that 
hepatic  tuberculosis  is  set  up  in  this  manner.  It  is  also  conceivable  that  from 
tuberculosis  of  the  glands  in  the  portal  fissure,  secondary  to  intestinal  disease,  an 
extension  of  the  disease  to  the  inside  of  the  liver  may  result.  But,  as  already 
pointed  out,  this  spread  of  tuberculosis  is  against  the  current  of  lymph,  the  lym- 
phatics at  the  portal  fissure  running  away  from,  not  towards,  the  liver. 

By  the  Common  Bile-duct. — It  has  been  suggested  that  tubercle  bacilli  from  the 
duodenum  pass  up  the  bile-ducts,  work  their  Avay  through  the  mucous  membrane 
of  the  ducts  into  the  portal  spaces,  and  there  give  rise  to  the  formation  of  caseous 
tubercles.  This  view,  which  on  the  face  of  it  was  improbable  from  the  absence 
of  motility  on  the  part  of  the  tubercle  bacilli,  has  been  disproved  by  Sergent' s 
experiments  of  injecting  tubercle  bacilli  into  the  bile-ducts,  which  showed  that 
unless  the  walls  of  the  ducts  were  previously  damaged,  as  by  ligature,  they  did 
not  allow  tubercle  bacilli  to  pass  through  them.  It  is  noticeable  that  the  extra- 
hepatic  ducts  are  not  affected  by  tubercle  except  in  the  rarest  instances,  and  that 
there  is  no  condition  of  ascending  or  descending  tuberculous  cholangitis  to  corre- 
spond with  tuberculous  disease  of  the  ureter.  Pilliet  **  suggested  that  tubercle 
bacilli  might  be  excreted  from  the  blood  into  the  lumen  of  the  ducts  and  that 
tuberculous  cholangitis  then  results.  Microscopic  examination,  however,  of  such 
cases,  viz.,  where  the  ducts  are  involved  {vide  p.  342)  shows  that  the  tuberculous 
process  always  begins  outside  the  ducts. 

To  sum  up:  Tubercle  bacilli  reach  the  liver  by  the  hepatic  artery  in  generalised 

*  D'Arrigo:  Centralbl.  f.  Bakt.,  1900. 
t  Sabouraud:  Soc.  de  biolog.,  1891,  p.  674. 
X  Nocard:  Rev.  de  la  Tuberculose,  1895. 
§  MacFadvean,  J.:  Trans.  Path.  Soc,  vol.  1,  p.  268. 
II  Sergent,- E.:  The.se  Paris,  1895. 
**  Pilliet:  These  Paris,  1891. 
22 


338  DISEASES    OF   THE    LIVER. 

tuberculosis  and  in  conditions  which  fall  short  of  generalised  tuberculosis.  The 
portal  vein  also  conveys  tubercle  bacilli  to  the  liver,  but  there  is  no  evidence  that 
tubercle  bacilli  travel  up  the  bile-duct  and  very  little  to  show  that  hepatic  tubercu- 
losis is  conveyed  through  the  lymphatics. 

FORMS  OF  HEPATIC  TUBERCULOSIS. 

It  might  be  thought  more  methodical  to  consider  hepatic  tuberculosis 
under  two  heads — (i)  tuberculous  disease  of  the  liver  substance  proper 
and  (ii)  tuberculosis  of  the  bile-ducts.  But  since,  as  will  be  shown  later, 
the  ducts  themselves  are  not  affected  primarily  and  only  suffer  as  the 
result  of  extension  from  without,  whether  the  starting-point  is  in  the 
hver  substance,  the  portal  space,  or  in  exceptional  instances  the  lymphatic 
glands  in  the  hilum,  it  is  more  practical  to  divide  the  subject  of  hepatic 
tuberculosis  into — 

(I)  Miliary  tuberculosis, — (a)  part  of  acute  generalised  tuberculosis; 
(h)  due  to  infection  from  the  intestine. 

(II)  Local  tuberculosis — (a)  involving  the  ducts;  (6)  not  involving 
the  ducts. 

MILIARY  TUBERCULOSIS, 

The  presence  of  miliary  tubercles  in  the  liver  is  part  of  generalised 
tuberculosis,  and  though  sometimes  not  seen  on  naked-eye  examination, 
they  will  be  found  to  be  constantly  present  when  microscopic  sections  of 
the  liver  are  made.  Miliary  tubercles  are  found  in  the  liver  in  chronic 
pulmonary  tuberculosis  as  a  result  of  two  processes:  (a)  tubercle  bacilli 
reaching  the  liver  by  the  hepatic  artery,  and  (5)  tubercle  bacilli  derived 
from  secondary  tuberculous  ulcers  in  the  intestine  and  passing  to  the 
liver  by  the  portal  vein. 

Simmonds  *  found  hepatic  tubercles  in  82  per  cent,  of  476  cases  of  tuberculosis, 
76  per  cent,  in  adults,  92  per  cent,  in  children.  Zehden  f  found  miliary  tubercles  in 
50  per  cent,  of  all  fatal  cases  of  puhnonary  tuberculosis,  thus  corresponding  with  the 
frequency  of  tuberculous  ulceration  of  the  intestine  in  that  disease.  My  own  ex- 
perience would  put  the  occurrence  of  mihary  hepatic  tubercle  in  fatal  cases  of 
ordinary  pulmonary  tuberculosis  lower  than  50  per  cent. 

Miliary  tubercle  in  babies  at  birth  is  almost  a  pathological  curiosity. 
When  there  is  tuberculosis  of  the  placenta  the  bacilli  may  infect  the  liver 
by  the  channel  of  the  umbilical  vein.  Bar  and  Renon  J  have  found 
tubercle  bacilli  in  the  bloqd  of  the  umbilical  vein  of  two  foetuses  from 
mothers  affected  with  tuberculosis.  Sabouraud  ^  met  with  miliary 
tubercles  in  the  liver  and  spleen  of  a  newly  born  infant  eleven  da3^s  old 
whose  mother  had  pulmonary  tuberculosis. 

Morbid  Anatomy. — Miliary  tubercles  in  the  liver  are  small  and 
isolated,  grey,  and  when  older  yellow  in  colour,  and  are  better  seen  on 
the  surface  of  the  capsule  than  on  section  of  the  organ.  In  some  instances 
the  liver  may  be  crowded  with  minute  miliary  tubercles  which  can  only 
be  seen  when  microscopic  sections  are  made;  to  the  naked  eye  the  liver 
may  merely  show  cloudy  swelling.     In  the  substance  of  the  liver  the 

*  Simmonds:  Centralblatt  f.  Path.,  1S9S,  Bd.  ix,  S.  865. 
t  Zehden:  Centralblatt  f.  Path.,  1897,  Bd.  viii,  S.  468. 
j  Bar  et  Renon:  Soc.  de  biolog.,  June  29,  1895,  p.  505. 
§  Sabouraud:  Soc.  de  biolog.,  Oct.  17,  1891,  p.  674. 


TUBERCULOSIS    OF   THE    LIVER   AXD    BILE-DUCTS.  339 

tubercles  are  nearly  always  situated  inside  the  lobules  and  thus  form  a 
contrast  to  the  local  and  chronic  form  of  tuberculosis  of  the  liver  occupy- 
ing the  portal  spaces.  Miliary  tubercles  are  not  infrequently  found  in 
cirrhosis  of  the  liver  and  are  then  usually  a  superadded  lesion  and  not 
the  cause  of  the  cirrhosis.  The  liver  is  generally  fatty  and  rather  in- 
creased in  weight;  there  may  be  considerable  venous  engorgement  from 
terminal  failure  of  the  right  side  of  the  heart.  Usually  there  is  little  or 
no  tuberculous  perihepatitis,  but  this  may  coexist  "with,  miliar}^  tubercles 
in  the  substance  of  the  liver  under  two  conditions:  (I)  When  there  is 
chronic  peritonitis  of  tuberculous  origin  in  which  the  capsule  of  the  liver 
shares,  or  (II)  in  rare  instances  where  there  is  a  subacute  fibrinous  peri- 
tonitis associated  with  acute  miliary  tuberculosis  of  the  capsule  of  the 


Fig.    40. — Photomicrograph    of    Liver   with    Caseous    Tubercles    showing    Giant   Cells. 
The  liver  substance  shows  chronic  venous  engorgement.     (S.  G.  Penny,  Esq.) 

liver.  It  is  possible  that  the  miliary  tubercles  in  the  hepatic  substance 
may,  if  the  process  is  not  very  acute  in  its  generalisation,  have  time  to 
unite  and  form  small  caseous  areas  which  may  soften  down  and  form 
small  tuberculous  abscesses. 

In  a  child  aged  three  months  who  died  in  St.  George's  Hospital  with  advanced 
tuberculous  bronchopneumonia  the  liver  contained  a  large  number  of  miliary 
tubercles  and  two  tul^erculous  cavities  stained  with  bile,  rather  larger  than  a  pea. 
The  intestines  were  free  from  tuberculosis.  Sergent  has  described  a  unique  case 
of  confluent  miliary  tuberculosis  of  the  liver. 

Histology. — In  then-  earliest  stage  tubercles  consist  of  small  round 
cells,  like  masses  of  lymphoid  tissue,  with  a  delicate  reticulum.  Mc- 
Weeney  *  considers  that  many  of  the  tubercles  begin  b}^  proliferation  of 

*  McWeeney:  Brit.  Med.  Journ.,  1900,  vol.  i,  p.  844. 


340  DISEASES    OF   THE    LIVER. 

the  endothelium  of  the  interlobular  capillaries.  After  a  time  larger  endo- 
thelioid  cells  are  found  in  the  miliary  tubercle;  they  are  the  result  of 
inhibited  hyperplasia  of  the  cells  which  at  first  were  small.  When  the 
tubercle  grows  to  a  larger  size,  according  to  McWeeney,  0.2  mm.,  giant 
cells  appear.  The  giant  cells  are  due  to  union  of  preexisting  cells,  though 
it  has  been  thought  that  continued  growth  and  nuclear  division  without 
cellular  division  in  endothelioid  cells  might  account  for  them.  The  cen- 
tral part  of  the  giant  cells  becomes  homogeneous  and  caseous,  while  the 
nuclei  form  prominent  objects  around  the  periphery.  It  is  often  impossi- 
ble to  demonstrate  bacilli  in  perfectly  typical  tubercles.  The  liver  cells 
at  the  margin  of  the  tubercles  are  compressed  and  may  undergo  fatty 
change.  In  some  cases  the  fatty  change  is  widely  diffused  throughout 
the  liver. 

Signs  and  Symptoms. — There  are  no  clinical  signs  or  syiwptoms  which 
can  be  relied  upon  to  indicate  the  presence  of  miliary  tubercles  in  the 
liver.  Hilton  Fagge  *  and  Frankel  t  have  seen  it  associated  mth  jaun- 
dice, but  this  is  so  rare  as  to  be  practically  a  curiosity.  When  there  are 
a  large  number  of  tubercles  on  the  surface  of  the  liver,  it  is  possible  that 
a  friction  rub  may  be  heard  on  auscultation. 

LOCAL  TUBERCULOSIS. 

(I)  Involving  the  bile-ducts. 

(II)  Solitary  tubercle  of  the  hver.     Tuberculous  abscess. 

Tuberculous  Disease  Involving  the  Bile-ducts. 

Synonyms:  Tuberculous  Cavities  in  the  Liver.     Tuberculous  Cholangitis  or  Peri- 
cholangitis. 

Incidence  and  Etiology. — Though  this  condition  was  described  by 
Bristowe  %  in  1858,  who  found  it  present  in  12  out  of  167  cases  of  tubercu- 
lous ulceration  of  the  intestines,  it  has  not  attracted  much  general  atten- 
tion, probably  because  it  has  no  clinical  features.  It  is  a  commoner  con- 
dition than  the  number  of  recorded  cases  would  lead  one  to  suppose. 
The  tubercle  bacilli  reach  the  liver  by  the  portal  vein,  being  derived  from 
the  intestines,  which  in  most  instances  show  tuberculous  ulceration. 
Tubercle  bacilli  having  reached  the  liver  settle  down  in  the  portal  spaces 
and  produce  miliary  tubercles,  and  later  masses  of  tuberculous  granula- 
tion tissue.  The  condition  might  well  be  spoken  of  as  tuberculosis  of  the 
portal  spaces. 

Sergent  §  insists  that  the  first  step  is  tuberculous  pylephlebitis  and  thrombosis 
of  the  intra-hepatic  branches  of  the  portal  vein,  and  that  at  a  later  stage  tuberculous 
granulation  tissue  develops  in  the  portal  spaces. 

The  tuberculous  granulation  tissue  caseates,  softens  clown,  and  even- 
tually breaks  into  the  bile-ducts  from  without  inwards.  The  discharge  of 
the  tuberculous  foci  into  the  ducts  is  analogous  to  rupture  of  a  caseous 
focus  in  the  lung  into  the  bronchi.     The  ducts  become  infected  and  may 

*  Hilton  Fagge:  Text-book  of  Med.,  vol.  ii,  p.  270,  1886. 
t  Frankel,  A.:  Zeitschrift  f.  khn.  Med.,  Bd.  v,  S.  107,  1882. 
j  Bristowe,  J.  S.:  Trans.  Path.  Soc,  vol.  ix,  p.  241. 
§  Sergent:  These  Paris,  1895,  No.  92. 


Plate  3. 


TUBERCULOSIS   OF  THE  LIVER  AXD   BILE-DUCTS.  341 

be  entirely  destroyed  localh'.  The  communication  between  the  ca^•ities 
thus  formed  and  the  chicts  is  not  always  visible,  but  from  the  bile-stained 
condition  of  the  "vomicae"  there  can  be  no  doubt  this  has  occurred. 
(Compare  Wethered's  case.*) 

As  stress  has  been  laid  on  the  statement  that  the  bile-ducts  are  invaded  from 
without  or  are  secondarily  involved  in  tuberculous  disease  of  the  liver,  it  ought 
to  be  mentioned  that  Lancereaiix  f  has  described  a  case  of  tuberculosis  of  the  com- 
mon bile-duct,  gall-bladder,  and  cystic  duct  in  a  woman  aged  thirty-two  years, 
which  he  regards  as  directly  due  to  infection  from  the  duodenum. 

Morbid  Appearance. — The  liver  is  usually  somewhat  larger  than 
natural,  and  on  section  shows  a  number  of  white  caseous  areas  or  of 
bile-stained  cavities  with  caseous  walls.  In  the  earUer  stages,  before  the 
tubercles  have  opened  into  the  ducts,  the  tuberculous  material  is  firm  and 
resembles,  and  is  therefore  sometimes  regarded  as,  lymphadenoma ;  in  the 
later  (excavation)  stage,  when  thej'^  have  opened  into  a  bile-duct,  their 
walls  have  a  greenish-yellow  colour  from  bile-staining,  and  exceptionall}" 
a  purple  colour  from  haemorrhage.  In  their  early  stage  the  tubercles  may 
be  ^  to  J  inch  in  diameter,  while  the  caAdties  subsec^uently  developed  are 
larger  and  may  measure  as  much  as  an  inch  or  even  two  inches  across. 

Structurally  the  masses  are  enclosed  in  a  capsule  representing  the 
fibrous  tissue  of  the  portal  space,  and  contain  caseating  granulation  tissue 
surrounding  a  cavity  which  in  its  turn  can  be  seen  opening  into  a  bile- 
duct  ;  the  ejDithelium  of  the  bile-duct  may  be  well  preserved  except  at  the 
point  where  it  has  been  destroyed  by  the  j^erforation  from  without.  The 
tuberculous  process  is  therefore  primarily  pericholangitic  not  cholangitic. 
Further,  the  bile-duct  is  not  affected  throughout  its  course  in  the  way 
that  a  tuberculous  ureter  is,  but  is  locally  infected  at  the  spot  where 
it  is  invaded  from  "^dthout.  The  larger  extra-hepatic  ducts  are  very 
seldom  involved ;  a  softened  tuberculous  gland  in  the  hilum  of  the  liver 
may  exceptionally  open  into  the  bile-duct. 

Kester  J  has  recorded  a  case  which  would  bear  this  interpretation.  A  boy  aged 
three  years  had  jaundice,  due  to  pressure  of  tuberculous  portal  glands,  and  tubercu- 
lous pneumonia.  The  liver  contained  tubercles  and  the  ducts  were  dilated  and 
the  lower  end  of  the  common  bile-duct  opened  into  a  caseous  cavity. 

Macroscopic  Diagnosis. — -Tuberculous  masses  and  cavities  in  the  liver  sometimes 
closely  resemble  other  conditions.  The  deep  bile-staining  is  extremely  suggestive  of 
tuberculous  cavities  in  connexion  vnth  the  bile-ducts,  but  before  this  staining  has 
occurred  the  masses  may  resemble  nodules  of  lymphadenoma,  etc.  The  tuberculous 
masses  are  whiter  and  may  show  signs  of  breaking  do^\'n,  which  lymphadenoma  never 
does.  In  cirrhosis  with  multiple  adenomata  fatty  change  in  the  nodular  areas 
of  hyperplasia  has  often  given  rise  to  a  mistaken  diagnosis  of  tuberculous  masses. 
In  exceptional  instances  secondary  carcinoma  maj'  very  closely  imitate  tuberculous 
masses  and  necessitate  microscopic  examination.  The  rare  condition,  chronic  peri- 
cholangitis, of  which  Strangeways  Pigg  and  I,§  and  Morley  Fletcher  H  have  recorded 
examples,  exactly  imitates  tuberculous  cavities  in  the  liver.  Psorospermial  disease 
of  the  bile-ducts  in  tame  rabbits  closely  imitates  tuberculous  lesions,  and  though  it 

*  Wethered,  F.  J.:  Trans.  Path.  Soc,  vol.  xl,  p.  139. 

t  Lancereaux:  Traite  des  Maladies  des  Foie  et  du  Pancreas,  p.  662,  1S99. 
t  Kester:  Centnalblatt  f.  inn.  Med.,  1896,  S.  213. 

§  Rolleston  and  Strangeways  Pigg:  Journ.  of  Pathology  and  Bacteriologv,  vol.  v, 
p.  221,  1898. 

11  Morley  Fletcher:  Trans.  Path.  Soc,  vol.  lii,  p.  193. 


342  DISEASES    OF   THE    LIVER. 

is  extremely  rare  in  man,  it  is  conceivable  that  some  examples  of  this  protozoan 
infection  have  been  erroneously  called  tuberculous.  Actinomycosis  and  the  sup- 
purating foci  in  pylephlebitis  and  cholangitis  are  hardly  likely  to  be  mistaken  for 
tuberculous  cavities,  though  abscesses  at  first  regarded  as  tuberculous  have  been 
subsequently  shown  to  be  actinomj^cotic* 

Histologically  the  portal  space  is  occupied  by  tuberculous  granulation 
tissue  containing  giant  cells  and  undergoing  caseation.  This  surrounds 
the  bile-duct  and  opens  into  it.  Eventually  the  bile-duct  may  be  de- 
stroyed, and  at  this  stage  the  portal  space  contains  a  central  mass  of 
caseous  debris,  stained  -^dth  bile,  and  surrounded  by  tuberculous  granula- 
.tion  tissue. 

Clinical  Features. — There  are  very  seldom  any  definite  symptoms 
j)ointing  to  the  liver.  It  is  indeed  remarkable  that  jaundice  is  constant^ 
absent,  inasmuch  as  there  is  very  definite  obstruction  in,  at  any  rate 
some  of,  the  bile-ducts. 

It  seems  possible  that  the  reason  why  jaundice  is  not  met  -n-ith  is  that  the 
lymphatic  vessels  which  should  carry  the  bile  from  the  obstructed  ducts  are  them- 
selves compressed  and  are  unable  to  convey  the  bile  into  the  general  circulation. 
If  this  be  the  case,  the  liver  substance  should  be  bile-stained.  Since  this  does  not 
occur  in  cases  of  tuberculous  cavities  in  the  liver,  this  explanation  cannot  be  urged. 

It  is  true  that  occasionally  attacks  of  abdominal  pain  have  been  re- 
ported in  cases  where  tuberculous  cholangitis  was  foimd  after  death. 
These  attacks  of  pain  are  not  accompanied  by  jamidice  or  by  bile  in  the 
urine  and  are  not  likely  to  suggest  biliary  colic  during  hfe.  The  ab- 
dominal pain  is  verj^  probably  due  to  tuberculous  ulceration  of  the  intes- 
tines or  concomitant  tuberculous  peritonitis.  Ascites  may  result  from 
tuberculous  peritonitis,  or  conceivably  from  compression  of  the  portal 
vein  by  enlarged  tuberculous  glands.  As  a  rule,  the  clinical  aspect  of  the 
cases  presenting  this  condition  after  death  are  those  of  pulmonaiy,  ab- 
dominal, or  generalised  tuberculosis. 

I  examined  after  death  a  child  aged  nine  months  who  had  advanced  tuberculous 
disease  of  the  lungs,  tuberculous  ulcers  in  the  intestine,  caseous  mesenteric  glands, 
and  tuberculous  cavities  in  the  liver.  During  life  the  signs  were  those  of  consolida- 
tion of  the  lungs;  there  was  no  diarrhcea  or  jaundice.  Dudgeon  showed  a  good 
specimen  of  tuberculous  cavities  in  the  liver  to  the  Pathological  Societj'  from  a  girl 
aged  two  years;  there  were  tuberculous  ulcers  in  the  intestine,  tuberculous  peritonitis, 
and  adenitis  of  the  lymphatic  glands  in  the  portal  fissure.  Plate  3  is  taken  from 
a  section  of  the  liver  presented  by  Dr.  Dudgeon  to  the  museum  of  St.  George's 
Hospital. 

Solitary  Tubercle. 
Under  the  heading  of  ''solitary  tubercle'^  it  will  be  convenient  to  con- 
sider comparatively  large  masses  of  caseous  material  which  do  not  com- 
municate with  the  bile-ducts.  It  is  true  that  such  masses  might  soften 
doWTi  and  effect  a  fistulous  communication  with  the  bile-ducts,  but  it 
would  then  be  impossible  to  be  certain  that  the  tuberculous  process  had 
not  started  near  the  bile-ducts.  Although  called  "solitary  tubercle," 
there  may  be  a  number  of  these  caseous  masses  in  the  liver.  This  form 
of  local  tuberculosis,  in  which  the  portal  spaces  and  bile-ducts  are  not 
specially  involved,  is  rare,  but  is  common  in  some  animals. 

*Harley,  J.:  Medico-Chirurg.  Trans.,  vol.  Ixix,  p.  135,  1886.  Shattock,  S.  G.: 
Trans.  Path.  Soc,  vol.  xxxvi,  p.  260. 


Plate  4. 


1.  Advanced  Stack  of  a  Tuberculous  Cavity  in  tiu:  I,ivi:it. 

There  is  a  dense  fibrous  capsule  derived  from  the  portal  space  wliicli  sinnmuds  tuberculous  granulalioii- 

tissue;  more  internally  there  is  a  mass  of  caseous  debris. 
2.  Earlier  stage,  showing  tuberculous  granulation  tissue  occupying  the  portal  space  and  opening  into  the 

bile-duct. 


TUBERCULOSIS  OF  THE  LIVER  AXD  BILE-DUCTS.  343 

Masses  of  hard  caseous  tubercle  are  very  common  in  birds;  in  fact,  tlie  liver 
is  the  chief,  and  in  20  per  cent,  of  the  cases  examined  by  W.  Hutchinson  *  the 
only,  organ  affected  in  avian  tuberculosis.  In  bovines  large  caseous  masses  are 
found  in  the  Hver;   they  soften  from  suppuration  and  have  a  thick  fibrous  capsule. 

These  solitary  caseous  masses  are  rather  less  rare  in  children  than  in 
adults. 

Craven  Moore, f  who  reports  a  case,  only  refers  to  four  other  published  instances, 
by  Clement,  Zehden,  and  Simmonds  two.  I  think,  however,  they  are  not  nearly 
so  rare  as  this,  and  have  certainly  seen  two.  F.  Craven  Moore's  case  was  extremely 
interesting  in  that  there  were  S  tu'oerculous  masses  in  the  liver  of  a  man  who  died 
with  carcinoma  of  the  pylorus.  It  was  thought  that  the  tubercle  bacilli  were  ab- 
sorbed from  the  ulcerated  surface  in  the  stomach  and  that  the  absence  of  HCl  in 
the  gastric  juice  rendered  this  infection  more  feasible.  Clement  t  has  described  an 
almost  exactty  similar  case.  Inasmuch  as  tubercle  bacilli  were  not  found  in  either 
Moore's  or  Clement's  cases,  the  possibility  arises  that  there  may  have  been  some 
other  cause  for  the  caseous  masses,  such  as  the  pseudo-tuberculosis  bacillus  de- 
scribed by  A.  Pfeiffer  and  by  Klein.  Klein  §  found  a  bacillus  in  Thames  and  Lee 
water  and  produced  caseous  masses  by  means  of  it  in  the  hver,  lung,  and  lymphatic 
glands.  It  is  possible  that  in  cases  of  carcinoma  of  the  stomach  these  bacilli  intro- 
duced into  the  stomach  in  water  might  set  up  caseous  lesions  in  the  liver. 

The  foUowdng  is  a  well-marked  example  of  multiple  ''solitarj^"  tubercu- 
lous masses  in  the  liver: 

A  boy  aged  eight  years  was  under  my  care  in  St.  George's  Hospital  for  the 
greater  part  of  thirteen  months;  he  was  admitted  with  pericarditis  and  advanced 
renal  disease;  he  recovered  from  the  pericarditis  and  gradually  developed  multiple 
tuberculous  lesions  of  the  limbs,  skull,  and  vertebra.  It  was  noticeable  that  as  the 
tuberculous  lesions  advanced  his  renal  symptoms  receded.  There  was  never  any 
jaundice.  He  eventually  died  of  exhaustion.  The  liver  was  much  enlarged  as 
compared  T^dth  his  emaciated  body;  weight,  20  ounces.  There  was  tuberculous 
perihepatitis  with  large  white  caseous  masses,  unstained  with  bile,  in  the  liver. 
They  were  the  size  of  filbert  nuts  and  had  been  felt  during  life  projecting  from  the 
surface  of  the  liver.  No  communication  with  the  bile-ducts  could  be  made  out; 
the  mesenteric,  tracheal,  inguinal,  and  axillary  glands  were  also  tuberculous. 

Milian  and  Hertz  ||  haA'e  recorded  the  case  of  a  man  aged  fifty-eight  with  ema- 
ciation, an  enlarged  spleen,  and  fever  unaffected  by  quinine.  The  clinical  aspect 
suggested  malaria  or  tuberculosis,  but  no  signs  were  found  in  the  lungs.  The  liver 
contained  miliar}^  tubercles  and  larger  ones  as  big  as  a  horse-chestnut;  the  spleen 
was  also  affected;  but  there  were  no  tubercles  in  the  alimentarj^  canal  or  lungs. 
In  a  somewhat  similar  case — a  woman  aged  sixty-six  years — described  by  Tolot** 
there  were  no  intestinal  or  pulmonary  lesions. 

Around  the  white  caseous  masses  there  is  a  thin  fibrous  capsule, 
while  outside  this  the  liver  substance  is  compressed  and  the  cells  elongated 
and  flattened.  The  caseous  masses  may  be  fairly  easily  enucleated. 
These  "solitary"  tubercles  closely  resemble  gummata,  and  must  be  dis- 
tinguished from  the  appearance  presented  by  the  adenomatous  forma- 
tions in  nodular  h}73er}3lasia  when  fatty  degeneration  has  occurred  in 
the  hyperplastic  liver  cells.  In  a  few  instances  encysted  caseous  masses 
have  also  been  found  in  the  spleen.     (Milian  and  Hertz;  Tolot.) 

The  clinical  aspect,  as  has  been  shown  incidentally  bv  the  foregoing 
cases,  is  vague   and   in  no  way  characteristic.     The  li^-er  may  not  be 

*  "Woods  Hutchinson:  .Studies  in  Human  and  Comparati\'e  Pathology,  p.  SOA. 
t  Craven  Moore:  Medical  Chronicle,  Oct.,  1899,  p.  5. 
J  Clement:  Virchow's  Archiv,  Bd.  cxxxix,  S.  35. 
ij  Klein,  E.  E.:  Lancet,  1899,  vol.  ii,  p.  1297. 
i|  MiUan  and  Hertz:  Bull.  Soc.  Anat.  Paris,  1900,  p.  153. 
**  Tolot:  Lyon  Medical,  vol.  xcix,  p.  323,  Sept.  7,  1902. 


344  DISEASES    OF   THE    LIVER. 

made  out  to  be  enlarged.     Exceptionally  a  tuberculous  mass  may  be 
sufficiently  large  to  be  felt  through  the  abdominal  walls  during  life. 

Thus,  in  a  case  related  by  T.  L.  Anderson  *  a  mass  the  size  of  a  Mandarin  orange 
in  the  left  lobe  of  the  liver  was  distinctly  felt  during  life.  The  patient  was  a  man 
aged  forty-one  who  had  extensive  intestinal  tuberculosis. 

In  a  few  cases  the  spleen  is  palpably  enlarged.  Jaundice  does  not 
occur,  and  a  diagnosis  can  hardly  be  made.  As  a  rule,  the  patients 
suffer  from  increasing  weakness,  loss  of  appetite,  and  general  debility. 

Excision  of  a  tubercular  mass  has  been  carried  out  by  Rome  f  and  Ranso- 
hoffjf  in  the  first  case  with  recovery. 

Tuberculous  Abscess. — The  solitary  tubercles  may  become  secon- 
darily infected  with  pyogenetic  micro-organisms,  soften  down,  and  form 
abscesses;  this  occurred  in  H.  Mackenzie's  §  case,  where  the  cavities 
were  purple  and  contained  blood  but  not  bile.  In  rare  instances  tuber- 
culous abscesses  may  reach  a  considerable  size;  they  may  set  up  local 
perihepatitis  or  even  perforate  into  the  peritoneal  cavity.  Waring,  || 
from  a  surgical  point  of  view,  considers  tuberculous  abscess  of  the  liver 
as  being  either  entirely  inside  the  liver,  and  so  resembling  an  ordinary 
hepatic  abscess,  or  when  near  the  surface  of  the  organ  setting  up  a  local- 
ised perihepatic  abscess  which  may  then  resemble  and  indeed  be  a  sub- 
phrenic abscess. 

A  single  tuberculous  abscess  of  the  liver  is  very  rare  indeed.  Some 
of  the  cases  that  have  not  been  examined  microscopically  may  have 
been  softened  gummata  or  actinomycotic  abscesses.     (Vide  p.  342.) 

Mayo  Robson  **  operated  upon  an  hepatic  abscess  which  proved  to  be  tubercu- 
lous and  was  evidently  single,  as  the  patient  was  in  good  health  more  than  two 
years  afterwards. 

There  may  be  other  evidences  of  tuberculosis  in  the  body,  such  as 
advanced  pulmonary  disease,  or,  on  the  other  hand,  the  liver  may  be 
exclusively  or  almost  exclusively  affected.  When  the  abscesses  are  large 
enough  to  attract  attention  during  life,  their  tuberculous  nature  cannot 
be  ascertained  until  their  contents  have  been  bacteriologically  examined. 
Tuberculous  abscesses  are  usually  small  and  multiple  and  belong  to  the 
group  of  local  tuberculosss  involving  the  bile-ducts. 

EFFECTS   OF   TUBERCULOSIS   ELSEWHERE   IN   THE    BODY  ON  THE 

LIVER. 

Tuberculosis  elsewhere  in  the  body  may  lead  to  other  clianges  in 
the  liver  besides  the  secondary  development  of  tubercles. 

1.  Focal  necrosis  and  coagulation  necrosis  due  to  the  virulent  action 
of  bacilli  on  the  liver  cells;  this  has  been  studied  experimentally  by  Pilliet 
and  is  the  same  as  that  described  by  Hanot  in  other  infective  disorders. 

*  Anderson,  T.  L.:  The  Australasian  Medical  Gazette,  March  20,  1S99,  p.  93. 
t  Annals  of  Rurgery,  part  cxxxiii,  p.  98. 
j  Medical  News,  April  16,  1904,  p.  727. 
§  Mackenzie,  H.  W.  G.:  Trans.  Path.  Soc,  vol.  xli,  p.  156. 
!|  Waring,  H.  J.:  Diseases  of  the  Liver,  Gall-bladder,  etc.,  p.  108. 
**  Mayo  Robson:  Trans.  Clinic.  Soc,  vol.  xx,  p.  83. 


TUBERCULOSIS  OF  THE  LIVER  AND  BILE-DUCTS.  345 

2.  Fatty  degeneration.  The  fatty  liver  met  with  in  piihiionar}'  tuber- 
culosis is  well  known.  It  is  described  and  discussed  under  Fatty  Change 
in  the  Liver,  page  423. 

3.  Lardaceous  change  is  not  uncommon  in  advanced  cases  where 
there  has  been  long-continued  suppuration.  This  change  is  due  not  to 
the  tuberculous  toxine,  but  in  all  probability  to  toxines  derived  from 
secondary  infection  of  tuberculous  abscesses  or  vomicse  with  pj^ogenetic 
cocci. 

TUBERCULOSIS   AND   CIRRHOSIS. 

As  has  been  already  pointed  out,  portal  cirrhosis  is  frequently  com- 
plicated by  tuberculosis.  It  has,  however,  been  thought  that  tubercu- 
losis may  set  up  hepatic  cirrhosis;  in  dealing  with  this  question  it  will 
be  clearer  to  consider  it  under  two  heads : 

(A)  Cirrhosis  of  the  liver  associated  with  tuberculosis  of  the  liver. 

(B)  Cirrhosis  of  the  liver  associated  with  tubercle  elsewhere,  but  not 
in  the  liver. 

(A)  Cirrhosis  Associated  with  Tuberculosis  of  the  Liver.— h\  a  patient  with  latent 
cirrhosis  of  the  liver  generaUsed  tuberculosis  may  of  course  arise,  and  miliary  tuber- 
cles develop  in  the  liver  in  common  with  the  other  viscera  of  the  body.  Tubercle 
bacilli  may  also  be  carried  to  a  cirrhotic  liver  from  the  intestines.  In  children 
with  nutmeg  livers  from  backward  pressure  in  heart  disease  secondary  infection  of 
the  portal  spaces  with  tuberculosis  has  been  known  to  supervene.  The  amount  of 
fibrosis  is  not  great  and  the  condition  is  essentially  a  complication  of  chronic  venous 
engorgement  of  the  liver;  it  is  referred  to  under  the  name  of  "  cardio-tuberculous 
cirrhosis"  (p.  101).  A  large  fatty  and  cirrhotic  liver  containing  miliary  tubercle 
is  sometimes  seen.  The  two  processes  of  hepatic  cirrhosis  and  tuberculosis  are 
probably  independent  of  each  other,  but  are  both  disposed  to  by  the  same  factors, 
viz.,  alcoholism. 

Hanot  and  Gilbert  *  describe  a  large  fatty  liver  with  small-cell  infiltration  and 
fibrous  hyperplasia  of  the  portal  spaces  and  miliary  tubercles  as  a  morbid  entity, 
due  to  tuberculosis,  under  the  names  "hypertrophic  fatty  tuberculous  hepatitis" 
or  "hypertrophic  fatty  cirrhosis."  Clinically  there  is  enlargement  of  the  liver, 
slight  jaundice,  and  a  little  ascites,  the  disease  running  a  rapid  course  in  about  six 
weeks.  These  authors  further  describe  two  less  acute  forms  of  tuberculous  cirrhosis: 
(a)  Without  any  enlargement  of  the  liver,  and  (6)  with  more  fibrosis  than  in  the 
previous  form,  but  with  similar  fatty  change  and  tuberculous  infiltration.  The 
two  latter  forms  only  differ  in  the  fact  that  one  shows  marked  nodules,  like  those 
seen  in  cirrhosis  with  adenoma.  Tliere  is  no  doubt  that  these  forms  occur,  but  I 
believe  that,  generally  speaking,  the  cirrhotic  changes  are  not  due  to  the  tuber- 
culosis. Around  tuberculous  masses  in  the  liver  substance  there  is  local  fibrosis 
which  sometimes  spreads  diffusely  into  the  surrounding  liver  tissue. 

On  the  other  hand,  it  is  quite  reasonable  to  believe  that  tubercle  bacilli  might, 
under  certain  conditions,  such  as  high  resistance  of  the  liver  or  a  low  degree  of 
microbic  virulence,  give  rise  to  fibrosis  in  the  liver  just  as  in  the  lungs.  This  does 
not  very  often  happen  in  man,  since  if  the  resistance  of  the  liver  is  good  or  the 
vitality  of  the  bacilli  feeble,  the  latter  would  probably  be  destroyed  outright.  Still 
there  are  experimental  grounds  for  believing  that  tubercle  bacilli  may  under  some 
conditions  have  a  sclerogenic  effect  on  the  liver.  Hanot  and  Gilbert  t  fovmd  that 
in  guinea-pigs  the  bacilli  of  avian  tuberculosis  produced  a  markedly  cirrhotic 
liver  with  deep  scars,  while  tubercle  bacilli  from  man  induced  fatty  change  or 
coagulation  necrosis.  (Pilliet.J)  A  small  deep]}'-  scarred  liver  with  lobulation  and 
cicatrices  like  that  of  acquired  syphilis  has  been  found  by  Hanot  to  be  associated 
with  scattered  miliary  tubercles  m  the  substance  of  the  organ.  It  resembles,  in 
fact,  the  lesion  produced  experimentally  in  guinea-pigs  by  avian  tubercle  bacilli. 

*  Hanot  and  Gilbert:  Archiv.  gdn^ral.  de  M(5d.,  tome  clxi^^,  p.  513. 
t  Hanot  and  Gilbert:  Soc.  de  biolog.,  Jan.  30,  1892. 
%  Pilliet:  Thise  de  Paris,  1891. 


346  DISEASES    OF   THE    LIVER. 

The  following  case,  recorded  by  Collet  and  Gallavardin,*  may  perhaps  be  re- 
garded as  an  example  of  cirrhosis  due  to  tuberculosis.  In  a  woman  aged  sixty  in 
whom  the  spleen  (4J  pounds)  showed  massive  tuberculosis  the  liver  was  greatly 
enlarged  and  showed  small  caseous  tubercles  in  connexion  with  the  portal  spaces 
and  a  diffuse  and  rather  delicate  fibrosis.  The  hepatic  changes  were  regarded  as 
secondary  to  those  of  the  spleen,  and  might  be  considered  as  an  exainple  of  cir- 
rhosis of  splenic  origin.      {Vide  p.  189.) 

{B)  Cirrhosis  Associated  with  Tuberculosis  Elseivhere,  hut  not  in  the  Liver. — This 
association  of  hepatic  cirrhosis  and  tuberculosis  elsewhere  in  the  body  is  a  common 
one;  in  most  cases  where  the  tuberculous  process  is  active  it  has  developed  sub- 
sequently to  the  cirrhosis  of  the  liver.  In  other  instances  there  may  be  obsolete 
and  latent  tubercle  of  old  date  and  independent  cirrhosis  of  the  liver,  which  are 
only  discovered  at  the  autopsy.  In  a  certain  number  of  cases  old  tuberculous 
lesions  in  the  lungs  are  lighted  up  and  make  rapid  progress  in  the  course  of  alcoholic 
cirrhosis. 

Nodular  cirrhosis  is  sometimes  found  in  fatal  cases  of  pulmonary  tuberculosis. 
Toxines  generated  in  the  lungs  may  lead  to  extensive  fatty  change  in  the  proliferated 
liver  cells  forming  the  adenomatous  projections  in  the  cirrhotic  liver.  The  appear- 
ance thus  produced  may  imitate  very  closely  that  of  multiple  nodules  of  growth. 
It  is  conceivable  that  tuberculous  lesions  in  other  parts  of  the  body  may,  by  the 
production  of  chemical  poisons,  induce  cirrhosis  of  the  liver  without  any  tubercu- 
losis of  that  organ.  Thus,  in  cases  of  pulmonary  tuberculosis,  in  which  streptococcal 
infection  of  cavities  is  very  common,  toxines  may  be  absorbed  from  the  suppurat- 
ing surfaces  and  carried  to  the  liver  by  the  general  circulation.  In  most  cases  of 
septic  absorption  from  the  lungs  fatty  degeneration  in  the  liver  without  any 
fibroses  results,  but  in  very  chronic  cases  it  is  conceivable  that  cirrhosis  might  be 
brought  about.  Again,  expectoration  when  swallowed  may  not  only  be  the  source 
of  toxic  bodies,  which  may  subsequently  be  carried  to  the  liver  by  the  portal  vein, 
but  may  set  up  gastro-enteritis  and  follicular  ulceration  of  the  intestines,  which  is 
not  necessarily  tuberculous,  and  thus  give  rise  to  dyspeptic  cirrhosis  of  the  liver. 
Mouisset  and  Bonnamour,t  however,  believe  that  cirrhosis  in  tuberculous  patients 
is  nearly  always  due  to  concomitant  alcoholism. 

Hanot  $  described  lobulation  of  the  liver  in  7  cases  of  chronic  tuberculosis  and 
believed  that  fibrosis  was  due  to  the  tuberculous  toxine.  I  have  notes  of  one  such 
liver  in  a  man  with  chronic  phthisis  in  whom  there  was  no  history  of  syphihs  and 
no  gummata  in  the  body;  there  was,  however,  a  scar  on  the  penis,  and  there  can 
be  little  doubt  that  it  was  in  reality  syphilis.  Possibly  some  of  Hanot's  cases  may 
have  been  examples  of  tardive  hereditary  syphilitic  disease  of  the  liver  with  secondary 
tuberculosis.  At  any  rate,  it  must  be  very  rare,  indeed,  to  find  such  a  condi- 
tion in  tubercle  pure  and  simple. 

In  conclusion,  although  from  a  pathological  point  of  view  tubercu- 
losis, both  in  the  liver  and  when  confined  to  some  other  part  of  the  body, 
may  under  certain  circumstances  set  up  some  fibrosis  in  the  liver,  there 
is  no  reason  to  think  that  genuine  cirrhosis  of  clinical  importance  is 
primarily  produced  in  this  way.  Tuberculosis,  whether  in  the  liver  or 
elsewhere,  may  produce  degenerative  changes  in  the  liver  cells,  and  when 
there  is  pre-existing  cirrhosis,  considerable  damage  may  be  done  in  this 
way. 

*  Collet  et  Gallavardin:  Archiv  de  Med.,  experiment,  et  d'Anat.  path., Mar.,  1901. 

t  Eev.  de  Med.,  1904,  p.  337. 

X  Hanot:  Gaz.  des  Hop.,  1893,  p.  902. 


SYPHILITIC  DISEASE  OF  THE  LIVER. 

History. — That  syphilis  affects  the  liver  is  a  very  ancient  idea;  according  to 
Frerichs,*  as  old  as  the  history  of  syphilis  itself.  But  the  earlier  views  naturally 
differed  from  those  of  the  present  day.  Fallopius  f  in  the  sixteenth  century  con- 
sidered that  the  liver  was  primarily  affected  in  syphilis  and  so  corrupted  the  humours 
of  the  body  that  ulcers  occurred  on  the  genitals.  Subsequently  Morgagni  opposed 
the  view  that  the  liver  was  affected  in  syphilis.  Later  Van  Swieten,  Portal,  and 
Ricord  described  syphilitic  lesions  of  the  liver,  but  very  little  attention  was  directed 
to  the  visceral  lesions  of  syphiUs  until  Dittrich  %  in  1849,  and  Sir  S.  Willcs  §  in  this 
country,  described  gummata  in  the  internal  organs.  The  distinction  between 
gummata  and  nodules  of  malignant  growiih  dates  from  this  time ;  previous  to  Wilks' 
observations  gummata  were  regarded  as  cancerous  nodules  or  even  as  evidence  of 
healing  of  malignant  growths. 

The  subject  of  syphilitic  disease  of  the  Hver  will  be  considered  under 
the  two  main  heads  of  (i)  the  accjuired  and  (ii)  the  congenital  or  hereditary 
forms. 

HEPATIC   LESIONS  IN  ACQUIRED  SYPHILIS. 

The  hepatic  changes  due  to  acquired  sy]3hilis  will  be  considered  under 
the  heads  of  (i)  the  secondary  and  (ii)  the  tertiary  manifestations,  while 
the  briefest  reference  only  will  be  made  to  the  possibility  that  remote — 
parasyphilitic — changes  in  the  liver  may  be  referred  to  syphilitic  in- 
fection. 

THE  SECONDARY  MANIFESTATIONS  OF  SYPHILIS  IN  THE  LIVER. 

The  diffuse  pericellular  cirrhosis  of  congenital  syphilis  is  generally 
regarded  as  being  pathognomonic  and  as  not  occurring  in  the  acquired 
form.  Whether  pericellular  cirrhosis  is  so  entirely  limited  to  the  con- 
genital form  may  be  very  seriously  questioned.  That  it  is  seldom  found 
except  in  that  disease  is  true  enough,  but  it  must  be  remembered  that 
congenital  syphilis  is  much  more  often  fatal  than  the  acquired  disease 
in  any  stage,  so  that  opportunities  for  examining  the  liver  in  the  secondary 
stage  of  acquired  syiDhilis  only  occur  in  rare  and  accidental  instances, 
and  that  hepatic  manifestations  of  acquired  sj^hilis  are  less  frequent 
than  those  of  the  congenital. affection. 

Sir  Hermann  Weber  ||  many  years  ago  described  a  case  of  acquired  syphilis 
in  a  man  aged  twenty,  in  whose  liver  the  lesions  appear  to  have  been  pericellular. 
I  have  examined  a  few  cases  in  which  the  liver  of  syphilitic  subjects  has  shown 
diffuse  pericellular  cirrhosis  without  there  being  any  gummata  present.  In  other 
cases  pericellular  cirrhosis  may  be  seen  at  a  considerable  distance  from  gummata. 

Since  then  few  cases  are  examined  during  the  secondary  stage,  and 
since  it  is  a  lesion  from  which  recovery  is  quite  possible,  it  is  not  unlikely 

*  Frerichs:  Diseases  of  Liver  (Transl.  New  Sydenham  Soc),  vol.  ii,  p.  150. 
+  Fallopiiis:  Tract,  de  Morbo  Gallico. 

X  Dittrich:  Prager  Vicrteljahresschrift,  1849,  S.  1 ;    1S.50,  S.  33. 
§  Wilks,  S.:  Trans.  Path.  Soc,  vol.  viii,  p.  240. 
II  Weber:  Trans.  Path.  Soc,  vol.  xvii,  p.  152. 

347 


348  DISEASES    OF   THE    LIVER. 

a  priori  that  the  condition  occurs  temporarily  and  usually  passes  away. 
As  an  argument  in  support  of  this  it  ma}'^  be  pointed  out  that  in  those 
rare  cases  of  acute  yellow  atrophy  supervening  after  s}^ohilis  the  micro- 
scopic appearances  are  at  least  compatible  -^dth  the  view  that  there 
has  been  pericellular  cirrhosis  and  that  excessive  necrosis  of  the  hepatic 
cells  has  supers^enecl. 

In  a  man  aged  forty-seven,  who  died  of  cerebral  hsemorrhage  and  had  gummata 
in  his  testes,  the  hver  showed  very  diffuse  intercellular  fibrosis  which  varied  in 
different  areas,  but  was  compatible  with  the  views  that  there  had  been  partial  acute 
atrophy  with  recover}^,  or  that  it  was  intercellular  cirrhosis.  In  describing  this 
specimen  Dr.  Parkes  Weber,^''  who  kindly  showed  the  slides  to  me,  drew  attention 
to  the  fact  that  the  situation  of  the  fibrosis,  viz.,  around  the  capillaries  of  the  hepatic 
artery,  resembled  that  of  lardaceous  change  and  pointed  to  the  poison  being  carried 
by  the  hepatic  artery. 

The  views  as  to  an  anatomical  substratum  of  the  jaundice  occurring 
during  the  exanthematous  stage  vdll  be  referred  to  directly.  Finger,! 
and  AdamiJ  suggest  that  it  is  a  generalised  toxic  disturbance  of  the  organ, 
which  may  or  may  not  lead  to  the  generalised  intercellular  cirrhosis 
characteristic  of  congenital  syphilis.  If  this  toxic  disturbance  is  ex- 
cessive, necrosis  of  the  hepatic  cells  may  follow  and  give  rise  to  icterus 
gravis.  {Vide  Acute  Yellow  Atrophy  in  the  Course  of  S3T3hihs.)  In 
exceptional  instances  gummatous  lesions  have  been  found  in  the  hver 
during  the  period  of  secondary  manifestation.     {Vide  p.  358.) 

To  sum  up,  in  acquired  syphilis  the  Uver  may  be  affected  in  the 
secondar}^  stage  so  as  to  give  rise  to  jaundice,  either  innocent  or  malignant; 
while  anatomical  changes  allied  to  or  resulting  in  pericellular  cirrhosis 
and  underlying  the  clinical  manifestations  must  not  be  forgotten. 

Jaundice  in  the  Secondary  Stage  of  Syphilis. — Jaundice  may  occur 
early  in  the  secondary  stage  at  the  same  time  as  the  cutaneous  roseola. 
Gubler  §  in  1853  first  drew  attention  to  this  association  in  a  memoir 
containing  fiA^e  cases.  It  is,  however,  uncommon,  and  more  so  in  Ger- 
many than  in  France;  in  15,799  cases  of  syphihs  S.  Werner  ||  met  with 
jaundice  in  57,  or  only  0.37  per  cent.  In  1868  Lancereaux  **  collected 
21  cases,  and  in  1900  Laschtt  referred  to  49  cases,  almost  aU  from  French 
literature.  These  figures  would  suggest  that  jaundice  during  the  rose- 
olous  stage  is  far  rarer  than  it  is  in  realit}'. 

It  must  be  admitted  that  there  are  more  theories  to  explain  the  oc- 
currence of  jaundice  in  the  early  stages  of  sj^liilis  than  facts  to  appeal 
to.  Inasmuch  as  it  coincides  with  the  exanthem,  it  was  first  thought 
that  it  is  due  to  a  somewhat  similar  condition,  in  the  mucous  mem- 
brane of  the  bile-duct  (Gubler);  or,  in  other  words,  a  specific  catarrhal 
cholangitis.     A  condyloma  of  the  bile-duct  has  also  been  suggested. 

*  Weber,  F.  P.:  Brit.  Med.  Journ.,  1899,  vol.  i,  p.  72S. 

t  Finger:  Die  Syphilis  u.  d.  vener.  Krankh.,  1892. 

X  Adami:  New  York  Med.  Journ.,  April  22,  1899. 

§  Gubler:  Mem.  Soc.  biolog.,  vol.  v,  p.  235,  185.3. 

II  Werner,  S.:  Miinchen.  med.  AVochen.,  1897. 
**  Lancereaux:  Svphilis,  vol.  i,  p.  182.     In  New  Svdenham  Soc.  Library. 
tt  Lasch,  O.:  Berlin,  khn.  Wochen.,  1894,  S.  904.    "Selected  essays,  New  Syden- 
ham Soc.  Library,  1900,  p.  145. 


SYPHILITIC    DISEASE    OF   THE    LIVER.  349 

According  to  another  view,  pressure  is  exerted  on  the  ducts  by  syphiUtic 
enlargement  of  the  lymphatic  glands  in  the  portal  fissure;  in  favour  of 
this  it  may  be  mentioned  that  out  of  "Werner's  57  clinical  cases  of  sj'phil- 
itic  jaundice  there  was  marked  enlargement  of  the  superficial  Ijaiiphatic 
glands  in  41. 

In  Talamon's  *  case  of  acute  yellow  atrophy  in  a  girl  aged  seventeen  with  a 
secondary  cutaneous  eruption  and  other  signs  of  syphilis  the  glands  in  the  portal 
fissure  were  enlarged  but  did  not  compress  the  common  bile-duct. 

It  is  probably  not  simply  catarrhal  jaundice  occurring  in  a  person 
who  has  recently  contracted  s}']3hilis,  since  the  successful  treatment  is 
that  of  syphilis  and  not  of  catarrhal  jaundice.  The  most  probable  ex- 
planation of  the  jaundice  is  a  catarrhal  condition  of  the  small  intra- 
hepatic bile-ducts  which  is  merely  part  of  a  general  sj'jDhilitic  hepatitis. 
The  change  in  the  liver  is  probably  a  pericellular  infiltration  with  small 
round  cells,  like  that  seen  in  hereditary  syphilis.  When  this  change  is 
excessive,  it  may  nm  on  into  acute  yellow  atrophy.  There  is  no  proof 
that  the  jaundice  is  due  to  the  administration  of  mercury,  for  in  onl}^ 
4  of  49  cases  of  benign  jaundice  occurring  in  the  early  stage  of  S3q3hilis, 
collected  by  Lasch,  had  mercury  been  given  before  the  icterus  appeared. 

Sex. — It  is  seen  in  about  an  equal  number  of  men  and  women;  in 
Lasch's  49  cases  25  were  men  and  24  women,  but  as  more  cases  of  syphilis 
are  seen  in  men,  syphilitic  jaundice  is  proportionately  more  frequent  in 
women. 

Its  onset  is  usually  sudden  without  any  apparent  cause  and  is  not 
accompanied  by  any  special  disturbance,  such  as  is  seen  in  cholelithiasis 
or  catarrhal  jaundice.  It  comes  on  simultaneously  with  the  cutaneous 
roseola  and  may  coincide  with  a  particularly  copious  eruption.  It  may 
appear  as  soon  as  five  weeks  after  infection,  or  later  up  to  the  sixth 
month. 

Clinical  Features. — The  jaundice  is  well  marked,  and  unless  treated 
with  mercury,  tends  to  become  chronic;  thus  it  may  last  three  months 
if  treated  with  the  ordinary  remedies  for  catarrhal  jaundice.  The  aspect 
of  the  patient  with  a  jaundiced  syphilitic  eruption  is  very  characteristic 
and  somewhat  repulsive.  There  is  an  absence  of  gastro-intestinal  s^ymp- 
toms  and  the  appetite  is  well  preserved,  though  distaste  for  fatty  food 
may  be  experienced.  The  liver  is  usually  slightly  enlarged  and  the 
spleen  may  be  palpable. 

Diagnosis. — ^The  important  point  is  to  recognize  that  in  a  patient 
with  recent  syphilis  jaundice  may  be  a  specific  manifestation  and  not 
an  independent  attack  of  catarrhal  jaundice.  From  the  presence  of 
the  roseola  and  enlarged  glands  the  recognition  of  syphilis  is  easy. 

The  treatment  is  that  of  secondary  syphilis;  it  is  noteworthy  that  the 
ordinary  treatment  of  catarrhal  jaundice  is  without  any  good  result. 
If  the  mercurial  treatment  is  prematurely  discontinued,  jaundice  may 
recur. 

The  'prognosis  is  good,  as  a  rule,  l)ut  in  some  rare  cases  the  jaimdice 

*  Talamon:  La  Medecine  Moderne,  Feb.  13,  1897. 


350  DISEASES    OF   THE    LIVER. 

passes  into  acute  yellow  atrophy.  There  are  probably  intermediate 
grades  between  the  benign  jaundice  and  the  acute  yellow  atrophy  occur- 
ring in  the  early  stage  of  syphilis. 

THE  TERTIARY  LESIONS  OF  SYPHILIS  IN  THE  LIVER. 

The  specific  tertiary  lesions  in  the  liver  are  polymorphic  and  include 
gummata,  gummatous  infiltration,  cicatrices,  and  a  combination  of 
gummata  and  cicatrices  (sclero-gummatous  form).  Lardaceous  disease, 
which  may  be  considered  as  a  parasyphilitic  lesion,  is  often  combined 
with  gummata  and  with  cicatrices. 

The  manifestations  of  tertiary  syphilis  in  the  liver  may  be  divided 
into  (a)  those  that  are  progressive  and  (b)  those  that  are  merely  the 
relics  of  past  syphilitic  activity.  In  other  words  (a)  the  late  secondary 
and  tertiary  lesions  seen  in  the  gummata  and  gummatous  infiltration 
of  the  organ  and  (b)  the  cicatrices,  calcified  remains,  and  deforixdties 
left  behind  by  the  first-named  lesions  are  both  included  under  the  tertiary 
manifestations.  Lardaceous  disease,  which  is  such  a  well-known  sequela 
of  syphilis,  is  dealt  with  elsewhere.     {Vide  p.  430.) 

GUMMA. 

The  word  gumma  was  employed  in  its  present  sense  by  Fallopius  in  the  sixteenth 
century  in  his  Tractatus  de  Morbo  Gallico.*  But  it  was  not  generally  used  until 
comparatively  recent  times.  In  his  work  on  the  liver  in  1857  Budd  t  gave  a  careful 
description  of  gummata  under  the  name  of  "encysted  knotty  tumours  of  the 
liver,"  and  separated  them  from  cancerous  growths,  with  which  they  had  been 
generally  confounded,  but  did  not  recognise  their  syphilitic  origin  or  speak  of  them 
as  gummata. 

Method  of  Formation  of  Gummata. — In  the  early  or  secondary 
stage  the  future  gumma  is  a  mass  of  syphilitic  granulation  tissue  of  a 
pink  colour,  sharply  localised,  and  contrasting  with  the  healthy  liver 
substance.  At  this  stage  it  is  better  to  speak  of  it  as  a  syphiloma,  since 
the  term  gumma  describes  a  central  mass  of  caseous  material  surrounded 
by  a  fibrous  capsule.  After  a  time  necrosis  occurs  in  the  centre  of  the 
syphiloma;  this  is  partly  due  to  syphilitic  endarteritis  in  the  neighbour- 
hood whereby  the  blood-supply  is  cut  off,  and  probably  in  part  to  an 
increase  in  amount  or  concentration  of  the  sy[3hilitic  poison  which  kills  the 
granulation  tissue  of  the  sj^hiloma.  At  this  stage  there  is  a  yellowish- 
white  centre  surrounded  by  pink  granulation  tissue.  Later  the  syiDhiloma 
of  the  secondary  stage  is  transformed  into  a  caseous  mass  surrounded 
by  a  fibrous  capsule,  a  condition  resembling  a  caseous  tubercle  of  some 
duration.  By  the  union  of  several  small  gummata  a  large  gummatous 
area  may  result. 

Structure,  etc, — A  well-marked  gumma  consists  of  a  firm,  yellowish- 
white  mass,  not  unlike  cheese,  surrounded  by  a  fibrous  capsule  which 
spreads  out  for  a  short  distance  into  the  surrounding  liver  tissue.  In  rare 
instances  the  caseous  part  of  gummata  is  yellow  from  bile-staining. 

*  Fagge  and  Pye  Smith:  (Ed.  i,  1S86),  vol.  i,  p.  123. 
t  Budd:  Diseases  of  the  Liver,  p.  416,  ed.  iii,  1857. 


SYPHILITIC    DISEASE   OF  THE    LIVER. 


351 


(Marie.)*  There  are  thus  three  zones  in  a  gumma:  (1)  The  central 
area  of  necrosed  or  necrosing  granulation  tissue;  (2)  the  surrounding 
fibrous  capsule;  (3)  the  invasion  of  the  surrounding  parts  of  the  liver  by 
interstitial  fibrosis. 

Old  gummata  consist  of  the  central  caseous  portion  and  the  well- 


Upper 

lobe  of 
lung 


Lower 

lobe  of 

lung 


Fibro-gummatous 

mass     replacing 

the  greater  part 

of  the  liver,  part  of 

the  diaphragm, 

and  the  lower 

part  of  the  right 

lung 


i  Diaphragm 

la 


Anterior 
part  of 
a*  ';'/)         right  lobe 
''  of  liver 


^'^^l§ 


Fig.  41.— a  Large   Gumma    of   the  Liver  Extending  through  the  Diaphragm   into   the 

Lower  Lobe  of  the  Right  Lung. 

From  a  specimen  (Series  ix,  18.3  g)  in  St.  George's  Hospital  Museum. t 

formed  fibrous  capsule,  there  being  no  advancing  margin.  In  recent 
gummata  where  the  capsule  is  indefinite  there  is,  on  the  other  hand, 
well-marked  infiltration  of  the  liver  tissue,  the  lesion  being  progressive. 

*  R.  Marie:  Bull.  Soc.  Anat.  Paris,  1901,  p.  62.5. 

t  I  am  indebted  to  Professor  S.  Delepine  for  this  l)lock,  which  appeared  in  the 
Transactions  of  the  Pathological  Society  of  London,  vol.  xlii,  p.  151. 


352  DISEASES   OF  THE   LIVER. 

The  amount  of  fibrous  tissue  enclosing  a  gumma  varies;  with  large 
and  advancing  gummata  it  may  be  slight  and  indistinct,  with  old  gum- 
mata  it  is  firm  and  dense.  As  it  contracts  it  presses  on  the  caseous 
centre,  and  at  the  same  time,  if  near  the  capsule  of  the  liver,  produces 
thickening,  puckering,  and  cicatrices  on  the  surface  of  the  organ.  Peri- 
hepatitis and  thickening  of  the  capsule  are  thus  produced;  in  rare  in- 
stances, of  which  an  example  is  given  on  page  168,  there  may  be 
chronic  universal  perihepatitis.  Adhesions  frequently  form  between  the 
liver  and  adjacent  organs,  the  diaphragm  and  the  anterior  abdominal 
wall;  in  rare  instances  gummatous  change  may  behave  like  malignant 
disease  and  invade  the  anterior  abdominal  wall  or  the  diaphragm. 

In  a  specimen  (series  ix,  183  g)  in  St.  George's  Hospital  Museum  an  immense 
gumma  of  the  right  lobe  of  the  liver  passed  through  the  diaphragm  and  extensively 
infiltrated  the  lower  lobe  of  the  right  lung  (Del6pine  and  Sisley*).  {Vide  Fig.  41.) 
In  a  case  of  late  hereditary  syphilis  with  the  usual  tertiary  changes,  recorded  by 
Post,t  gummatous  inflammation  extended  into  the  anterior  abdominal  walls  and 
produced  a  definite  tumor. 

The  naked-eye  appearances  of  caseous  gummata  may  sometimes 
closely  resemble  those  of  certain  cases  of  primary  massive  carcinoma 
and  multiple  carcinomatous  growths  in  the  liver. 

Gouget  J  has  described  a  case  in  which  columnar-celled  carcinomatous  growths 
were  at  first  thought  to  be  gummata;  I  have  seen  similar  appearances  on  several 
occasions.  As  a  rare  coincidence  secondary  growths  may  occur  in  a  liver  containing 
gummata.  Microscopical  examination  is  necessary  before  one  can  be  certain  that 
both  gummata  and  secondary  new-growths  are  present.  In  1891  I  examined  such 
a  case;  a  man  had  primary  carcinoma  of  the  colon  with  small  secondary  growths 
in  a  scarred  and  gummatous  liver.     The  left  testis  also  contained  gummata. 

The  microscopic  appearances  of  a  gumma  present  differences  according 
to  the  age  of  the  formation.  In  the  stage  when  caseation  has  begun 
the  central  necrotic  part,  which  to  the  naked  eye  appears  white,  is  fibrillar 
or  granular,  shows  a  few  nuclei  but  is  otherwise  structureless,  and  does 
not  take  the  stain  properly;  around  it  there  is  granulation  tissue,  which 
occasionally  contains  giant  cells.  These  giant  cells,  which  are  rare  in 
gummata,  are  formed  by  the  union  of  pre-existing  young  connective- 
tissue  cells,  probably  in  order  to  absorb  the  caseous  debris.  It  is  note- 
worthy that  the  giant  cells  seen  in  gummata  are  not  so  large  or 
so  well  developed  as  those  seen  in  tuberculosis.  Necrosis  and  caseation 
may  be  seen  to  be  extending  into  this  surrounding  granulation  tissue  in 
young  or  recent  gummata,  while  in  older  ones  organization  is  going  on 
and  a  capsule  of  connective  tissue  is  formed  around  the  caseous  mass. 
The  fibrous  capsule  contains  elastic  fibres  and  if  stained  with  osmic  acid 
shows  globules  of  fat. 

The  granulation  tissue  spreads  into  the  surrounding  liver  tissue  for 
a  short  distance,  so  that  there  is  intercellular  cirrhosis  in  the  immediate 
neighbourhood  of  the  gumma.  Later  groups  of  liver  cells  become  sur- 
rounded by  bands  of  young  connective  tissue,  and  in  recent  cases  the 
solid  columns  of  small  cubical  cells  which  stain  deeply  are  prominent 

*  Del^pine  and  Sisley:  Trans.  Path.  Soc,  vol.  xlii,  p.  141. 
t  Post:  Boston  City  Hospital  Reports,  1898,  p.  233. 
j  Gouget:  Bull.  Soc.  Anat.  Paris,  1898,  p.  605. 


SYPHILITIC    DISEASE    OF   THE    LIVER. 


353 


objects  at  the  margin  of  a  gumma.     These   pseudobile    canaHcuU  are 
very  probably  due  to  compensatory  hyperjolasia  of  the  hver  cells.     The 


Fig.  42. — Recent  Gumm.^  of  Liver.     X  30. 
A,  fibrous  capsule;    b,  syphilitic  granulation  tissue;     c,  caseating  granulation  tissue;  d,  caseous 


Fig.  43. — Old  GuiMma  of  I  iver. 
The  lighter  part  is  the  caseous  material;  it  is  .surrounded  by  a  dense  fibrous  capsule  which  ex- 
tends into  the  surrounding  liver  substance.      (Photomicrograph  by  S.  G.  Penny,  Esq.) 


liver  cells  near  the  margin  of  a  gumma  are  flattened  from  pressure  and 
may  be  spindle  shaped. 
23 


354 


DISEASES    OF   THE    LIVER. 


The  small  arteries  at  the  margin  of  a  gumma  show  well-marked  end- 
arteritis obliterans.  There  is  sometimes  lardaceous  change  immediately 
around  the  gumma.  In  old  gummata,  where  the  lesion  is  no  longer  ad- 
vancing, the  fibrous  capsule  is  dense  and  well  formed  and  there  is  no 
small-cell  infiltration  around  the  gumma,  while  giant  cehs  are  not  seen. 
Particles  of  calcareous  salts  may  be  seen  in  the  caseous  material  or  in 
the  surrounding  fibrous  tissue.  The  caseous  material  and  the  prolif- 
erating zone  around  it  contain  a  good  deal  of  fat  and  thus  differ  from 
tuberculous  caseation,  in  which  fatty  change  is  slightly  marked,  the 
degenerative  change  being  of  a  hyaline  nature.  (Gaylord  and  Aschoff  *.) 
Retrogressive  Changes  in  Gummata. — The  caseous  material  may 
diixiinish  in  amount  from  the  circumferential  pressure  exerted  upon  it  by 

the  contraction  of  its  fibrous  capsule; 
at  the  same  time  it  becomes  drier  from 
absorption  of  fluid.  Calcification  may 
then  occur.  A  certain  amount  of  cal- 
careous change  is  not  very  rare,  but  it 
is  usually  only  in  small  particles  which 
do  not  offer  any  real  resistance  to  the 
knife.  In  these  cases  the  presence  of 
calcareous  matter  is  best  seen  on 
making  microscopic  sections  of  the 
gumm.a.  In  other  instances  calcifica- 
tion is  best  seen  in  the  capsule  of  the 
gumma.  (Vide  Cambridge  Museum, 
Nos.  504,  505.)  In  exceptional  cases 
calcification  is  very  prominent. 


Dr.  Fooks  kindly  sent  me  the  liver  of  a 
woman  aged  fifty-nine  who  died  in  the  Brent- 
ford Union  Asylum,  Isleworth,  in  April,  1898. 
It  weighed  31  §  ounces  and  was  two-thirds 
the  natural  size.  The  surface  was  scarred 
and  puckered  all  over,  especially  on  the 
right  side.  These  cicatrices  were  all  calci- 
fied, and  on  cutting  into  the  organ  several 
calcareous  masses  the  size  of  a  walnut  were 
found. 

Targett  f  showed  before  the  Pathological 
Society  a  specimen  of  diffuse  calcification  of 
the  liver  which  probably  supervened  on  gum- 
matous change.     A  slice  of  this  liver  is  in  St.  George's  Hospital  Museum.     (Vide 
Fig.  44.) 


Fig.  44. — Section  of  Liver  Showing 
Diffuse  Calcification  Probably  Sub- 
sequent TO  Gummatous  Infiltra- 
tion. 

St.  George's  Hospital  Museum,  Series  ix. 
172  B.   (Drawn  by  Dr.  E.  A.  Wilson.) 


Calcification  of  the  liver  may  in  very  rare  instances  occur  independently  of 
syphilis  {vide  p.  437)  and  is  met  with  in  animals.  There  is  a  dried  section  of  a  horse's 
liver  showing  infiltration  with  carbonate  and  phosphate  of  Ume  in  St.  Bartholomew's 
Hospital  Museum  (No.  2239). 

Occasionally  gummata  may  soften  down ;  this  may  very  probably  be 
the  result  of  treatment  with  iodides  and  be  a  stage  in  the  process  of 
absorjotion.  It  may  also  be  due  to  septic  infection,  and  when  it  occurs 
in  a  large  gumma  the  condition  is  practically  a  chronic  abscess. 

*  Gaylord  and  Aschoff:  Pathological  Histology,  p.  95. 
t  Targett:  Trans.  Path.  Soc,  vol.  xl,  p.  123. 


SYPHILITIC    DISEASE    OF   THE    LIVER.  355 

Moxon*  described  a  large  gumma,  which  softened  down  and  communicated  with 
a  bile-duct.  In  former  days  gummata  have  actually  been  described  as  "retiring 
abscess  of  the  liver"  {vide  Cambridge  Museum,  No.  503),  and  were  supposed  to  be 
due  to  concentration  and  solidification  of  material  originally  fluid. 

Unless  the  gumma  is  very  large,  it  slowly  undergoes  absorption. 
This  is  carried  on  by  phagocytosis  and  depends  on  the  neighbouring 
blood-vessels  and  lymphatics  being  permeable  and  not  obstructed  by 
S5^hilitic  changes.  The  more  the  gumma  contracts,  the  more  it  resem- 
bles the  scars  and  cicatrices  which  are  in  many  "cases  the  only  remains 
of  obsolete  gummata.  This  probably  accounts  for  the  rarity  of  gummata 
in  old  persons.  The  scars  may,  however,  result  from  the  organization  of 
inflammatory  products  without  any  central  caseation  having  taken  place. 

Number  and  Striation. — Gummata  may  be  circumscribed  and  multi- 
ple, or  there  may  be  diffuse  gummatous  infiltration  of  a  large  part  of  one 
or  even  of  both  lobes.  The  right  lobe  is  much  more  often  affected  and 
thfi  anterior  surface  far  more  frequently  than  the  under  aspect.  They 
are  much  more  often  multiple;  in  86  cases  of  hepatic  gummata  collected 
by  J.  L.  Allen  t  only  11  were  single.  It  is  said  that  the  neighbourhood  of 
the  falciform  ligament  is  a  favourite  situation  for  gummata,  but  in  my  ex- 
perience I  have  not  noticed  any  such  special  localisation  of  gummata  ex- 
cept the  anterior  surface.  They  may  occur  in  any  part  and  may,  when 
present  in  an  exceptional  position,  i.  e.,  near  the  portal  fissure,  press  on 
the  main  trunks  or  branches  of  the  bile-ducts  or  portal  vein. 


SYPHILITIC    CICATRICES. 

Deep  furrows  on  the  surface  of  the  liver,  due  to  cicatricial  contraction, 
are  the  result  of  organisation  of  syphilitic  granulation  tissue.  Cicatrices 
may  be  formed  directly  from  syphilomata  or  be  the  last  stage  of  a  gumma 
which  has  undergone  absorption.  The  cicatrices  may  be  linear  or  may 
be  star-like.  The  linear  cicatrices  may  divide  a  lobe  into  a  number  of 
lobules;  the  star-like  cicatrices  are  depressed  with  well-formed  fibrous 
tissue  radiating  into  the  capsule  on  all  sides  of  it.  The  liver  may  be  so 
widely  fissured  and  lobulated  by  cicatrices  that  it  has  a  slight  resemblance 
to  the  coarse,  hobnailed  liver  of  portal  cirrhosis,  but  the  irregularity  of 
this  diffuse  syphilitic  fibrosis  or  ''syphilitic  cirrhosis,"  as  it  is  often  called, 
distinguishes  it  from  genuine  portal  cirrhosis.  Like  gurhmata,  these 
scars  are  said  to  be  frequent  in  the  neighbourhood  of  the  falciform  liga- 
ment. When  they  occur  around  the  portal  fissure,  they  may  involve 
the  portal  vein,  giving  rise  to  ascites,  or  the  bile-ducts,  thus  producing 
jaundice;  or  if  they  occur  near  the  coronary  ligament,  they  may  lead 
to  narrowing  or  obliteration  of  the  hepatic  veins  {vide  p.  49). 

Bosanquet,t  "w^^o  records  a  case  of  obliteration  of  the  inferior  vena  cava  by 
syphilitic  cicatrices  spreading  from  a  gummatous  liver,  could  not  find  any  other 
published  instances  of  syphilitic  obstruction  of  the  inferior  vena  cava. 

*  Moxon :  Trans.  Path.  Soc,  vol.  xxiii,  p.  153. 
t  J.  L.  Allen :  Unpublished  Thesis  for  M.  B.  degree,  Cambridge,  1899. 
J  Bosanquet,  W.  C:  Edinburgh  Medical  Journ.,  New  Series,  vol.  xii,  p.  250, 
Sept.,  1902. 


356  DISEASES    OF   THE    LIVER. 

The  scars  may  contain  a  central  caseous  mass,  showing  that  they  are 
receding  gummata ;  sometimes  calcification  has  commenced  in  the  caseous 
material.  The  older  the  scar,  the  denser  it  is,  and  the  more  depressed 
the  surface  of  the  liver  over  it. 

GUMMATA  AND  CICATRICES  COMBINED   (SCLERO-GUMMATOUS  FORM). 

The  contraction  of  syphilitic  cicatrices  and  gummata  may  lead  to 
great  deformity,  so  that  the  organ  is  nodular  and  irregularly  lobulated. 
Such  lobulation  must  not  be  regarded  as  persistence  of  a  congenital 
condition,  for  the  liver  is  not,  like  the  kidney,  normally  lobulated 
in  the  foetus. 

In  a  girl  aged  twenty-five  years  who  died  under -my  care  in  St.  George's  Hospital 
with  syphilitic  stenosis  of  both  bronchi  *  the  liver  (.52  ounces)  was  occupied  by 
multiple  caseous  gummata  and  was  so  extensively  scarred  that  as  many  as  16  lobes 
could  be  counted  on  its  anterior  surface. 

The  shape  of  the  liver  may  be  altered  out  of  all  recognition.  The 
relative  size  of  the  two  chief  lobes  of  the  liver  may  be  greatly  altered; 
thus,  the  left  lobe  may  be  almost  entirely  destroyed  by  fibrous  contrac- 
tion or  enlarged  from  gummatous  infiltration,  while  in  some  cases  it  may 
be  enlarged  from  hyperplasia  of  the  liver  substance  to  compensate  for 
extreme  destruction  of  the  right  lobe.  As  a  rule,  the  syphilitic  changes 
and  enlargement  are  much  more  marked  in  the  right  than  in  the  left  lobe. 

Association  of  Gummata  and  Lardaceous  Change  in  the  Liver» 
■ — As  already  pointed  out,  local  lardaceous  change  may  be  found  around 
a  gumma.  In  other  instances  gummata  may  be  found  in  a  universally 
lardaceous  liver.  In  86  cases  of  gummata  collected  by  J.  L.  Allen  the 
liver  was  lardaceous  in  12,  or  14  per  cent. 

Incidence  of  Gummata  in  Universally  Cirrhotic  Livers. — It 
might  naturally  be  supposed,  since  alcoholic  excess  and  exposure  to 
syphilitic  infection,  or,  as  Osier  puts  it,  the  worship  of  Bacchus  and 
Venus,  are  frequently  associated,  that  gummata  would  be  common  in 
universally  cirrhotic  livers.  This,  however,  is  not  the  case,  and  it  is 
remarkable  how  seldom  gummata  and  ordinary  portal  cirrhosis  coexist 
in  the  same  liver. 

In  86  cases  of  hepatic  gvimmata  collected  by  J.  L.  Allen  only  4  were  combined 
with  genuine  cirrhosis.  In  Flexner's  f  88  cases  of  hepatic  syphilis  these  conditions 
were  combined  in  9  instances. 

A  certain  amount  of  fibrosis  is  usually  present  in  the  liver-  tissue 
immediately  surrounding  a  gumma,  and  cicatrices  leading  to  scarring 
and  lobulation  of  the  organ  may  be  associated  with  gummata,  but 
genuine  multilobular  cirrhosis  is  rare. 

INCIDENCE  OF  TERTIARY  HEPATIC  LESIONS. 

Though  well  recognized  and  exhaustively  described,  the  tertiary 
hepatic  manifestations  are  by  no  means  very  common.     It  is  true  that 

*  Vide  Trans.  CUnic.  Soc,  vol.  xxxii,  p.  158. 

t  Flexner:  New  York  Med.  Journ.,  Jan.  18,  1902,  p.  101. 


SYPHILITIC    DISEASE    OF   THE    LIVER.  357 

cicatrices  of  old  gummata  are  usually  entirely  latent,  so  that  they  are 
less  frequently  detected  clinically  than  in  the  postmortem  room.  Cica- 
trices are  apparently  more  often  seen  than  gummata,  though  in  many 
instances  gummata  and  cicatrices  are  of  course  present  in  the  same  liver. 
But  even  in  the  postmortem  room  they  cannot  be  said  to  be  common. 

In  a  critical  examination  of  the  postmortem  records  of  St.  George's  Hospital, 
dealing  witli  a  period  of  forty-two  years  (from  1857  to  1898),  J.  L.  Allen  only 
found  37  cases  of  undoubted  hepatic  gummata;  during  this  same  period  there  were 
11,629  autopsies;  there  were,  in  addition,  27  other  cases  in  which  cicatrices  alone 
were  present.  In  a  period  of  thirty-five  years  during  which  there  were  5088  autop- 
sies at  the  Philadelphia  Hospital,  Flexner  *  found  that  gummata  were  present  in 
23  cases,  cicatrices  in  38,  and  in  all  88  cases  of  hepatic  syphilis,  half  this  number 
being  cases  of  diffuse  syphilitic  fibrosis. 

There  is  indeed  a  great  contrast  between  the  frequency  of  hepatic 
lesions  in  congenital  and  in  acquired  syphilis. 

Predisposing  Causes. — It  has  been  thought  that  previous  disease 
of  the  liver  or  conditions  such  as  alcoholism,  malarial  infection,  or  a 
previous  attack  of  jaundice,  would,  by  diminishing  the  resistance  of  the 
liver,  render  it  more  likely  to  be  affected.  Traumatism,  such  as  blows 
or  previous  injury  to  the  liver,  may  very  probably,  as  elsewhere  in  the 
body,  determine  the  occurrence  of  gummata  in  the  organ.  It  is  inter- 
esting to  note  that  gummata  have  been  found  in  the  pendulous  portion 
of  the  right  lobe  seen  in  the  tight-laced  or  corset  hvers  of  women.  In 
this  connexion  it  would  be  interesting  to  know  what  proportion  of  cases 
of  hepatic  gummata  occur  in  women. 

In  83  cases  of  gummata  of  the  liver  collected  from  various  sources  by  J.  L. 
Allen,  60  were  males  and  23  females;  he  could  not  find  any  evidence  to  support  the 
hypothesis  that  tight  lacing  disposed  the  liver  to  gummatous  change. 

It  is  difficult  to  prove  anything  with  regard  to  the  influence  of  trauma 
in  determining  the  incidence  of  gummata  in  the  liver,  but  the  greater 
frequency  of  hepatic  gummata  in  the  male  sex,  nearly  3  to  1,  and  the 
fact  that  gummata  are  more  commonly  met  with  on  the  anterior  surface 
of  the  liver,  are  certainly  in  favour  of  this  hypothesis. 

In  a  case  recorded  by  Pitt  f  the  irritation  of  an  old  hydatid  cyst  in  the  liver 
seemed  to  have  determined  an  extensive  syphilitic  formation  around  it. 

ETIOLOGY. 

Age  Incidence. — The  great  majority  of  hepatic  gummata  are  found 
between  the  ages  of  twenty-five  and  fifty  years.  In  78  cases  of  hepatic 
gummata  collected  by  J.  L.  Allen,  69,  or  88.5  per  cent.,  occurred  within 
this  limit.  The  average  age  of  these  78  cases  was  thirty-nine  years, 
and  was  almost  the  same  in  the  two  sexes.  The  cases  were  arranged  as 
follows : 

Number  Number 

Age.  of  Cases.        Age.  of  Cases 

15-20 1  46-50 11 

21-25 2  51-55 3 

26-30 15  61-65 1 

31-35.  .  : 10  66-70 1 

36-40 21  71-75 1 

41-45 12 

*  Flexner:   New  York  Medical  Jour.,  1902,  p.  101. 
t  Pitt:  Trans.  Path.  Soc,  vol.  xxxvii,  p.  276. 


358  DISEASES    OF   THE    LIVER. 

Gummatous  disease  in  the  liver  has  been  observed  at  the  advanced 
age  of  eighty-nine  (Wagner*). 

Interval  between  Infection  and  the  Appearance  of  Gummata. — Usually 
a  number  of  years,  from  ten  to  twenty,  elapse  between  the  primary 
chancre  and  evidence  of  gummata  in  the  Hver;  but  exceptionally  gum- 
mata have  been  found  within  a  year  of  infection. 

Key  t  found  a  gumma  the  size  of  a  walnut  in  the  hver  of  a  woman  aged  twenty- 
six  who  died  of  generahsed  tuberculosis  six  months  after  infection;  and  Fleisch- 
hauer,t  a  gumma  in  the  liver  of  a  man  who  died  seven  months  after  infection.  These 
cases  are  analogous  to  the  occurrence  in  rare  instances  of  gummata  in  the  livers 
of  foetuses  and  still-born  children,     {yide  p.  370.) 


CLINICAL  MANIFESTATIONS. 

Clinically  the  occurrence  of  manifestations  clue  to  hepatic  lesions, 
apart,  from  lardaceous  disease,  is  comparatively  rare  in  the  subjects  of 
tertiary  sj^hiHs. 

Mauriac,§  combining  the  statistics  of  Fournier,  Ehlers,  and  Hjalmann,  found 
that  in  7497  cases  of  tertiary  syphihs  symptoms  pointing  to  the  liver  occurred  in 
only  41. 

It  is  remarkable  how  rare  sj^jliilitic  lesions  in  the  hver  are  in  cases  of 
locomotor  ataxia,  and  it  has  been  suggested  that  there  is  some  kind  of 
antagonism  between  hepatic  sj-philis  and  paras^T^hilitic  lesions  of  the 
nervous  system.  Gummata  and  especialh'  cicatrices  are  not  uncommonly 
latent,  and  are  only  found  after  death  as  a  surprise. 

The  factors  which  determine  the  development  of  S3'mptoms  are:  (1) 
the  size  and  extent  and  (2)  the  position  of  s^-pliilitic  lesions  in  the  hA^er. 

1.  If  a  gumma  is  large,  it  Mill  give  rise  to  the  signs  of  a  tumor,  and  by 
irritating  the  capsule  of  the  liver  to  periliepatitis  and  pain,  while  the 
morbid  metabohsm  going  on  inside  it  may  lead  to  the  production  and 
absorption  of  poisons  which  will  lead  to  constitutional  symptoms,  such  as 
ansemia,  asthenia,  and  perhaps  fever. 

2.  A  cicatrix  or  small  gumma  on  the  convexity  of  the  liver  need  give 
rise  to  no  symptoms,  but  if  situated  in  the  portal  fissure,  jaundice  and 
ascites  may  foUow. 

There  is  a  great  difference  between  the  relative  importance  of  the 
symptoms  produced  by  a  caseous  gumma  and  by  an  old  cicatrix;  for 
symptoms  due  to  the  pressure  of  a  gumma  may  be  relieved,  or  disappear 
under  the  influence  of  iodides,  whereas  it  is  highly  improbable  that  an 
old  cicatrix  -udll  be  altered  by  such  treatment. 

As  has  just  been  pointed  out,  there  is  usually  a  very  considerable 
interval  (ten  to  twent}^  3^ears)  between  the  onset  of  sj^mptoms  and  the 
primary  infection;  it  may  be  postponed  for  thirty  or  forty  jxars,  so  that 
it  has  been  said  that  no  one  can  be  regarded  as  cured  of  sj-philis  until 
he  has  been  examined  postmortem.     Some  cases  show  signs  of  hepatic 

*  Wagner:  Archiv  der  Heilkunde,  Bd.  v,  S.  126,  1S64. 
tKey:  Schmidt's  Jahrb.,  1S74,  Bd.  161. 
X  Fleischhauer;  XII.  Congress  f.  inn.  Med.,  Wiesbaden,  1S03. 
§  Mauriac-  Gaz.  hebdom.  de  Med.  et  de  Chirurg.,  ISSS. 


SYPHILITIC    DISEASE    OF    THE    LIVER.  359 

involvement  within  three  years  of  infection,  and  exceptionally  hepatic 
symptoms  develop  with  great  rapidity.  In  the  early  stages  of  tertiary 
syphilitic  disease  of  the  liver,  before  very  definite  locahsing  symptoms 
and  signs  appear,  there  is  very  commonly  weakness,  general  loss  of  health, 
failure  of  appetite,  and  gastro-intestinal  symptoms.  According  to  Mar- 
cuse,*  two-thirds  of  the  cases  show  gastro-intestinal  symptoms  in  the  early 
stages.  As  gummata  nearly  always  reach  the  surface  of  the  liver,  a 
certain  amount  of  local  perihepatitis  is  common,  which,  according  to  its 
intensity,  accounts  for  feelings  of  discomfort,  pain,  and  tenderness  in  the 
right  hypochondrium;  the  pain  may  radiate  up  to  the  right  shoulder, 
and  is  sometimes  accompanied  by  local  tenderness.  Pain  is  one  of  the 
most  frequent  symptoms  in  tertiary  syphilis  of  the  liver. 

The  clinical  manifestations  of  tertiary  syphilitic  disease  of  the  liver 
vary,  and  may  for  convenience  be  grouped  under  different  headings : 

(I)  Where  the  symptoms  suggest  portal  cirrhosis,  or  simple  chronic 
peritonitis  and  perihepatitis. 

(II)  Presenting  the  features  of  widespread  lardaceous  disease. 

(Ill)  Suggesting  tumor  of  the  liver,  such  as  malignant  growth, 
hydatid,  or  enlarged  gall-bladder. 

(IV)  Imitating  suppuration  in  the  liver. 
(V)  Resembling  cholelithiasis. 
(VI)  Resembling  chronic  splenic  angemia. 

(VII)  Where  the  clinical  features  resemble  hypertrophic  biliary 
cirrhosis. 

I.  Cases  Imitating  Cirrhosis. — ^These  cases  are  frequent  and  impor- 
tant, as  they  probably  account  for  some  of  the  reputed  cures  of  ordinary 
cirrhosis.  There  is  ascites  which  is  serous,  but  in  rare  instances  has 
been  noticed  to  be  chyliform  (Veil,  Galvagni,t  Poljakoff  J)  or  even 
hsemorrhagic.  Other  signs  of  portal  obstruction,  such  as  hsematemesis, 
dilated  veins  in  the  abdominal  walls,  and  dyspepsia,  are  much  less 
frequent  than  in  cirrhosis.  There  may  be  enlargement  of  the  spleen. 
Jaundice  is  very  infrequent.  Ascites  may  be  produced  in  several  ways: 
(i)  by  the  pressure  of  cicatrices  or  gummata  on  the  intrahepatic  branches 
of  the  portal  vein,  or  in  some  instances  on  the  trunk  of  the  vein  in 
the  portal  fissure  of  the  liver;  (ii)  by  constriction  of  the  hepatic  veins; 
(iii)  by  perihepatitis  over  gummata;  this  is  usually  local,  but  may  be 
more  widespread  and  give  rise  to  some  chronic  peritonitis. 

Under  iodide  of  potassium  the  gumma  undergoes  absorption  and  the 
symptoms  will  pass  off  unless  there  is  enough  cicatricial  tissue  left  to 
exert  permanent  pressure  on  the  portal  vein  or  its  branches.  In  a  number 
of  cases  the  absorption  of  the  gumma  leads  to  relief;  these  cases  are 
responsible  for  some  of  the  reputed  cures  of  portal  cirrhosis,  for  iodides 
are  commonly  given  in  that  disease.  In  other  instances  where  there  is 
no  means  of  telling  that  there  is  a  firm  cicatrix,  and  not  a  gumma,  em- 

*  Marcuse:  Wien.  med.  Wochen.,  Nov.  17,  1900.  S.   2219. 

t  Veil,  Galvao;ni:  Quoted  bv  Hoix:  Archiv.  General,  de  MM.,  May  23,  1903, 
p.  1302. 

:  Poljakoff:   Berlin,  idin.  Woclien.,  Jan.  1,  1900. 


360  DISEASES    OF    THE    LIVER. 

barrassing  the  portal  circulation,  antisyphilitic  treatment  fails,  and  the 
case  more  closely  resembles  common  cirrhosis. 

The  Differential  Diagnosis  of  Portal  Obstruction  due  to  Syphi-itic 
Disease  of  the  Liver  from  Ordinary  Cirrhosis. — The  history  and  the  pres- 
ence of  other  signs  of  sj^hilis  should  always  suggest  s}Tohilitic  disease  of 
the  hver  and  lead  to  adequate  antisj^jhilitic  treatment.  In  sj'philis 
the  liver  may  be  irregularly  enlarged,  especially  the  right  lobe,  while  in 
cirrhosis  enlargement,  if  present,  is  more  uniform.  Definite  enlarge- 
ment of  the  spleen  in  the  absence  of  lardaceous  disease,  which  itself 
points  to  SATphilis  and  should  then  be  accompanied  by  albuminuria,  is 
rather  in  favour  of  cirrhosis.  An  alcoholic  history  and  dyspepsia  of 
long  standing  are  also  in  favour  of  cirrhosis.  Ascites  which  recurs  after 
paracentesis  is  probably  not  due  to  cirrhosis,  but  to  chronic  peritonitis 
and  perihepatitis  or  to  syphilitic  disease  of  the  liver.  ^A^ien  ascites  is 
due  to  cirrhosis,  the  patient  is  usually  thin  or  emaciated,  while  in  syphil- 
itic disease  of  the  liver  nutrition  may  be  fairly  well  presented. 

Cases  Resembling  Simple  Chronic  Peritonitis  and  Perihepatitis. — Cases 
of  syphilitic  disease  of  the  liver  in  which  ascites  recurs  T\dll  closely  re- 
semble simple  chronic  peritonitis,  of  which  chronic  universal  perihepatitis 
is  only  a  part.  Chronic  and  recurrent  ascites  only  occurs  in  a  certain 
proportion  of  the  cases  of  hepatic  S}'philis,  while  it  is  a  constant  feature 
in  simple  chronic  peritonitis.  There  must,  therefore,  be  undoubted 
evidence  of  syphihs  in  the  body,  or  enlargement  and  irregularity  of  the 
hver,  which  point  to  gummatous  disease  rather  than  to  universal  chronic 
perihepatitis,  before  the  diagnosis  of  S3rphilitic  disease  is  made  offhand 
in  preference  to  chronic  peritonitis.  The  effect  of  a  thoroughly  efficient 
course  of  iodides  should,  however,  always  be  tried  to  settle  the  c[uestion 
of  diagnosis.  But  the  fact  that  the  treatment  fails  does  not  absolutely 
put  S}T)hilitic  disease  out  of  court.  Universal  chronic  perihepatitis  may 
in  some  rare  instances  be  associated  with  and  possibly  due  to  sj^philis. 
{Vide  Perihepatitis,  p.  167.)  Cheadle  *  considers  that  s}^hihs  is  the 
most  important  cause  of  perihepatitis.  My  own  experience  is  that 
syphihtic  gummata  commonly  give  rise  to  local  perihepatitis  and  thick- 
ening of  the  capsule,  but  that  syphilitic  infection  is  quite  an  exceptional 
cause  of  universal  perihepatitis.  In  22  cases  collected  by  Hale  "WHiitef 
syphilis  was  the  apparent  cause  in  3. 

II.  Cases  with  the  Features  of  Lardaceous  Disease. — "\ATien  a 
gummatous  liver  is  associated  with  lardaceous  disease,  the  renal  affection 
gives  rise  to  albuminuria  and  dropsy,  and  the  aspect  of  the  case  may  be 
that  of  renal  disease.  Under  these  circumstances  the  presence  of  a 
gumma  in  the  hver  may  naturally  not  be  suspected.  The  presence  of 
albuminuria  in  syphilis  is  not,  however,  to  be  regarded  as  undeniable 
proof  of  lardaceous  disease,  though  very  suggestive  of  this  change,  since 
it  may  be  due  to  a  s^T^hilitic  nephritis.  In  some  cases  where  the  liver 
and  spleen  are  both  very  considerably  enlarged,  the  clinical  aspect  has 

*  Cheadle:  Some  Cirrhoses  of  the  Liver,  1900,  pp.  41,  4.3. 
t  Hale  White:  Allbutt'.s  Svstem  of  Medicine,  vol.  iv,  p.  121. 


SYPHILITIC    DISEASE    OF   THE    LIVER.  3G1 

been  described  as  that  of  Hanot's  hypertrophic  l^iliary  cirrhosis  but  with- 
out jaundice.     (Boix.*) 

The  following  is  a  well-marked  case  of  s^i^hilitic  gummata  of  the  liver 
combined  with  lardaceous  disease: 

Large  Gumma  in  the  Liver;  Extensive  Lardaceous  Disease;  AJbuminuria;  Ascites, 
Paracentesis;  Peritonitis. — A  man  aged  forty-two  yeans  Avas  under  m}^  care  in 
August-September,  1900,  in  St.  George's  Hospital,  with  ascites,  albuminuria,  and 
casts;  there  was  no  trace  of  jaundice  and  his  facial  aspect  was  that  of  cirrhosis. 
There  was  no  cardiac  disease  or  hypertrophy;  the  tension  of  the  pulse  was  low. 
It  was  thought  possible  that  he  had  lardaceous  disease  of  the  kidneys  and  syphilitic 
disease  of  the  liver,  but  the  diagnosis  was  open  to  doubt,  as  there  was  no  history 
or  signs  of  lues  veneris.  The  testes  were  not  enlarged  and  there  were  no  scars  in 
any  part  of  the  body.  The  spleen  could  not  be  felt.  The  liver  was  felt  to  be  some- 
what enlarged.  He  was  put  on  iodide  of  potassium,  but  without  any  improvement, 
and  his  abdomen  was  tapped;  a  week  later  he  vomited,  complained  of  abdominal 
pain,  and  as  there  was  considerable  ascites,  he  was  again  tapped;  the  fluid  with- 
dra-nm  was  turbid  and  contained  numerous  pus  corpuscles;  the  patient  got  rapidly 
weaker  and  died  on  September  6.  At  the  autopsy  there  were  recent  peritonitis  and 
extensive  lardaceous  disease  of  the  viscera.  The  liver  weighed  8  pounds  10  ounces, 
was  somewhat  scarred,  and  showed  a  large  gumma  in  the  posterior  part  of  the  right 
lobe  which  was  the  size  of  a  cocoanut;  it  compressed  the  right  branch  of  the  portal 
vein  and  had  running  through  its  centre  a  large  Ijile-duct.  There  were  other 
small  gummata  in  the  Uver,  which  was  lardaceous.  The  spleen,  20  ounces,  was  in 
a  condition  of  diffuse  waxy  change.  The  left  kidney  was  atrophied;  the  right 
weighed  15  ounces  and  was  lardaceous. 

III.  Gummata,  etc.,  Imitating  Hepatic  Tvunors. — AMien,  as  they 
usually  are,  gummata  are  situated  on  the  anterior  surface  of  the  liver,  the 
irregularities  they  give  rise  to  may  be  readily  felt  through  the  abdominal 
wall.  The  elevations  of  the  liver  substance  due  to  the  contraction  of 
cicatrices  are  also  easily  palpable.  A  large  gumma  or  gummatous  in- 
filtration of  a  lobe  or  part  of  a  lobe  may  give  rise  to  the  suspicion  of 
primary  massive  carcinoma,  but  if  watched  for  a  short  time  it  will  be 
seen  that  it  does  not  enlarge  at  the  same  rate  that  a  growth  would. 
Iodides  in  full  doses  and  mercur}^  should  be  given  in  the  absence  of  strong 
evidence  that  the  enlargement  is  of  a  malignant  nature.  Jaundice  and 
ascites,  especially  together,  are  more  likely  to  be  met  mth  in  malignant 
disease;  other  points  in  favour  of  growth  are  rapid  increase  in  the  size 
of  the  liver,  marked  constitutional  symptoms,  and,  of  course,  any  signs 
of  a  grovrth.  elsewhere.  In  a  sj-philitic  subject  enlargement  and  irregu- 
larity of  the  liver  may  be  due  either  to  gummatous  disease  or  to  new- 
gro\\1:h,  for  syphilis,  of  course,  in  no  way  protects  against  malignant 
disease.  The  vigourous  administration  of  iodides  and  mercury  should 
decide  the  cjuestion,  diminution  in  size  of  the  liver  settling  the  diagnosis 
in  favour  of  gumma. 

An  eminent  member  of  the  medical  profession  who  had  lieen  unfortunately 
inoculated  with  syphilis  died  with  hepatic  cancer,  which  he  had  naturally  at  first 
hoped  and  beUeved  to  l)e  gummatous  disea.se. 

Enlargement  of  the  spleen  from  lardaceous  or  gummatous  change 
is  more  hkely  to  accompany  s^q^hilitic  disease  of  the  liver  than  malignant 
disease,  and  is  a  point  to  be  borne  in  mind  in  diagnosis.     When  gummata 

*  Boix:  Archiv.  Gen<5ral.  de  Med.,  June  2,  1903. 


362  DISEASES   OF  THE   LIVER. 

are  associated  with  lardaceous  change  in  the  same  Hver  the  enlargement 
may  be  very  marked,  and  the  resemblance  to  carcinoma  very  consid- 
erable. The  irregularities  produced  by  cicatrices  in  a  lardaceous  liver 
have  a  similar  resemblance  to  malignant  disease.  In  such  cases  albumin- 
uria points  to  lardaceous  disease,  and  therefore  in  favour  of  syphilis. 
Moreover,  albuminuria  is  rare  in  malignant  disease  of  the  liver.  In  the 
following  case  adhesions  over  the  surface  of  a  lardaceous  liver  gave 
rise  during  life  to  a  diagnosis  of  malignant  disease: 

A  man  aged  forty-one  who  had  had  a  sore  on  the  penis  followed  by  a  bubo, 
but  who  presented  no  other  history  or  signs  of  syphihs  or  suppuration,  was  admitted 
to  St.  George's  Hospital  with  ascites  and  albuminuria.  After  tapping  nodules 
were  felt  over  the  surface  of  an  enlarged  liver  and  the  tentative  diagnosis  of  cirrhosis 
was  given  up  in  favour  of  maUgnant  disease.  At  the  autopsy  the  irregularities  felt 
as  nodules  were  due  to  peritoneal  adhesions  over  the  convexity  of  the  hver;  the 
liver  weighed  9  pounds,  was  fatty  and  lardaceous,  but  presented  no  fibrosis,  gummata, 
or  new-growth.  The  spleen,  13  ounces,  kidneys,  suprarenal  bodies,  and  intestines 
were  lardaceous.     One  testis  showed  fibroid  change  in  the  body  of  the  organ. 

Difficulty  sometimes  arises  in  deciding  between  gummatous  infiltra- 
tion of  a  lobe  of  the  liver  and  a  hydatid  cyst  covered  over  by  a  layer 
of  liver  substance.  The  general  health  in  hydatid  is  unaffected  unless 
suppuration  has  occurred,  and  the  liver  is  smooth,  whereas  in  syphilis 
other  signs  of  the  disease  and  irregularity  of  the  liver  should  be  present. 
In  any  doubtful  case  iodides  should  be  given  at  once.  Gummatous  and 
cicatricial  deformity  of  the  right  lobe  may  produce  a  mass  which  imitates 
malignant  disease  of  the  gall-bladder. 

IV.  Cases  with  Fever,  Resembling  Hepatic  Suppuration. — Occa- 
sionally irregular  fever  may  occur  in  gummatous  disease  of  the  liver,* 
and  may  perhaps  be  explained  as  being  due  to  secondary  infection  having 
occurred  in  gummata.  The  fever  may  suggest  hepatic  suppuration, 
malaria,  latent  tuberculosis,  or  even  typhoid  fever.  It  is,  as  a  rule, 
removed  by  antisyphilitic  treatment.  When  secondary  infection  takes 
place  in  a  gumma,  it  may  soften  down  and  imitate  an  abscess.  The 
association  of  a  fluctuating  swelling  in  the  region  of  the  liver  and  a  raised 
temperature  would  render  the  resemblance  to  an  ordinary  hepatic  abscess 
so  close  that  unless  the  patient  was  known  to  have  had  syphilis  there 
would  be  no  reason  to  delay  ordinary  surgical  treatment.  A  softened 
gumma  may  present  anteriorly  or  may  perforate  through  the  ribs  and 
project  posteriorly  or  laterally.  In  a  case  operated  upon  by  Newbolt  t 
a  softened  gumma  at  the  back  of  the  right  lobe  was  associated  with  and 
probably  the  cause  of  an  empyema  on  the  right  side. 

The  abdomen  of  a  woman  aged  twenty-six  years,  who  had  a  well-marked  syph- 
ilitic history,  was  opened  during  hfe,  and  a  small  gumma  excised  from  the  anterior 
margin  of  the  liver.  A  hard  mass  was  felt  in  the  right  lobe  posteriorly  and  was 
thought  to  be  a  gumma.  She  was  put  on  iodide  of  potassimn  and  the  right  base 
was  aspirated  several  times,  but  without  success.  At  the  autopsy  there  was  an 
empyema  on  the  right  side  and  a  suppurating  gumma,  apparently  communicating 
with  the  empyema,  in  the  posterior  part  of  the  right  lobe  of  the  Uver. 

*Bristowe:  Brit.  Med.  Journ.,  1886,  vol.  i,  p.  878.  Gerhardt:  Sem.  M6d., 
June  22,  1898.     Migliorato:  Settim.  Med.,  Nov.  26,  1898. 

t  Newbolt:  Medical,  Surgical,  and  Pathological  Reports  of  Royal  Southern 
Hosp.,  Liverpool,  1901,  pp.  148.  248. 


SYPHILITIC    DISEASE    OF    THE    LIVER.  363 

Tropical  hepatitis  around  a  previously  quiescent  gumma  may  imi- 
tate an  abscess,  and  the  true  state  of  affairs  be  only  revealed  when 
caseous  material  instead  of  pus  is  removed  at  operation. 

V.  Cases  Resembling  Gall-stones,  etc. — Jaundice  is  not  really 
common  in  tertiary  syphilitic  disease  of  the  liver,  but  occasionally  the 
pressure  of  a  gumma  or  the  traction  exerted  by  syphilitic  cicatrices  in 
the  portal  fissure  may  lead  to  obstructive  jaundice.  In  rare  cases  this 
obstructive  jaundice  is  accompanied  by  attacks  of  pain  resembling  biliary 
colic,  but  not  due  to  the  presence  of  gall-stones.  The  chnical  aspects  of 
such  a  case  will  closely  resemble  gall-stones.  In  any  case  of  probable 
cholelitliiasis  with  well-marked  signs  of  tertiary  syphilis  iodides  should 
be  given  before  proceeding  to  operation.  The  following  case  recorded  by 
Billings  *  bears  on  this  point: 

A  single  man  aged  thirty-seven  who  had  contracted  syphilis  one  and  one-half 
years  previously  had  constant  pain  in  the  region  of  the  gall-bladder  with  attacks 
of  colic  followed  by  jaundice  and  accompanied  by  intermittent  hepatic  fever.  A 
tumor  was  felt  in  the  region  of  the  gall-bladder  and  Finger  operated  for  cholecystitis 
and  calcuU  in  the  gall-bladder  and  cystic  duct.  Multiple  gummata  were  found  at 
the  operation;  the  largest  gumma  was  at  the  edge  of  the  liver,  close  to  the  gall- 
bladder. The  main  ducts,  however,  did  not  appear  to  have  been  pressed  upon, 
so  the  obstruction  must  have  been  in  their  branches.  Finger  had  met  with  a  similar 
case. 

Gummata  very  seldom  behave  in  such  a  way  that  they  imitate  a 
distended  gall-bladder,  as  in  the  case  just  referred  to  and  in  another 
operated  upon  by  R.  Parker.f  Such  a  case  might  naturally  be  thought 
to  be  one  of  impaction  of  a  calculus  in  the  cystic  duct  and  secondary 
distension  of  the  gall-bladder.  In  a  case  of  suppurating  gumma  operated 
upon  by  Lilienthal  +  the  most  probable  diagnosis  was  cholec3^stitis. 

VI.  Cases  Resembling  Chronic  Splenic  Anaemia. — In  some  cases 
of  s}T3hilitic  disease  of  the  liver  the  spleen  is  greatly  enlarged  from  lar- 
daceous  disease,  or  in  rare  instances  from  gummatous  change,  while 
the  Hver  is  little,  if  at  all,  enlarged.  In  such  cases  there  may  be  a  con- 
siderable resemblance  to  chronic  splenic  anaemia  which  is  characterised 
by  anaemia  of  the  chlorotic  type,  leucopenia  or  a  diminution  in  the  number 
of  leucocytes,  and  great  splenic  enlargement.  In  a  case  of  Coupland's  § 
the  spleen  was  removed  for  supjDOsed  splenic  anaemia  with  great  apparent 
benefit.  Subsequently  the  woman  died  from  hsematemesis  and  ascites 
and  the  liver  was  found  to  be  s}T3hilitic.  Osier  ||  refers  to  similar  ex- 
amples of  S3^3hilis  imitating  chronic  splenic  anaemia  in  adults. 

VII.  Cases  Resembling  Hypertrophic  Biliary  Cirrhosis. — In  rare 
instances  syphihs  may  lead  to  an  enlarged  liver  with  chronic  jaundice 
and  splenic  enlargement  (Hanot**).  There  are  signs  of  syphilis  else- 
where in  the  body,  the  progress  of  the  case  is  more  rapid  than  in  hyper- 
trophic Vjiliary  cirrhosis,  while  the  splenic  enlargement  is  not  so  marked. 

*  Billings:  Philadelphia  Med.  Journ.,  1900,  p.  670. 
t  Parker,  R.:  Lancet,  1899,  vol.  i,  p.  301. 
X  LiUenthal:  Annals  of  Surgery,  July,  1902,  p.  1.32. 
§  Coupland,  S.:  Brit.  Med.  Journ.,  1S96,  vol.  i,  p.  1445. 

II  Osier,  W. :  American  Journal  of  Medical  Sciences,  vol.  cxxiv,  p.  765,  Nov.,  1902. 
**  Hanot:  Presse  Medicale,  Sept.  30,  1896,  p.  505. 


354  DISEASES    OF   THE    LIVER. 

Lancereaux  *  assumes  that  Hanot  was  in  error  and  that  the  condition  was 
really  leukEemia.  A  good  example  of  syphilitic  disease  imitating  hypertrophic 
biliary  cirrhosis  is  given  on  page  324;  the  patient  had  tardive  hereditary  syphihs, 
chronic  jaundice  for  years,  enlarged  li^^er  and  spleen,  and  clubbed  fingers.  Fer- 
rannini  described  the  case  of  a  woman  aged  forty-eight  years,  mth  jaundice,  clay- 
coloured  stools,  a  large  spleen  and  liver  which  resembled  hypertrophic  biliary  cirrhosis. 
At  the  autopsy  the  enlargement  of  the  liver  and  spleen  were  found  to  be  due  to 
syphilis  and  the  jaundice  to  a  retention  cyst  in  the  head  of  the  pancreas  compressing 
the  common  bile-duct. 

DIAGNOSIS. 

A  history  of  syphilitic  infection  or  the  evidence  of  syphilitic  lesions 
in  some  accessible  part  of  the  body,  such  as  the  skin,  tongue,  throat, 
testes,  or  bones,  in  an  obscure  case  of  hepatic  enlargement  or  tumor, 
should  always  be  regarded  as  an  indication  for  antisyphilitic  treatment. 
A  patient  may  deny  infection  or  may  be  entirely  ignorant  that  he  has 
contracted  the  disease. 

In  the  following  case  the  patient  complained  of  hepatic  pain,  had  an  enlarged 
liver  without  jaundice  or  ascites,  and  denied  syphilitic  infection.  A  labourer  aged 
fifty  was  under  my  care  in  St.  George's  Hospital  in  October,  1900.  For  a  month 
he  had  constant  pain  in  the  right  hypochondrium,  worse  at  night  when  lying  on  the 
right  side  and  on  respiration.  Married,  no  children,  but  his  wife  has  had  four 
miscarriages.  The  liver  extends  below  the  costal  arch  in  the  nipple  line  and  is 
tender.  Spleen  not  enlarged.  Testes  not  enlarged.  There  is  a  rupial  scar  near 
the  umbilicus.  The  tongue  is  greatly  deformed  and  caniiot  be  put  out;  it  is  scarred, 
shows  superficial  glossitis,  and  is  lobulated,  but  not  ulcerated.  The  tongue  had 
been  sore  for  six  months  and  was  ascribed  by  the  patient  to  heavy  smoking.  On 
full  doses  of  iodides  and  mercury  the  hepatic  pain  and  the  condition  of  the  tongue 
rapidly  improved.  The  case  was  one  of  gummatous  disease  of  the  tongue  with 
probably  a  similar  change  in  the  liver. 

Hepatic  syphilis  is  probably  very  commonly  overlooked,  the  disease 
being  regarded  as  cirrhosis  or  early  new-growth.  It  is  therefore  impor- 
tant to  bear  in  mind  the  possibility  of  syphilis  in  all  obscure  enlargements 
of  the  liver  and  to  give  the  patients  the  chance  afforded  by  antisjrphilitic 
treatment.  Moreover,  in  doubtful  cases  invahiable  assistance  to  diag- 
nosis is  obtained  by  watching  the  effects  of  a  thorough  course  of  mer- 
curials and  iodides.  In  the  early  stages  of  malignant  disease  it  may  be 
quite  impossible  to  come  to  a  correct  decision  until  this  has  been  tried. 
The  differential  diagnosis  of  syphilitic  disease  of  the  liver  from  cirrhosis, 
chronic  peritonitis,  malignant  disease,  etc.,  has  already  been  referred  to 
under  the  description  of  the  clinical  aspects  of  sj^philitic  disease  of  the 
liver. 

PROGNOSIS. 

When  treated  with  sufficient  doses  of  the  iodides  the  prognosis  is 
much  better  than  in  most  of  the  conditions  which  resemble  it,  such  as 
carcinoma,  cirrhosis,  chronic  peritonitis,  and  perihepatitis.  Gummata 
undergo  absorption  and  the  bad  effects  due  to  their  mechanical  effects 
will  disappear.  On  the  other  hand,  firm  cicatrices  will,  as  has  already 
been  pointed  out,  not  be  affected,  and  the  results  of  antis3^3hilitic  treat- 
ment are  therefore  disappointing,  and,  in  addition,  misleading  if  absence 
of  a  good  result  be  regarded  as  necessarily  eliminating  sj^hilis.     The 

*  Laicereaux:  Traits  des  Maladies  du  foie  et  du  Pancreas,  p.  513.  1897. 


SYPHILITIC    DISEASE    OF    THE    LIVER.  365 

prognosis  of  syphilitic  enlargement,  which  is  often  gummatous,  is  therefore 
rather  better  than  that  of  ascites  or  jaundice  thought  to  depend  on 
syphilitic  disease  of  the  liver,  since  the  latter  may  be  due  to  cicatrices. 

TREATMENT, 

If  S3^3hilitic  disease  is  suspected,  mercurial  inunction  and  iodide 
of  potassium  internally  should  be  employed.  Iodide  of  potassium 
should  be  combined  with  iodide  of  sodium  and  "^dth  an  ammonia 
salt  such  as  spiritus  ammonise  aromaticus.  In  this  way  the  depress- 
ing effects  of  the  potassium  are  avoided.  The  usual  course  is  to  begin 
with  fifteen  grains  of  the  combined  iodides  three  times  daily,  which  is 
increased  until  30  grains  are  being  taken  three  times  a  day.  If  mercurial 
inunction  be  not  employed  at  the  same  time,  liquor  hydrargyri  per- 
chloridi,  n^  xx,  should  be  added  to  each  dose  of  the  medicine.  The 
medicine  should  be  taken  shortly  before  meals.  If  taken  after  meals, 
dyspepsia  may  occur,  probably  because  some  free  iodine  is  liberated  by 
the  action  of  the  hydrochloric  acid  of  the  gastric  juice  on  the  iodides. 

The  use  of  iodide  of  potassium  in  tertiary  syphilis  appears  to  have  been  first 
discovered  in  1831  by  Dr.  R.  WilUams,  of  St.  Thomas'  Hospital  (Sir  'J.  Paget*); 
though  Dr.  Wallace,  of  Dublin,  who  employed  it  in  1S32  and  pubhshed  his  results 
in  the  "Lancet"  in  1836,  is  generally  credited  as  the  first  to  use  this  drug.f 

It  is  important  to  remember  that  the  good  effects  of  iodides  and 
mercury  may  take  a  considerable  time  to  show  themselves.  It  is  essen- 
tial, therefore,  that  several  weeks'  thorough  treatment  should  be  insisted 
upon  before  it  can  be  concluded  that  the  condition  is  not  of  a  syphilitic 
nature. 

An  interesting  speculation  is  opened  up  by  a  consideration  of  the  marvellous 
way  in  which  iodides  produce  absorption  of  gummatous  material.  This  action  can 
hardly  be  considered  specific  in  the  strict  sense  of  the  term,  inasmuch  as  a  similarly 
marked  effect  follows  its  adequate  administration  in  actinomycosis.  Possibly  iodides 
act  by  preventing  further  disease  of  the  vessels  in  the  neighbourhood,  and  that 
this  enables  the  natural  process  of  absorption  to  go  on  unchecked  by  endarteritis 
of  the  neighbouring  vessels,  while  it  prevents  any  further  manifestations  of  the 
syphilitic  virus.  Stockmanj  takes  a  different  view,  and  l)elieves  that  iodides  act 
by  bringing  about  increased  secretion  of  the  thyroid  gland,  which  has  a  powerful 
absorptive  action.     If  this  be  the  case,  thyroid  extract  should  be  given  in  gumnuita. 

Flexner  §  attributes  the  absorption  of  gummata  to  autolysis  or  the  action  of 
intracellular  ferments,  and  supposes  that  this  ferment  action  is  accelerated  by 
iodides. 

If  the  patient  is  ansemic,  iron  should  be  given  and  ioditle  of  iron  is 
a  convenient  form.  When  gummata  dovelo])  Avith  great  ra])idity  and 
soon  after  infection,  subcutaneous,  or  better  intranmscular,  injection 
of  mercurial  salts  may  be  employed.  The  benzoate  of  merctry,  which 
is  soluble,  has  been  used  witli  advantage. 

Pain  due  to  perihepatitis  may  be  relieved  by  hot  fomentations,  by 

*  Sir  James  Paget:  Address  to  the  Abernethian  Society  of  St.  Bartholomew's 
Hospital,  1885,  p.  19.  Privately  printed.  Quoted  by  Howard  Marsh  in  obituary 
notice  of  Sir  J.  Paget,  St.  Bariliolomew's  Hospital  Reports,  vol.  xxxvi.  p.  6. 

t  See  Lancereaux:  Syphilis,  vol.  ii,  p.  300.  In  New  Sydenham  Society's  Li- 
brary, t  Stockman:  Glasgow  Hospital  Reports,  1899,  p.  69. 

§  Am.  Jour.  Med.  Sc,  vol.  cxxvi. 


366  DISEASES    OF   THE    LIVER. 

poultices,  or  by  the  application  of  a  few  leeches  over  the  painful  area. 
The  general  health  should  be  maintained  by  a  generous  diet  and  by 
fresh  air,  preferably  that  of  the  sea.  In  severe  cases  with  cachexia  the 
medicinal  treatment  may  with  advantage  be  carried  out  at  spas  of  high 
elevation;  Sir  Hermann  and  Dr.  Parkes  Weber  recommend  Bareges,  Cau- 
terets,  Bagneres-de-Luchon,  or  Wildbad-Gastein.  Aix-la-Chapelle  and 
Wiesbaden  are  well  adapted  for  the  treatment  of  visceral  S3^1iihs. 

The  surgical  treatment  of  gunainata  of  the  hver  by  removal  may 
be  possible  when  the  anterior  margin  of  the  liver  is  affected,  and  when 
the  lesion  is  single  and  localised,  but  it  is  only  hkely  to  be  performed 
in  cases  where  an  exploratory  operation  has  been  undertaken  for  pur- 
poses of  diagnosis  and  where  a  tumor  of  uncertain  nature  is  found  and 
can  be  fairly  easily  removed.  In  exceptional  instances  when  a  breaking- 
down  gumma  is  ulcerating  through  the  abdoirdnal  wall,  scraping  out  the 
gummatous  sloughs,  as  in  a  case  described  by  W.  G.  Spencer,*  is  ad- 
visable, inasmuch  as  septic  absorption  is  thus  prevented. 

In  a  case  where  an  exploratory  operation  revealed  a  very  large  gumma  4  or  5 
inches  across,  R.  Parkerf  removed  some,  but  not  all,  of  the  caseous  contents  and  then 
closed  the  wound;  antisyphilitic  remedies  were  afterwards  given  and  the  man 
recovered. 

Removal  of  a  localised  gumma  or  of  a  gummatous  constriction  lobe 
in  cases  where  laparotomy  has  been  undertaken  to  clear  up  the  diagnosis, 
or  under  the  impression  that  some  other  condition  was  present,  is  ad- 
missible, inasmuch  as  it  may  accelerate  the  cure  by  antisyphilitic  treat- 
ment. But  a  very  thorough  course  of  antisyphilitic  treatment  should  be 
carried  out  before  an  operation  is  undertaken  with  the  view  of  remov- 
ing a  gumma. 

Keen  J  in  1899  collected  twelve  cases  where  resection  of  the  liver  had  been  per- 
formed for  gumma,  and  in  1903  Cumston  §  brought  the  number  up  to  twenty-seven. 
In  most  cases  operation  was  undertaken  under  the  idea  that  the  hepatic  condition 
was  other  than  a  giunma.  Steiner  ||  has  collected  thirteen  cases  in  which  laparot- 
omy was  planned  on  what  turned  out  to  be  errors  of  diagnosis. 


PARASYPHILITIC   AFFECTIONS. 

By  parasyphihtic  or  metasyphilitic  lesions  are  meant  changes  which 
are  not  in  their  nature  pathognomonic  of  syphilis,  but  which  develop 
when  the  soil  has  been  prepared  by  the  poison  of  syphihs,  such  as  tabes 
dorsalis  and  general  paralysis  of  the  insane.  The  question  of  para- 
syphilitic  multilobular  cirrhosis  occurring  in  the  subjects  of  congenital 
syphilis  is  cUscussed  elsewhere.  Pathologists  have  insisted,  and  rightty, 
on  the  difference  between  ordinary  alcoholic  cirrhosis  and  the  specific 
forms  of  hepatic  fibrosis — namely,  pericellular  cirrhosis  in  hereditar}^ 
syphilis  and  multiple  scarring  by  cicatrices.    This  may  account  for  the 

*  Spencer,  W.  G.:  Brit.  Med.  Journal,  1898,  vol.  ii,  p.  1686;  and  Trans.  Clin. 
Soc,  vol.  xxxii,  p.  46. 

t  Rushton  Parker:  Lancet,  1899,  vol.  i,  p.  301. 

I  Keen,  W.  W.:  Annals  of  Surgery,  Sept.,  1899,  p.  267. 

§  Cumston.  C.  G.:  (Boston.  U.  S.  A.)  Archiv.  (general,  de  Med.,  t.  191. 

!1  Steiner:  These  Paris,  1902,  No.  380,  p.  897,  1903. 


SYPHILITIC    DISEASE    OF   THE    LIVER.  367 

fact  that  little  attention  has  been  paid  to  the  question  whether  a  para- 
syphilitic  multilobular  cirrhosis  need  be  recognised  as  a  sequela  of  s}nph.- 
ilis.  That  it  not  uncommonly  happens  that  a  person  who  has  had  syphilis 
becomes  the  subject  of  ordinary  multilobular  cirrhosis  is  quite  natural, 
since  sjqDhilis  does  not  protect  in  any  w-ay  against  the  effects  of  alco- 
holism, and,  moreover,  Bacchus  and  Venus  are  frequently  worshiped 
by  the  same  devotees.  It  is  reasonable  to  believe  that  parasyphilitic 
multilobular  cirrhosis  may  occur  in  adults,  but  there  are  considerable 
difficulties  in  recognising  it  or  in  establishing  its  existence. 

Lardaceous  Disease. — ^AVith  the  advance  of  antiseptic  surgery  pro- 
longed suppuration  is  so  much  less  common  than  formerly  that  syphilis 
is  responsible  for  a  much  larger  proportion  of  cases  of  lardaceous  disease 
than  formerly.  Lardaceous  liver  is  considered  elsewhere;  it  need  only 
be  stated  here  that  lardaceous  change  may  accompany  gummatous  and 
other  syphilitic  lesions  in  the  hver  and  that  in  some  instances  the  larda- 
ceous change  is  limited  around  gummata. 

CONGENITAL  SYPHILIS  OF  THE  LIVER. 

The  hepatic  lesions  due  to  congenital  or  hereditary  sji^hilis  may  con- 
veniently be  considered  as:  (1)  Those  found  in  infants  at  the  same  time 
that  other  manifestations  of  congenital  syphilis  are  present.  (2)  Those 
of  delayed  or  tardive  congenital  syphiHs.  (3)  Multilobular  cirrhosis 
supervening  in  children  with  a  history  or  signs  of  former  hereditary 
syphilis,  or  parasyphilitic  cirrhosis. 

The  first  of  these  categories  is  far  the  most  important  and  contains 
the  account  of  what  is  ordinarily  understood  by  the  liver  of  congenital 
s5Tohilis. 

History. — Gubler  *  first  gave  a  full  description  of  the  lesions  of  the 
liver  in  hereditary  or  congenital  syphihs  in  1852.  Bamburger,  Virchow, 
and  Parrot  further  described  the  condition,  while  in  Great  Britain  Sir 
S.  Wilks  recorded  a  case  in  1866.  The  reader  will  find  references  to  the 
history  of  hereditary  hepatic  syphilis  in  Lancereaux's  t  work  on  s\q3hilis. 
More  recently  the  tertiary  effects  of  congenital  syphilis  on  the  liver  have 
been  specially  described  in  cases  of  sylDhilis  hereditaria  tardiva. 

THE  ORDINARY  HEPATIC  MANIFESTATION  OF  CONGENITAL  SYPHILIS. 

Incidence. — The  hver  is  found  to  be  affected  in  a  ^-ery  high  pro- 
portion of  the  infants  dying  with  congenital  syphilis. 

In  infants  with  congenital  syphilis  the  hver  has  been  found  to  be  affected  in 
from  39  per  cent.  (HofmeisterJ)  to  65  per  cent.  (Feige  §). 

This  contrasts  with  acquired  syphilis,  in  which  the  liver  very  fre- 
quently escapes.     It  is  generally  considered  that  antenatal  syphilis  may 

*  Gubler:  Soc.  debiolog.,  tome  iv,  p.  25,  1852. 

t  Lancereaux:  Syphilis,  vol.  ii,  pp.  132,  151.     Transl.  New  Sydenham  Soc. 
t  Hofmeister:  Dissertation,   Kiel,   1SS6.     Quoted  by   Quincke  in  Nothnagcl's 
Encyclopaedia  of  Practical  Medicine,  Enghsh  translation,  p.  745. 
§  Feige:  Dissertation,  Kiel,  1896.     Ibid. 


368  DISEASES    OF    THE    LIVER. 

be  either  (I)  hereditary,  and  due  to  the  spermatozoon  being  the  carrier 
of  the  s}T^)hilitic  germ  or  poison  to  the  ovum,  while  the  mother  escapes 
though  rendered  immune  to  further  infection;  or  (II)  congenital,  and 
due  to  the  SA^Dhihtic  toxine  passing  from  the  mother  through  the  placenta 
into  the  umbilical  vein  of  the  fcetus.  The  frequency  of  hepatic  lesions 
in  congenital  syphilis  is  an  argument  in  favour  of  the  view  that  antenatal 
sjTjhiUs  is  maternal,  the  infection  passing  through  the  placenta  into  the 
umbihcal  vein  and  damaging  the  hver,  which  is  the  first  organ  of  the 
foetus  "^"ith  which  it  comes  in  contact;  while  if  the  ovum  were  primarily 
infected  by  a  syphiUsed  spermatozoon  it  is  improbable  that  the  embrv^o 
would  survdve;  and  further,  if  it  did,  the  s^i^hilitic  toxine  would  reach 
the  hver  by  the  hepatic  artery,  and  the  liver,  being  thus  exposed  to  the 
same  risk  of  infection  as  in  postnatal  sj-pliilis,  should  be  affected  in 
much  the  same  joroportion  as  in  the  acc{uired  disease.  In  postnatal 
syphihs  when  the  disease  is  conveyed  by  suckling  from  a  wet-nurse,  by 
inoculation,  or  other  means,  the  lesions  are  the  same  as  those  of  acquired 
syphilis. 

Morbid  Anatomy. — Liver. — There  is  ver\'  considerable  variation  in 
the  changes  found  in  the  hvers  of  infants  dying  with  congenital  s^-phihs; 
but  the  two  main  points  in  regard  to  the  morbid  anatomy  are,  (I)  that 
the  change  tends  to  be  diffuse,  and  (II)  that  it  is  a  secondare''  sjTDhihtic 
manifestation.  Congenital  hepatic  s^^^hilis  thus  differs  markedly  from 
the  circumscribed  lesions  of  the  liver  characteristic  of  the  tertiary  stage 
of  the  acquired  disease.  The  appearance  of  the  hA'er  is  by  no  means 
constant;  there  is  sometimes  little  or  no  manifest  change  to  the  naked 
eye,  and  microscopic  examination  alone  may  make  it  certain  that  there 
is  s\q)hihtic  infection.  The  liver  is  enlarged,  usually  retains  its  shape, 
and  weighs  more  than  natural,  being  one-twelfth  or  one-sixteenth  instead 
of  one-twenty-fifth  of  the  bodj'-weight  at  birth.  The  surface  may  show 
adhesions,  due  to  intrauterine  perihepatitis  and  peritonitis,  but  except 
for  these  adhesioiLs  the  liver  is  smooth,  and  is  firmer  and  more  resistant 
than  normal.  The  healthy  colour  is  altered;  occasionally,  in  the  early 
stages  of  the  disease,  it  is  congested,  but  usualh'  its  tint  is  hghter  than 
in  health;  it  may  be  violet,  greyish-yellow,  and  approaching  the  colour 
of  fhnt  {Foie  Silex  of  Gubler)  or  yellow.  On  section  it  is  firmer  than 
natural  and  resistant,  but  not  to  the  same  extent  as  in  cirrhosis  or  in 
congenital  obhteration  of  the  bile-ducts.  The  organ  tends  to  be  uniformly 
affected,  but  often  some  parts  are  more  affected  than  others,  so  that  a 
marked  or  mottled  appearance  is  presented.  The  alteration  in  colour 
is  the  same  as  described  above,  but  the  mottling  may  be  more  marked; 
areas  presenting  the  yellow  change  may  alternate  with  parts  preserving 
the  more  or  less  healthy  red  colour,  and  the  appearance  may  suggest 
primary  sarcoma.  In  other  instances  the  glistening,  semi-translucent 
aspect  resembles  that  of  a  lardaceous  liver. 

On  carefully  examining  the  cut  surface  small  grey  spots  like  grains 
of  semolina  are  generally  visible;  they  are  small  granulomata  or  svphil- 
omata,  and,  though  not  caseous,  are  often  spoken  of  as  miliary  gummata. 
The  left  lobe  is  said  to  be  more  often  affected  with  these  syphilomata. 


SYPHILITIC    DISEASE    OF    THE    LIVER. 


369 


To  the  naked  eye  these  look  Hke  small  miHary  tubercles,  and  micro- 
scopically they  so  far  resemble  them  in  being  localised  collections  of 
small  round  cells.  Tubercle  may  indeed  be  associated  \\'ith  intercellular 
cirrhosis,  and  the  distinction  between  these  small  s^iohilomata  and 
mihary  tubercles  depends  on  the  absence  of  tubercle  bacilh.  In  rare 
instances  definite  caseous  gummata  have  been  found  in  infants  and  even 
in  still-born  cliildren  and  jaremature  fcetuses. 

Canton  *  has  figured  multiple  hepatic  gummata  in  a  child  of  seven  weeks,  and 
Sir  T.  Barlow  t  gave  a  description  of  "receding  gummata"  in  a  child  twelve  weeks 
old.  Bittner  X  has  recorded  gummata  in  the  liver  of  a  still-born  child  and  in  a 
six  months'  foetus.  A  number  of  other  cases  are  given  by  Lancereaux  §.  and  by 
Hutinel  and  Hudelo.  11 


r;!  - 


4:-- -A     •V!J -^  ♦'  V,.i  V.' V-'  --^v;.     -mNrr\ 


Fig.  45. — Microscopic  Appeakanci-s  in  Pericellular  Cirrhosis. 
There  is  delicate  connective  tissue  between  the  small  groups  of  liver  cells. 


The  microscopic  appearances  vary  very  greatly  according  to  the  dura- 
tion and  virulence  of  the  infection.  In  the  earliest  stage  there  is  capillary 
congestion  mth  commencing  small-cell  infiltration,  which  subsequently 
becomes  diffuse,  spreads  widely  between  the  liver  cells,  and  may  invade 
the  portal  spaces.  These  newly  formed  cells  are  the  outcome  of  pro- 
liferation of  (a)  the  pre-existing  connective-tissue  cells  of  the  organ;  (b) 
of  the  endothehum  of  the  capillaries  and  lymphatics  inside  the  hepatic 

*  Canton,  E.:  Trans.  Path.  Soc,  vol.  xiii,  p.  113. 

t  Barlow,  T.:  Ibid.,  xxvii,  p.  202. 

t  Bittner:  Prag.  med.  Wochen.,  Bd.  xviii,  S.  581,  1893. 

§  Lancereaux:  A  Treatise  on  Syphilis,  vol.  ii,  p.  152.  Translat.  New  Syden- 
ham Soc,  1869. 

II  Hutinel  and  Hudelo:  Archiv  de  Med.  experiment,  et  d'Anat.  path.,  p.  509, 
tome  X,  1890. 
24 


370  DISEASES    OF   THE    LIVER. 

lobules,  while  Kupffer's  star-like  cells,  which  are  intimately  connected 
with  the  endothelial  lining  of  these  vessels,  share  in  this  process.  This 
diffuse  infiltration  closely  resembles  an  infiltrating  sarcoma,  and  natur- 
ally, since  proliferation  of  the  connective  tissues  during  foetal  life  or  soon 
after  birth  leads  to  a  formation  which  is  structurally  much  the  same  as 
that  of  a  sarcoma.  It  is  extremely  probable  that  some  cases  described 
as  diffuse  sarcoma  in  early  life  were  in  reality  examples  of  the  hepatic 
lesion  of  hereditary  s}T)hilis. 

At  a  rather  later  stage  the  infiltrating  cells  have  become  elongated 
and  as  fibroblasts  separate  the  individual  liver  cells  from  each  other. 
There  is  thus  a  pericellular,  unicellular,  or  monocellular  cirrhosis.  This 
appearance  is  occasionally  seen  in  the  secondary  stage  of  syphilis,  and 
locally  in  some  cases  of  ordinary  portal  cirrhosis.  Sometimes  the  micro- 
scopic appearances  of  pericellular  cirrhosis  at  this  stage  are  like  those 
of  an  infiltrating  carcinoma,  the  liver  cells  representing  the  epithelial  cells 
of  carcinoma  and  the  cirrhosis  the  alveolar  walls. 

It  is  interesting  to  note  that  Adami  *  described  pericellular  cirrhosis  in  the 
Pictou  cattle  disease  of  Nova  Scotia.  The  change  is  due  to  a  minute  diplo-bacillus, 
and  gives  rise,  unlike  congenital  syphilitic  disease  of  the  liver,  to  ascites,  diarrhoea, 
and  muscular  weakness — in  short,  to  symptoms  like  those  of  ordinary  cirrhosis. 

As  time  goes  on  the  organisation  of  young  connective  tissue  may 
advance  and  lead  to  well-formed  fibrous  tissue.  The  chronic  nature  of 
the  inflammation,  if  allowed  to  run  its  course,  is  often  well  shown  by 
the  presence  of  both  well-formed  fibrous  tissue  and  recent  inflammatory 
or  granulation  tissue  in  the  same  specimen.  The  fibrous  tissue  of  Glis- 
son's  capsule  in  the  portal  canals  is  also  increased  in  amount.  In  places 
there  may  be  collections  of  small  round  cells — syjDhilomata — or,  as  they 
are  often  called,  miliary  gummata,  though  the  word  "gumma"  should 
iDe  reserved  for  the  further  stage,  where  necrosis  and  caseation  have 
supervened.  These  small  syphilomata  may  be  found  in  association  ^vith 
•early  pericellular  infiltration,  or  later,  when  there  is  well-formed  fibrous 
tissue. 

The  hepatic  lesions  which  can  be  regarded  as  a  remote  result  of  con- 
:genital  syphilis  will  be  referred  to  again  under  the  heading  of  Delayed 
Congenital  Syphilis,  but  here  it  may  be  pointed  out  that  although  ordinarv 
cirrhosis  may  very  probably  supervene  in  a  liver  recovering  from  peri- 
cellular cirrhosis,  it  does  not  appear  reasonable  to  imagine  that  peri- 
cellular cirrhosis  can  be  directly  transformed  into  multilobular  or 
mo  no  lobular  cirrhosis.  Very  marked  fibrosis  attacking  large  areas  of 
the  liver  and  producing  a  tumor-like  mass  is  a  change  sometimes  seen 
as  the  result  of  congenital  syphilis.  Some  cases  of  the  kind  have  been 
described  as  fibroma  of  the  liver.  Marchand  f  has  insisted  on  the  S}q3hil- 
itic  nature  of  these  cases. 

As  an  example  of  very  extensive  fibrosis  Morley  Fletcher's  J  case  of  a  child 
aged  eight  weeks  may  be  referred  to.     The  mother  had  had  seven  other  health}^ 

*  Adami,  J.  G.:  Middleton-Goldsmith  Lecture,  1896. 

t  Marchand:  Centralblatt  f.  allg.  Path.,  Bd.  vii,  S.  273,  1S96. 

j  Morley  Fletcher,  H.:  Trans.  Path.  Soc,  London,  vol.  1,  p.  13S. 


SYPHILITIC    DISEASE    OF   THE    LIVER. 


371 


children  and  one  still-born  infant,  but  no  other  evidence  of  syphiUs  was  forthcom- 
ing. The  liver  was  much  enlarged  and  easily  felt.  There  was  no  jaundice  or 
ascites.  The  liver  weighed  28  ounces  and  microscopically  showed  great  fibrosis, 
the  fibrous  tissue  being  well  formed;  in  addition,  there  were  areas  mth  much  small- 
cell  infiltration.  The  hepatic  cells  were  greatly  atrophied,  compressed,  and  in  many 
places  formed  columns  resembling  pseudo-bile  canaliculi  {vide  Fig.  46);  there  was 
a  considerable  amount  of  extravasation  of  red  corpuscles.  The  spleen  was  not 
enlarged.  The  right  suprarenal  was  enlarged  to  the  size  of  its  corresponding  kidney 
and  there  were  fibrosis  and  extravasation  into  the  medulla.  In  this  case,  as  in  those 
recorded  by  Marchand,  some  doubt  as  to  the  existence  of  syphihs  might  arise. 

The  liver  cells  are  atrophied  and  compressed  as  if  from  pressure,  and 
may  show  granular  and  degenerative  changes.  Fatty  change  is  not 
frequent,  and  when  present  is  usually  quite  sporadic  and  locahsed.  As 
the  result  of  necrosis  they  may  disappear  from  considerable  areas,  their 
place  being  taken  by  organising  granulation  tissue.     The  liver  cells  may 


Fig.  46. — -Microscopic  Section  from  a  Case  of  Congenital  Syphilis. 

Showing  extensive  fibrosis,  areas  of  small-cell  infiltration  (c),  compressed  liver  cells,  and  columns 

of  cells  resembling  small  bile-ducts  (6).     (Drawing  kindly  lent  by  Dr.  H.  Morley  Fletcher.) 


be  so  compressed  that  they  closely  resemble  newly  formed  bile-ducts. 
This  may  be  explained  in  two  ways:  (a)  on  the  supposition  that  the 
specific  changes  began  early  in  foetal  life  and  arrested  the  de'S'elopment 
of  the  liver  parenchyma  so  that  it  remained  in  many  parts  as  a  tubular 
gland,  while  in  other  areas  the  liver  cells,  being  less  interfered  with,  were 
able  to  develop  more  or  less  normally;  (b)  on  the  hyjjothesis  that  these 
pseudo-bile  canaliculi  are  an  attempt  at  compensation  by  hypeiplasia 
of  the  remaining  liver  cells. 

Adanii  *  regards  the  changes  in  the  liver  cells  as  primary,  and  due  to  the  action 
of  the  poison,  and  the  pericellular  infiltration  as  secondary  and  of  the  nature  of  a 
replacement  fibrosis.     Tlie  view  which  appeals  more  to  nay  mind  is  that  both  the 

*  Adami,  J.  G.:  New  York  Med.  Journ.,  April  22,  1899. 


372  DISEASES   OF  THE   LIVER. 

degenerative  changes  in  the  Hver  cells  and  the  pericellular  cirrhosis  are  concomitant 
results  of  the  same  factor — the  poison. 

The  hepatic  artery  is  normal  and  is  free  from  endarteritis,  a  change 
which  would  naturally  be  expected  if  the  syphilitic  virus  reached  the 
liver  from  the  general  circulation.  In  exceptional  instances,  however, 
endarteritis  and  peri-arteritis  and  phlebitis  are  present.  (Obernderfer.*) 
There  is  an  increase  in  the  amount  of  fibrous  tissue  and  in  exceptional 
instances  marked  inflammatory  changes  around  the  bile-ducts  and  portal 
vein  in  the  portal  spaces.  Endophlebitis  of  the  branches  of  the  hepatic 
veins  sometimes  occurs,  and  if  allowed  to  progress,  may  eventually  lead 
to  stenosis  of  the  orifice  of  these  veins.     (Vide  p.  50.) 

The  variations  met  with  in  the  liver  in  congenital  syphilis  depend  on 
the  severity  of  the  infection  and  its  duration.  The  following  conditions 
may  be  recognised : 

I.  The  commonest  change  is  a  diffuse  embryonic  infiltration  which 
subsequently  develops  into  young  connective-tissue  cells  separating  the 
individual  liver  cells;  this  is  pericellular,  unicellular,  or  monocellular 
cirrhosis. 

II.  The  previous  condition  may  be  combined  with  small  collections 
of  round  cells  or  miliary  gummata. 

III.  Further  organisation  of  the  pericellular  infiltration  leads  to  wide- 
spread or  local  areas  of  fibrosis. 

IV.  Occasionally  well-formed  caseous  gummata  like  those  seen  in 
adults  are  present. 

V.  A  combination  of  gummata  with  fibrosis  (gummatous  hepatitis) 
not  affecting  the  whole  organ,  but  forming  circumscribed  areas  which 
occasionally  may  be  so  marked  as  to  imitate  a  new-growth  or  tumor. 

The  diffuse  monocellular  cirrhosis  is,  like  the  lesions  of  secondary 
syphilis  elsewhere  in  the  body,  an  essentially  curable  condition  if  treated 
with  mercury.  It  may,  however,  pass  into  the  tertiary  lesions,  and 
gummata,  cicatrices,  and  lardaceous  changes  may  develop.  (Vide  De- 
layed Congenital  Syphilis,  p.  375.) 

The  spleen  is  generally  enlarged,  and  from  fibrosis  becomes  firmer  than 
natural.  Lardaceous  disease  may  be  seen  in  older  children.  Gummata 
are  extremely  rare;  Still  f  could  only  find  two  cases  in  infants.  There 
may  be  adhesions  between  the  capsule  and  adjacent  parts.  Microscopi- 
cally there  is  fibrosis. 

The  kidneys  may  also  present  interstitial  fibrosis. J  This  is  a  point 
of  interest  in  connexion  with  Payne's  §  view  that  granular  kidneys  in 
young  children  depend  on  hereditary  syphilis.  There  may  be  diffuse 
small-cell  infiltration  in  the  pancreas  and  testes,  while  changes  in  the 
lungs  are  comparatively  frequent.  The  suprarenal  bodies  are  larger  than 
natural.  There  may  be  small-cell  infiltration,  haemorrhage,  or  fatty 
change. 

*  Obernderfer:  Centralblattf.  allg.  Path.  u.  path.  Anat.,  March  25,  1900. 

t  Still:  Trans.  Path.  Soc,  vol.  xlviii,  p.  205. 

t  Hebb,  R.  G.:  Trans.  Path.  Soc,  vol.  xlviii,  p.  117. 

§  Payne,  J.  F.:  Ibid.,  vol.  H,  p.  364. 


SYPHILITIC    DISEASE    OF   THE    LIVER.  373 

Clinical  Features. — When  the  infection  is  advanced,  the  child  may 
be  still-born  or  die  a  few  days  after  birth.  In  many  cases  the  child  is 
healthy  when  born  and  subsequently  develops  evidences  of  congenital 
syphilis.  As  a  general  rule,  signs  pointing  definitely  to  the  liver,  such 
as  jaundice  and  ascites,  are  absent,  and  it  is  only  on  examination  that 
the  liver  and  spleen  are  found  to  be  enlarged.  The  clinical  features  may 
be  summarised  in  a  word.  The  well-known  manifestations  of  hereditary 
syphilis  are  present,  and,  in  addition,  there  is  evidence  of  enlargement 
of  the  spleen  and  liver. 

The  liver  is  enlarged :  it  may  even  reach  down  to  the  iliac  crest.  This 
enlargement  is  frequent  in  congenital  syphilis;  in  148  cases  it  was  pal- 
pably so  in  48.  (Hochsinger.*)  In  connexion  with  the  enlargement  of 
the  hver  it  must  be  borne  in  mind  that  normally  in  young  children  the 
liver  projects  further  down  than  in  adults;  this,  Henoch  points  out,  is 
not  merely  due  to  the  relatively  larger  size  of  the  organ  in  children,  but 
also  to  the  ribs  being  more  horizontal  and  so  leaving  the  organ  more 
uncovered.  Hence  slight  apparent  enlargement  must  not  be  regarded 
as  of  any  importance  in  the  absence  of  other  evidence.  The  degree  of 
hepatic  enlargement  corresponds  with  that  of  the  other  manifestations 
of  the  disease,  and  may  therefore  be  taken  as  an  index  of  the  severity 
of  the  infection. 

The  hver  is  firm,  tender,  and  somewhat  resistant.  In  some  cases 
there  is  a  localised  tumor  formation  which  is  readily  felt  during  life. 
These  cases  are,  of  course,  very  rare;  reference  to  Marchand's  cases  has 
already  been  made. 

In  a  child  three  months  old,  icterus,  ascites,  and  cerebral  symptoms  were  asso- 
ciated with  a  gummatous  growth  projecting  from  the  under  surface  of  the  right 
lobe  of  the  liver.     (Cohn.t) 

The  spleen  is  enlarged  in  cases  of  hereditary  syphilis.  This  univer- 
sally accepted  fact  was  pointed  out  by  Gee  {  in  1867,  who  found  cUnical 
evidence  of  splenic  enlargement  in  one-fourth  of  the  cases  of  hereditary 
syphilis. 

More  recently  the  incidence  of  splenic  enlargement  in  congenital  syphilis  has 
been  estimated  at  45  per  cent,  by  Still, §  and  at  63  by  Coutts.  || 

Jaundice  occasionally  occurs,  and  is  probably  not  so  extremely  rare 
as  is  often  stated.  It  may  be  explained  as  due  to  various  factors.  It 
may  possibly  depend  on  pressure  of  enlarged  glands  in  the  portal  fissure 
on  the  ducts,  or  on  pressure  exerted  by  masses  of  syphilitic  granulation 
tissue,  but  is  more  probably  due  to  inflammatory  changes  in  the  small 
bile-ducts  which  form  part  of  the  diffuse  pericellular  hepatitis.  In  the 
latter  case  it  is  much  the  same  as  the  jaundice  occasionally  seen  in  the 
secondary  stage  of  acquired  syi^hilis.  IVIilon  **  has  drawn  attention  to 
secondary  infection  as  a  cause  of  jaundice  in  congenital  syphilis;  in  two 

*  Hochsinger:  Wiener  med.  Wochen.,  Bd.  xlvi,  S.  345,  1896. 
t  Cohn,  M.:  Virchow's  Archiv,  Bd.  cxlvi,  S.  468. 
t  Gee,  S.:  Brit.  Med.  Journ.,  1867,  vol.  i,  p.  435. 

§  Practitioner,  vol.  Ixxiii,  p.  101.  ||  Brit.  Med.  Jour.,  1896,  vol.  i,  p.  1025. 

**  Milon:  Thdse  Paris,  1897,  No.  434. 


374  DISEASES    OF   THE    LIVER. 

of  his  cases  the  infective  agent  was  Proteus  vulgaris  and  the  colon  bacillus 
respectively.  The  micro-organisms  may  enter  through  the  umbilical 
vein  and  find  a  suitable  nidus  in  the  liver,  the  resistance  of  which  has 
been  reduced  by  the  sj^hilitic  lesion.  The  development  of  jaundice  is 
thus  comparable  to  icterus  gravis  supervening  in  ordinary  cirrhosis.  The 
aspect  of  the  case  may  then  be  one  of  multiple  haemorrhages  and  resemble 
the  acute  umbilical  infections  in  the  newly  born.  Perr}"  and  Shaw  * 
refer  to  a  case  of  this  kind,  which  was  regarded  as  primarily  s}T3hilitic, 
in  an  infant  two  weeks  old. 

When  jaundice  is  met  with  in  congenital  s}"philis,  it  is  usually  present 
at  birth,  but  it  may  not  come  on  until  some  weeks  later.  In  rare  cases 
the  jaundice  may  be  seen  to  pass  away  and  return  again. 

Still  t  refers  to  a  boy  who  was  j  aundiced  for  the  first  six  weeks  of  life ;  he  then 
recovered  and  appeared  perfectly  healthy  until  the  age  of  two  j^ears  and  three  months, 
when  he  again  became  attacked  by  jaundice,  which,  after  lasting  some  weeks,  proved 
fatal.     Microscopically  the  liver  showed  intercellular  cirrhosis. 

Ascites  in  hke  manner  is  very  rare;  it  may  be  due  to  concomitant 
peritonitis  and  perihepatitis,  which  are  not  very  rare  in  severe  cases  of 
the  disease;  or  possibly  to  the  pressure  of  enlarged  glands  in  the  portal 
fissure.  In  intrauterine  life  hepatic  syphilis  may  so  interfere  vith  the 
circulation  through  the  umbilical  vein  as  to  produce  tydramnios,  and  a 
number  of  premature  deaths  are  thus  accounted  for.  But  in  infants 
which  survive  there  is  not  sufficient  phlebitis  of  the  portal  vein  to  produce 
ascites.  The  abdomen  is  somewhat  distended,  partly  from  enlargement 
of  the  liver  and  spleen,  and  partly  from  tympanites.  As  already  pointed 
out,  ascites  is  very  rarely  present.  Prominence  of  the  subcutaneous  ab- 
dominal veins  is  sometimes  noticeable.  The  usual  symptoms  and  signs 
of  congenital  S}q3hilis,  such  as  debility,  wasting,  the  cutaneous,  mucous, 
and  bony  lesions,  anaemia,  and  in  some  cases  multiple  haemorrhages, 
vomiting,  and  diarrhoea,  are  present. 

Diagnosis. — This  is  usually  verj^  much  easier  than  in  acquired 
syphilitic  disease  of  the  liver  in  adults,  inasmuch  as  there  are  usually 
well-marked  signs  of  S}q3hilis  elsewhere  in  the  body  of  the  infant.  In  the 
absence  of  these  signs  other  causes  for  enlargement  of  the  liver  and 
spleen,  such  as  rickets,  tuberculosis,  gastro-intestinal  infection,  and 
the  various  forms  of  anaemia,  must  be  considered  and  as  far  as 
possible  eliminated.  In  cases  where  there  is  jaundice  from  birth  without 
any  manifest  signs  of  sj^phihs  simple  catarrhal  jaundice  and  co.ngenital 
obliteration  of  the  ducts  must  be  borne  in  mind.  In  cases  of  doubt 
much  assistance  will  be  obtained  by  a  course  of  mercurial  treatment. 

Prognosis. — The  prognosis  depends  on  the  general  state  of  nutrition 
and  on  efficient  and  prompt  anti-syphilitic  treatment.  If  the  liver  and 
spleen  are  greatly  enlarged,  the  prognosis  is  grave.  Visceral  enlargement 
may  be  regarded  as  an  index  of  the  severity  of  the  infection.  The  occur- 
rence of  hemorrhages  is  of  bad  omen,  and  cases  with  jaundice  usuallv  do 
badly. 

*  Perry  and  Shaw:  Guy's  Hosp.  Reports,  vol.  1,  p.  226. 
t  Still":  Clinical  Journal,  vol.  xvii,  p.  322,  1901. 


SYPHILITIC    DISEASE    OF   THE    LIVER.  375 

Treatment. — The  treatment  is  that  of  cfingenital  syphihs  with  mer- 
cury b}'  inunction  or  by  the  mouth.  Hydrargyrum  cum  creta  may  be 
given  in  the  form  of  a  powder:  to  a  child  under  two  months  h  grain 
twice  a  day;  after  that  age  the  dose  being  increased  to  one  grain.  Liquor 
hydrargyri  perchloridi  may  be  given  instead  or  the  French  preparation 
of  Liqueur  de  ^  an  Swieton  in  doses  of  10  minims  daily  for  a  child  of 
one  month  old,  increasing  the  doses  by  5  or  10  minims  every  month  or 
so.  A  more  satisfactory  method,  both  because  it  acts  more  rapidly  and 
is  less  likely  to  lead  to  salivation,  is  mercurial  inunction.  ^Mercurial  oint- 
ment is  rubbed  on  with  flannel,  into  the  axilla,  over  the  liver,  and  over 
the  spleen,  a  fresh  situation  being  selected  daily.  To  begin  with,  about 
15  grains  of  the  ointment  should  be  used  every  day. 

The  mercurial  treatment  should  be.  carried  out  daily  for  three  months, 
and  then  relaxed  gradually;  in  the  fourth  month  the  treatment  being 
intermitted  for  a  week  at  a  time,  and  in  the  fifth  month  for  two  weeks^ 
In  the  second  year  of  treatment  mercurial  inunction  should  be  performed 
during  one  month  out  of  three,  and  small  doses  of  iodide  of  potassiuni 
given.  In  the  third  year  the  dose  of  the  iodide  may  be  increased,  and 
in  the  fourth  year  the  mercurial  treatment  may  be  dropped,  while  the 
iodide  is  continued.  In  this  way  the  appearance  of  tertiarj^  manifesta- 
tions should  be  prevented.  As  a  means  of  preventing  both  abortion  and 
syphilitic  infection  of  the  foetus  a  pregnant  woman  known  to  be  the 
subject  of  syphilis  should  go  through  a  course  of  ant i -syphilitic  treatment- 

THH   HEPATIC   MANIFESTATION   OF   DELAYED   CONGENITAL   SYPHILIS. 
Synonym:  Tardive  Hereditary  Syphilis. 

Description. — The  changes  in  the  liver  are  the  same  as  in  the  tertiary 
stage  of  the  accj[uired  disease,  but  they  occur  in  the  subjects  of  undoubted 
hereditary  or  congenital  syphilis. 

History. — The  recognition  of  this  form  of  syphilis  is  usually  credited 
to  Fouriiier  in  1886.  Probal)h'  the  earliest  recorded  case  was  described 
in  1863  by  Sir  S.  Wilks;  *  the  patient  was  a  girl  aged  twelve  years  whose 
mother  had  had  secondary  syphilis.  The  child's  liver  was  much  de- 
formed and  contained  gummata  and  numerous  cicatrices. 

H.  Morris'  f  case  is  worth  referring  to  as  one  of  the  earlier  examples  of  tardive 
hereditary  syphilis.  The  patient  was  a  girl  aged  twenty  years  with  a  family  history 
of  syphilis  and  a  personal  history  of  interstitial  keratitis.  The  liver  was  noticed 
to  be  enlarged  at  eighteen  and  ascites  appeared  in  the  course  of  the  next  year. 
At  the  autopsy  the  liver,  which  weighed  thirty-nine  oimces,  was  fissured,  puckered, 
lardaceous,  and  contained  gummata;   the  kidneys  and  spleen  were  also  lardaceous. 

Incidence. — The  disease  is  not  very  I'aro.  In  1885  Fournior  J  col- 
lected 25,  and  in  1890  Hudelo  ^  referred  to  49,  cases.  In  1902  Forbes  || 
collected  132. cases  showing  the  lesions  of  late  hereditary  syphilis  in  one 

*  Wilks,  S.:  Guv's  Hosp.  Rep.,  1803. . 
t  Morris,  H.:  Trans.  Path.  Soc,  vol.  xxi,  p.  214. 
X  Fournier:  La  Syphilis  hereditaire  tardive,  1S.S6. 

§  Hudelo:  Quoted  by  Chauffard,  Traitf'-  de  Medecine  [Bouchard,  Bri.ssaud],  tome 
V,  p.  265.  II  Forbes:  St.  Bartholomew's  Hosp.  Reports,  vol.  xxxviii,  p.  37. 


376  DISEASES    OF    THE    LIVER. 

form  or  another.  In  34  per  cent,  of  Forbes'  cases  the  hver  was  affected 
with  changes  other  than  lardaceous  disease,  such  as  cicatrices,  gunimata, 
cirrhosis,  or  perihepatitis.  It  may  come  on  in  any  of  the  first  three 
decades  of  life  or  even  later;  more  than  half  occur  in  the  second  decade. 

In  Forbes'  cases  26.5  per  cent,  came  on  in  the  first  decade,  57.5  in  the  second, 
12.3  in  the  third,  and  3.7  in  the  fourth. 

The  presence  of  gummata  in  the  hvers  of  infants  or  in  exceptional 
instances  in  new-born  children  shows  that  the  same  changes  may  occur 
very  early  in  Ufe.  The  hepatic  lesions  are  tertiary  in  character  and 
exactly  resemble  those  seen  in  the  acquired  disease.  The  secondary 
lesions  having  persisted,  and  instead  of  being  cured  by  treatment  have 
been  succeeded  by  the  tertiary  lesions  commonly  present  in  accjuired 
hepatic  syphihs  and  sometimes  seen  in  the  early  stage  of  the  hereditary' 
disease.  Tardive  congenital  sypliilitic  disease  of  the  liver  therefore  forms 
a  connecting  link  between  the  ordinary  congenital  and  acquired  types 
of  hepatic  syphilis.  In  order  to  be  sure  that  the  case  is  one  of  delayed 
congenital  syphilis  there  must  be  some  other  evidence  of  the  congenital 
affection,  such  as  interstitial  keratitis,  otherwise  the  disease  might  have 
been  acquired  in  early  life;  for  example,  from  a  wet-nurse. 

Morbid  Anatomy. — The  liver  is  nearly  always  enlarged  and  is  changed 
in  much  the  same  way  as  in  the  tertiary'  stage  of  the  acquired  disease. 
It  may  be  very  greatly  deformed  and  cut  up  into  numerous  lobes;  it  is 
highly  probable  that  some  of  the  recorded  anatomical  abnormaUties  of 
multiple  lobulation  (as  many  as  16  lobes  have  been  described)  can  be 
thus  explained.  The  lesions  are  gummata,  cicatrices,  fibrosis,  pericellular 
cirrhosis,  and  lardaceous  change  in  varjdng  degrees  and  combinations. 
(Vide  Lesions  of  the  Liver  in  Acquired  Syphilis.)  It  is  weU  to  remember 
that,  as  in  early  congenital  syphilis,  the  naked-eye  appearance  of  the 
liver  may  suggest  malignant  disease;  this  was  the  first  naked-eye  diag- 
nosis in  a  boy  aged  fifteen  years  with  tardive  hereditary  hepatic  syphilis 
described  by  H.  W.  G.  Mackenzie.*  Perihepatitis  is  common  and  may 
be  the  means  by  which  gummatous  inflammation  spreads  to  the  ab- 
dominal wall.  The  other  organs  may  show  SA^philitic  lesions  and  ad- 
vanced lardaceous  disease. 

Clinical  Features. — The  subjects  of  tardive  hereditary  syphilis  usu- 
ally display  copious  signs  of  syphilitic  infection  in  the  bones,  sense 
organs,  or  in  the  existence  of  widespread  lardaceous  disease.  They  are 
ill  developed,  look  much  less  than  their  years,  and  are  examples  of  what 
has  been  called  infantilism.  The  liver  is  nearly  always  enlarged  and 
may  even  appear  as  a  tumor;  this  point  is  illustrated  in  cases  recorded 
by  Post  t  and  Bristowe.| 

In  Po.st's  case,  a  boy  aged  twenty-two  years,  the  subject  of  late  hereditary 
syphiUs,  there  were  gummata  in  various  bones,  in  the  pancreas,  and  in  the  Hver. 
A  gumma  in  the  liver  had  become  adherent  to  and  in^-aded  the  abdominal  wall, 
giving  rise  during  life  to  a  very  definite  tumor.     Besides  gummata  the  liver  showed 

*  MacKenzie,  H.  W.  G.:  Trans.  Path.  Soc,  vol.  xhii,  p.  84. 
t  Post:  Boston  Citv  Hospital  Reports,  1898,  p.  233. 
t  Bristowe:  Brit.  Med.  Journ.,  1886,  vol.  i,  p.  878. 


SYPHILITIC    DISEASE    OF   THE    LIVER. 


377 


very  diffuse  fibrosis.  As  is  not  uncommonly  seen  in  severe  examples  of  syphilis, 
the  patient  died  from  an  acute  secondary  infection  with  streptococci.  Bristowe's 
case,  a  boy  aged  fifteen  years,  had  a  tumor  of  uncertain  nature  connected  with 
the  hver  which  yielded  nothing  on  aspiration.  The  temperature  was  hectic.  As 
there  was  reason  to  believe  that  the  boy  was  the  subject  of  congenital  syphihs, 
anti-syphihtic  remedies  were  employed  and  the  signs  and  symptoms  all  disappeared. 

The  spleen  is  enlarged  either  from  lardaceoiis  change  or  independ- 
ently, as  in  the  following  case,*  which  imitated  hypertrophic  bihary 
cirrhosis. 

A  boy  aged  seventeen  years,  under  the  care  of  my  colleague,  Dr.  Ewart,  had 
chronic  jaundice  of  some  years'  duration,  subcutaneous  gummata,  periostitis, 
enlargement  of  the  spleen  and  hver,  and  clubbed  fingers.  He  was  the  subject  of 
congenital  syphihs.  Death  was  due  to  erysipelas  comphcated  by  pericarditis  and 
peritonitis.  The  liver  weighed  5  pounds,  the  right  lobe  was  much  scarred  by  gum- 
mata and  was  small,  a  fibrous  mass  compressed  the  common  hepatic  duct  just  at 
its  commencement  and  obstructed  the  entrance  of  the  two  hepatic  ducts  into  it. 
The  spleen  weighed  45  ounces.     None  of  the  organs  were  lardaceous. 


Fig.  47. — Photograph    Showing  Clubbing  of    Fingers  in  a  Case  of  Tardive  Hereditary 
Syphilis.     (Photographed  by  Dr.  H.  G.  Drake  Brockman.) 


There  may  be  oedema  of  the  feet  and  evidence  of  lardaceous  disease 
of  the  kidneys,  and  eventually  ursemia.  Jaundice  is  rare,  while  ascites 
is  very  common.  Jaundice  and  ascites  may  be  due  to  pressure  exerted 
by  gummata  or  cicatrices  in  the  portal  fissure,  while  ascites  may  be  part 
of  the  general  dropsy  of  lardaceous  kidney  disease.  In  some  instances 
there  is  widespread  arteriosclerosis,  with  so  much  narrowing  of  the  arteries 
(endarteritis  obliterans)  that  the  pulses  in  the  limbs  may  be  absent. 
Death  may  be  due  to  secondary  infections,  such  as  erysipelas,  or  be  due 
to  urgemia,  cardiac  failure,  or  asthenia. 

Diagnosis, — The  diagnosis  rests  on  the  evidence  of  congenital  syphilis, 
as  shown  by  interstitial  keratitis,  Hutchinson's  teeth,  deafness,  and 
infantilism,  together  with  hepatic  enlargement.  If  evidences  of  syphilis 
common  to  the  congenital  and  the  acquired  forms,  such  as  gummata  and 
lardaceous  disease,  are  present  and  none  of  the  stigmata  of  the  congenital 
variety  are  obvious,  the  infection  may  have  been  acquired  in  early  life. 
But  from  the  point  of  view  of  treatment  an  accurate  distinction  between 

*  Lazarus-Barlow,  W.  S.:  Trans.  Path.  Soc    vol.  1,  p.  158. 


378  DISEASES    OF   THE    LIVER. 

tardive  congenital  and  ordinary  syphilitic  disease  of   the  liver  is  im- 
necessar}'. 

The  following  case  illustrates  the  difficulties  which  may  arise  in 
classification:  there  was  tardive  hereditary  syphilis,  but  the  hepatic 
lesions  were  of  the  secondar}^  and  not  of  the  tertiary  stage.  Chnically 
the  hepatic  enlargement  must  have  appeared  to  have  been  undoubtedly 
of  a  tertiary  nature. 

In  a  marked  case  of  the  congenital  syphilitic  disease  with  Parrot's  pseudo- 
paralysis, deafness,  and  other  stigmata  in  a  girl  aged  twenty-one  years,  recorded 
by  Touche,*  the  liver,  which  weighed  104  ounces,  only  showed  pericellular  cirrhosis, 
although  gummata  and  tertiary  lesions  were  present  in  the  bones. 

When,  as  is  often  the  case,  the  most  proixdnent  features  are  those 
of  enlarged  liver,  ascites,  and  lardaceous  disease,  the  diagnosis  turns  on 
evidence  of  past  syphilis;  failing  this  and  any  other  cause  for  lardaceous 
disease,  such  as  prolonged  suppuration,  the  possibility  of  tardive  heredi- 
tary syphilis  should  be  thought  of. 

Prognosis. — The  prognosis  is  not  so  favourable  as  in  acquired  tertiary 
syphiHs  of  the  liver;  the  effects  of  the  poison  are  more  "widespread,  and 
the  frequency  with  which  extensive  lardaceous  disease  is  present  makes 
the  outlook  very  grave.  The  treatment  is  that  of  acquired  S3'philis  in  its 
tertiary  stage.     {Vide  p.  365.) 

REFERENCES. 

Alexejew:  Monats.  f.  prakt.  Dermat.,  1897,  xxiv,  S.  8. 

Barthelemy:  Archiv.  General,  de  Med.,  May,  June,  1886. 

Bristowe:  Medical  Press  and  Circular,  1886,  vol.  i,  p.  405. 

Fournier:  Svphilis  hereditaire  tardive,  1896. 

Mackenzie,  H.  W.  G.:  Trans.  Path.  Soc,  vol.  xliii,  p.  84. 

Moore,  X.:  Trans.  Path.  Soc,  vol.  xxxvii,  p.  271. 

Morris,  H.:  Trans.  Path.  Soc,  vol.  xxi,  p.  214. 

Osier:  Diagnosis  of  Abdominal  Tumours. 

Pitt:  Brit.  Med.  Journal,  1891,  vol.  i,  p.  995. 

Plicciue:  Gaz.  des  Hop.,  Jan.  8,  1898. 

Post:  Boston  City  Hosp.  Report,  1898,  p.  233. 

Touche:  Bull.  Soc  Anat.  Paris,  1900,  p.  852. 

Tzevtline:  These  Paris,  1896. 

Wilks:  Guy's  Hosp.  Reports,  vol.  ix,  p.  24,  1863. 

Wills:  Liverpool  Medico-Chirurg.  Journ.,  July,  1892. 

PARASYPHILITIC    MULTILOBULAR    CIRRHOSIS. 

The  subsequent  development  of  multilobular  cirrhosis  in  young  per- 
sons the  subjects  of  congenital  syphilis  is  a  point  of  considerable  interest. 
The  diffuse  pericellular  cirrhosis  of  infants  suffering  from  congenital 
syphilis  is,  like  the  lesions  of  the  secondary  stage  of  the  acquired  disease, 
a  curable  condition.  Microscopic  examination  of  the  livers  of  children 
formerly  affected  with  well-marked  hereditary  sy]3hilis  may  show  no 
disease.  On  the  other  hand,  every  now  and  again  the  liver  of  a  child 
who  bears  undoubted  stigmata  of  congenital  syphilis  in  the  body  is 
found  to  show  ordinar}^  cirrhosis.  The  arrangement  of  the  two  lesions 
is  so  dissimilar  that  pericellular  cirrhosis  cannot  be  thought  to  be  trans- 
*  Touche:  Bull.  Soc.  Anat.  Paris,  1900,  p.  852. 


SYPHILITIC    DISEASE    OF   THE    LIVER.  379 

formed  into  multilobular  cirrhosis;  it  would  rather  lead  to  diffuse  fibrosis 
or  gummatous  change.  It  seems  probable  that  the  pericellular  cirrhosis 
undergoes  absorjDtion,  but  that  some  vulnerability  or  diminished  re- 
sistance of  the  liver  is  left  behind.  If  causes  then  arise  that  tend  to 
produce  ordinary  cirrhosis,  this  change  will  be  readily  produced.  In 
other  words,  the  multilobular  cirrhosis  is  a  parasyphilitic  lesion,  and  is 
comparable  to  general  paralysis  of  the  insane,  in  that  though  not  syph- 
ilitic, it  is  favoured  by  syphilisation  of  the  soil. 

Sometimes  multilobular  cirrhosis  due  to  its  ordinary  causes  may 
supervene  in  a  Hver  where  pericellular  cirrhosis  still  exists.  This  would 
account  for  some  cases  of  very  extensive  fibrosis,  chiefly  of  the  multi- 
lobular type,  but  where  there  are  in  addition  areas  of  fibrosis  suggesting 
that  pericellular  cirrhosis  has  gone  on  to  organisation.  Occasionally  in 
multilobular  cirrhosis  occurring  early  in  life  in  the  subjects  of  congenital 
S3^philis  there  is  early  lardaceous  change  in  the  organ. 

The  clinical  features  of  these  cases  of  ordinary  cirrhosis  supervening 
in  the  subjects  of  congenital  syphilis  are  much  the  same  as  those  of  portal 
cirrhosis  in  children,  viz.,  portal  obstruction,  ascites,  wasting,  etc.  In 
some  instances  it  will  be  difficult  to  distinguish  between  the  cases  of 
cirrhosis  -^dth  facial  and  other  stigmata  of  hereditary  disease  and  cases 
of  tardive  hereditary  s}T3hilis  with  ascites;  in  the  latter  disease  there 
may  be  lardaceous  disease  of  the  various  organs,  including  the  kidney, 
as  shown  by  albuminuria.  Wliat  proportion  of  the  cases  of  advanced 
portal  cirrhosis  of  the  liver  in  children  have  a  sj-iDhilitic  substratum  it 
is  difficult  to  say  with  certainty;  but  the  statistics  of  reported  cases 
make  it  clear  that  direct  evidence  of  syphilis  is  often  absent.  The  fol- 
lowing case  illustrates  the  very  marked  degree  of  cirrhosis  that  may 
develop  in  the  wake  of  congenital  syphilis  and  the  importance  of  a  careful 
microscopic  examination  in  distinguishing  this  condition  from  tardive 
hereditary  syjDhilis : 

A  boy  aged  thirteen  years,  who  had  never  taken  alcohol,  was  the  third  child 
of  his  mother,  who  had  four  miscarriages,  all  after  his  birth.  In  May,  1898,  the 
abdomen  enlarged,  he  became  languid  and  tired,  and  in  August  he  becaine  short 
of  breath,  and  ha^matemesis  and  mela?na  occurred.  When  admitted  to  St.  George's 
Hospital  under  the  care  of  Dr.  Penrose,  the  liver  was  found  to  be  much  enlarged, 
reaching  three  fingerbreadths  below  the  costal  arch,  and  dilated  veins  were  present 
on  the  abdominal  wall.  Ascites  developed  and  he  was  twice  tapped;  death  oc- 
curred three  weeks  after  the  last  tapping.  There  was  no  oedema  of  the  feet  or 
albuminuria.  At  the  autopsy  the  liver,  42  oimces,  was  enlarged  and  granular  on 
the  surface;  on  section  there  were  white  areas  suggesting  gummatous  infiltration. 
These  were  especially  well  marked  around  the  hepatic  veins,  and  by  narrowing 
them  had  induced  thrombosis.  Microscopically,  however,  these  areas  showed  no 
caseation,  while  there  was  a  high  degree  of  fibrosis,  multilobular  and  intercellular 
cirrhosis.  There  was  no  lardaceous  change.  The  spleen  was  enlarged,  weighing 
16  ounces,  and  contained  a  large  fibrous  area  in  its  centre.  The  oesophageal  veins 
were  dilated.  The  teste.s  and  kidneys  were  healthy.  The  liver  is  in  St.  George's 
Hospital  Museum,  Series  ix.  174.  T,  and  was  described  by  Dr.  Lazarus-Barlow.* 

Diagnosis, — It  may  be  difficult  to  differentiate  l)etween  these  cases 
of  cirrhosis  in  individuals  with  other  manifest  signs  of  congenital  sjq^hilis, 
on  the  one  hand,  and  cases  of  tardive  hereditary  syphilis  with  he]~»atic 

*  Lazarus-Barlow,  W.  S.:  Trans.  Path.  Sec,  vol.  1,  p.  146. 


380  DISEASES   OF  THE   LIVER. 

lesions  and  ascites,  on  the  other  hand.  In  the  latter  there  may  be  ex- 
cessive lardaceous  disease,  as  shown  by  albuminuria.  Iodide  of  potas- 
sium and  mercury  should  be  tried,  and  improvement  will  point  to  hepatic 
gummata  and  cicatrices  due  to  tardive  hereditary  syphilis,  and  the  treat- 
ment must  then  be  pushed. 

The  prognosis  of  these  cases  is  very  bad. 

The  treatment  is  that  of  ordinary  cirrhosis,  viz.,  milk  diet,  no  alcohol 
or  irritating  food.  Constipation  should  be  prevented  by  seeing  that 
plenty  of  water  is  taken,  and  if  necessary  by  calomel  and  saline  purges. 
Flatulence  and  excessive  intestinal  fermentation  and  putrefaction  should 
be  prevented  by  relieving  constipation  or  by  minute  doses  {-^  to  ^-^  grain) 
of  calomel  or  of  perchloride  of  mercury.  The  iodides  of  potassium,  sodium, 
and  ammonium  should  be  given,  as  is  often  done  in  common  cirrhosis 
of  adults,  to  prevent  if  possible  any  further  progress  in  the  disease.  But 
as  the  lesion  is  parasyphilitic  rather  than  sy[3hihtic,  iodide  of  potassium 
can  hardly  be  expected  to  remove  the  fibrosis.  In  other  respects  the 
treatment  is  on  the  same  lines  as  in  portal  cirrhosis. 


ACTINOMYCOSIS. 

Incidence. — Actinom3^cosis  («>=-:?,  "a  ray/'  iJ-'y^-^i^,  "a  fungus")  is 
rare  in  Great  Britain  and  America;  less  so  in  Germany,  Austria,  and 
Russia.  In  France  its  reputed  rarity  appears  to  be  due  to  the  disease 
having  escaped  recognition;  Duvau  *  has  collected  146  cases  obser\''ed 
in  that  countrv^  In  1902  Erving  f  collected  100  cases  in  America.  In 
1094  cases  of  human  actinomycosis  collected  by  Ruhrah,t  604,  or  56 
per  cent.,  were  in  the  head  and  neck,  223,  or  20  per  cent.,  in  the  digestive 
tract,  164,  or  15  per  cent.,  in  the  respiratory  tract,  26,  or  2  per  cent.,  in 
the  skin;  and  63,  or  6  per  cent.,  were  doubtful. 

Actinomycosis  is  about  three  times  commoner  in  men  than  in  women. 

On  the  basis  of  405  cases  Leith  §  estimated  that  73  per  cent,  were  males  and 
27  per  cent,  females. 

It  is  most  frequent  between  the  ages  of  twenty-five  and  forty-five 
years. 

The  fungus  may  gain  access  to  the  alimentary  canal  in  food;  milk 
from  cows  whose  udders  have  been  infected  from  contact  with  straw 
(Miillerll)  may  spread  the  disease.  The  disease  is  commoner  in  agri- 
culturists who  are  more  likely  to  chew  ears  of  wheat,  barley,  or  straw. 

Actinomycosis  of  the  liver  is  rare.  It  is,  indeed,  rather  surprising  that 
Auvray  **  has  only  been  able  to  collect  records  of  thirty-one  pubhshed 
cases,  and  he  disputes  the  correctness  of  Duvau's  statement  that  forty 
cases  have  been  published. 

Method  of  Origin. — Actinomycosis  of  the  liver  must  be  either 
metastatic,  the  infection  being  conveyed  by  the  blood-stream  from  a 
mucous  or  cutaneous  surface,  or  due  to  the  direct  spread  of  the  disease 
from  a  focus  in  the  neighbourhood.  In  the  majority  of  instances  the  pri- 
mary focus  is  in  the  alimentary  canal,  from  which  infection  may  spread 
either  by  the  blood-stream  or  by  continuity.  In  the  latter  event  there 
may  be  a  mass  of  inflammatory  tissue  extending  between  the  affected 
part  of  the  bowel,  usually  near  the  caecum,  and  the  liver.  In  rare  in- 
stances there  is  a  direct  spread  of  the  actinomycotic  growi;h  from  the 
skin  of  the  abdominal  wall  or  from  the  base  of  the  right  lung  into  the 
liver.  In  some  instances  the  primary  focus,  usually  in  the  intestine,  has 
healed  so  that  it  is  very  difficult  or  impossible  to  determine  its  situation. 
It  is  to  such  cases,  of  which  Aribaud  collected  seven,  that  the  term 
primary  actinomycosis  of  the  liver  has  been  applied. 

*  Duvau:  ThSse  Lyon,  No.  92,  1902.     La  Presse  Medicale,  May  7,  1902. 
t  Erving,  W.:  Johns  Hopkins  Hosp.  Bull.,  Nov.,  1902,  p.  261. 
t  Ruhrah:  Annals  of  Surjjerv,  Oct.  and  Nov.,  1899. 
§  Leith:  Edinburgh  Hospital  Reports,  vol.  ii,  p.  121,  1894. 
II  Muller:  Munch,  med.  Wochen.,  Dec.  18,  1894. 
**  Auvray:  Rev.  de  Chirurg.,  tome  xxiii,  1903. 

381 


382  DISEASES    OF   THE    LIVER. 

In  30  cases  of  hepatic  actinomycosis  collected  by  Aribaud  *  the  growth  was 
derived  from  the  intestinal  tract  in  20.  In  12  of  these  it  spread  by  metastases 
and  in  the  remaining  8  by  direct  extension. 

As  shown  by  Ruhrah's  statistics,  more  than  half  the  total  number 
of  cases  of  human  actinomycosis  occur  in  the  head  and  neck.  The  liver 
is  very  seldom  affected  in  these  cases;  though  it  is  quite  conceivable  that 
when  an  actinomycotic  abscess  discharges  into  the  mouth,  secondary 
infection  of  the  gastro-intestinal  tract,  and  so  of  the  liver,  might  result. 

Moodie  t  has  recorded  a  case  where  a  small  circumscribed  primary  actinomy- 
cotic tumor  of  the  upper  jaw  gave  rise  to  a  large  actinomycoma  of  the  liver. 

Actinomycosis  or  ray  fungus  belongs  to  the  streptothrix  group  and 
presents  pleomorphous  characters.  It  may  appear  as  filaments,  as  cocci, 
or  clubs.  The  clubs  are  often  absent  in  human  actinomycosis.  For  a 
description  of  the  parasite  the  reader  should  refer  to  bacteriological  text- 
books. Cases  of  other  varieties  of  streptotrichosis  have  been  described 
under  the  name  of  actinomycosis,  and  also  under  the  unfortunate  title 
of  pseudo-actinomycosis.     (Berestnew,J  Habershon  and  Hichens.§) 


MORBID  ANATOMY. 

The  liver  is  enlarged  and  shows  adhesions  on  the  surface.  The  morbid 
condition  shows  very  considerable  variation.  The  actinomycotic  abscess 
has  a  characteristic  honeycombed  aspect  and  has  been  compared  to  a 
sponge  soaked  in  pus.  The  alveolar  appearance  is  due  to  the  coalescence 
of  a  number  of  small  abscesses.  The  suppurative  process  spreads  by 
continuity,  and  is  accordingly  more  or  less  localised,  but  sometimes  small 
abscesses  are  seen  away  from  the  main  collection,  while  there  may  be 
merely  multiple  abscesses,  like  those  seen  in  pyaemia.  ||  The  individual 
abscesses  vary  in  size  from  a  pin's  head  to  that  of  a  walnut. 

There  is  a  great  tendency  to  get  inflammation  of  the  capsule  of  the 
liver  and  adhesions  to  adjacent  organs.  When  the  actinomycotic  lesion 
is  situated  anteriorly,  it  readily  extends,  after  adhesions  have  been  formed, 
to  the  abdominal  wall  and  may  lead  to  an  abscess.  This  may  be  the 
first  evidence  of  disease,  so  that  caution  is  necessary  in  assuming  that 
the  hepatic  lesion  is  secondary  to  an  abscess  of  the  abdominal  wall.  If 
an  actinomycotic  abscess  near  the  surface  of  the  liver  ruptures  into  the 
general  cavity  of  the  peritoneum,  acute  peritonitis  will  result,  as  in 
Grainger  Stewart  and  Muir's**  case.  But  from  the  frequency  with  which 
perihepatic  adhesions  are  found  it  is  more  usual  to  get  localised  collections 
of  pus  near  the  liver,  such  as  a  subphrenic  abscess.  An  actinomycotic 
abscess  may  even  perforate  into  the  stomach. 

*  Aribaud:  Thdse  Lyon,  1897. 

t  Moodie,  E.  L.:  Journ.  of  Path,  and  Bacteriol.,  vol.  viii,  p.  239,  1902. 
t  Berestnew:  Centralblatt  f.  Bakt.,  1899,  Bd.  xxvi. 
§  Habershon  and  Hichens:  Brit.  Med.  Journ.,  1900,  vol.  ii,  p.  14S9. 
II  Stewart,  F.  J.:  Guy's  Hospital  Reports,  vol.  liv,  p.  303. 
**  Grainger  Stewart  and  Muir:  Edinburgh  Hospital  Reports,  vol.  i. 


ACTINOMYCOSIS. 


383 


r' 


/ 


Duckworth  and  Marsh*  met  with  a  case  where  an  actinom3'cotic  abscess  in 
the  left  lobe  of  the  liver  and  a  subphrenic  abscess  of  the  same  nature  had  eroded 
the  stomach  wall  from  without  inwards. 

The  abscess  or  abscesses  in  the  Hver  may  work  their  way  through 
the  diaphragm  into  the  kmg  or 
pleural  cavity.  Cases  of  hepatic 
actinomycosis  may  thus  first 
present  themselves  as  chronic 
empyemata  of  obscure  origin. 
When  the  actinomycotic  tumor 
is  in  the  posterior  part  of  the 
right  lobe,  it  may  spread  into 
the  right  suprarenal  body,  and 
even  reach  the  right  kidney. 

The  pus  contains  the  charac- 
teristic granules  composed  of  the 
ray  fungus — actinomycotic  colo- 
nies— and  numerous  pyogenetic 
cocci.  Stewart  considers  that 
suppuration  is  due  to  secondary 
infection  and  that  it  does  not 
occur  until  this  has  taken  place. 
Suppuration  may,  however,  be 
found  to  be  associated  with  ap- 
parently pure  streptothricial  in- 
fections. 

Around  the  areas  of  suppura- 
tion there  is  fibrosis  with  pig- 
mentation of  the  walls  of  the 
abscesses.  Microscopically  there 
are  intercellular  fibrosis  and  atro- 
phy of  the  liver  cells.  The  re- 
mainder of  the  liver  may  be  fatty 

or  lardaceous.     In  rare  cases  actinomycosis  may  be  pysemic  and  spread 
by  the  blood-vessels. 


Fig.  48. 


Actinomycosis  of  the  Liver,  from  a 
Specimen  in  St.  George's  Hospital  Muse- 
um.    (Drawn  by  Dr.  E.  A.  Wilson.) 


In  Kanthack's  t  case  it  was  not  clear  whether  the  abscess  originated  in  the 
right  lobe  of  the  liver  or  at  the  base  of  the  right  lung;  from  this  it  had  spread  by 
continuity  into  the  right  suprarenal  body,  and  had  given  rise  to  secondary  pj'^femic 
abscesses  over  the  body.  In  Boari's  J  case  there  were  secondary  pysemic  abscesses 
due  to  pyogenetic  cocci  and  not  containing  actinomyces. 

Actinomycotic  lesions  in  the  liver  have  sometimes  been  regarded 
as  tuberculous  or  ordinar}^  hepatic  abscesses. § 

*  Duckworth  and  Marsh:  Brit.  Med.  Journ.,  1900,  vol.  ii,  p.  11 89. 
t  Kanthack:  Trans.  Path.  Soc,  vol.  xlv,  p.  23-3. 
t  Boari:  II  Pohchnico,  1897,  p.  19. 

^  Vide  Harley,  Medico-cliirurg.  Trans.,  vol.  l.xix,  p.  135.  Shattock:  Trans. 
Path.  Soc,  vol.  xxxvi,  p.  260. 


384  DISEASES    OF   THE    LIVER. 


CLINICAL   PICTURE. 

Before  there  are  any  symptoms  or  signs  indicating  disease  of  the  liver 
there  may  be  evidence  of  abdominal  disturbance,  such  as  pain,  constipa- 
tion, or  localised  swelhng  imitating  appendicitis.  Stewart  has  laid  stress 
on  the  occurrence  of  two  stages  in  the  disease — an  early  period  just  referred 
to,  and  a  later  one  when  the  liver  is  definitely  affected.  Between  these 
two  stages  there  may  be  an  interval  of  fair  health.  The  first  symptoms 
of  hepatic  actinomycosis  may  be  those  of  an  empyema,  of  an  abscess  in 
the  abdominal  wall,  or,  when  the  portion  of  the  liver  near  the  kidney 
is  involved,  of  a  perinephritic  abscess.  The  liver  may  be  enlarged,  and 
with  a  slight  degree  of  fever  and  pain  over  the  liver  the  resemblance  to 
an  ordinary  hepatic  abscess  may  be  very  close.  Jaundice  is  extremely 
rare. 

Ascites  has  been  noticed  to  occur  late  in  the  disease  (Eve*),  but  is 
usually  absent.  Anaemia  of  a  chlorotic  type,  viz.,  diminution  of  the  red 
blood-corpuscles  with  a  greater  reduction  in  the  amount  of  haemoglobin, 
is  an  important  feature  of  the  disease.     There  is  leucocytosis. 

Latimer  and  Welch  f  described  a  case  of  actinomycosis  of  the  liver  combined 
with  myelogenous  leukaemia. 

PROGNOSIS. 

The  prognosis  of  actinomycosis  of  the  liver  is  very  bad.  Duvau,J 
a  pupil  of  Poncet,  collected  40  cases  of  hepatic  actinomycosis,  all  of  which 
proved  fatal.  Presumably  the  prognosis  should  be  less  gloomy  if  the 
disease  could  be  recognised  in  an  early  stage  and  treated  vigourously  with 
iodide  of  potassium,  and  secondary  infection  with  pyogenetic  cocci  pre- 
vented. For  when  the  latter  event  has  occurred  the  prognosis  is  bad. 
Though  much  commoner  in  animals,  actinomycosis  is  rather  more  virulent 
in  man. 

DIAGNOSIS. 

The  diagnosis  depends  on  finding  the  fungus  in  the  pus  either  from 
the  liver  or  from  a  discharging  abscess  elsewhere.  Before  this  has  been 
done  the  condition  is  hardly  likely  to  be  thought  of,  and  recorded  cases 
show  that  the  disease  has  been  regarded  as  empyema,  phthisis,  sarcoma 
of  the  kidney  (Leith),  perinephritic  abscess,  hepatic  abscess,  suppurating 
hydatid,  or  gumma  of  the  liver.  It  has  been  observed  that  the  subjects 
of  actinomycosis  react  to  Koch's  tubercuhn  (Kahler,  Arloing) ;  this  might 
lead  to  an  erroneous  diagnosis  of  that  very  rare  condition,  massive  tubercle 
of  the  liver. 

■     TREATMENT. 
The  effect  of  iodide  of  potassium,  introduced  by  Thomassen,  on  actino- 
mycosis is  extremely  marked  and  does  fully  as  much  good  as  it  does  in 
tertiary  syphilis.     It  should  be  given  in  large  doses,  as  much  as  two 

*  Eve:  Trans.  Path.  Soc,  vol.  xl,  p.  405. 

t  Latimer  and  Welch:  Trans.  Assoc.  Americ.  Phys.,  vol.  xi,  p.  328. 

j  Duvau:  These  Lyon,  1902.     Abstract  La  Presse  M^dicale,  May  7,  1902. 


ACTINOMYCOSIS.  385 

drachms  or  even  more  daily.  Sawyer  *  has  urged  that,  in  addition  to 
its  administration  by  the  mouth,  iodide  of  potassium  should  be  injected 
directly  into  the  affected  part;  15  to  30  minims  of  a  1  per  cent,  aqueous 
solution  of  iodide  of  potassium  are  injected  into  the  area  infected  with 
actinomycosis;  at  first  this  is  done  at  inten^als  of  three  or  four  days, 
but  after  a  time  the  injections  can  be  given  more  frequently. 

When  an  actinomycotic  abscess  has  been  opened,  the  necrotic  tissue 
may  be  scraped  away  with  advantage,  while  of  course  iodides  should  be 
given  freely.  Iodoform  may  be  employed  locally,  and  carbolic  acid  or 
other  disinfectants  should  be  applied  in  order  to  minimise  the  risks  of 
septic  infection.  In  a  few  cases  tuberculin  has  seemed  to  have  a  good 
effect,  while  Ziegler  has  found  the  injection  of  a  proteid  body  obtained 
from  cultures  of  Staphylococcus  pyogenes  aureus  of  use.  Arsenic  has 
also  been  recommended  (Braun). 

*  Sawyer:  Journ.  American  Med.  Assoc,  May  11    1901 


25 


LYMPHADENOMA  AFFECTING  THE  LIVER, 

Synonym:  Hodgkin's  Disease. 

In  generalised  lymphadenoma  the  liver  may  contain  nodules  of  white 
growth.  As  a  rule,  the  growths  are  small,  discrete,  and  do  not  lead  to 
any  enlargement  of  the  organ  during  life.  In  exceptional  cases,  as  in 
a  boy  aged  six  years  under  the  care  of  my  colleague,  Dr.  Penrose,  with 
generalised  lymphadenoma,  there  may  be  a  large  diffuse  mass  of  growth 
in  the  liver. 

In  a  new-born  infant  the  pleura,  peritoneum,  intestines,  bladder,  and  supra- 
renal bodies  contained  growths  regarded  by  Bouvain  and  Ducloux  *  as  lymphade- 
noma. The  liver  was  greatly  enlarged  from  numerous  nodules  of  growth.  Such  a 
case  closely  resembles  generalised  sarcoma. 

Morbid  Anatomy. — The  appearances  of  lymphadenomatous  nodules 
in  the  liver  may  imitate  caseous  tuberculous  masses  and  secondary  new- 
growth.  They  are  firm,  white,  and  do  not  show  any  softening  or  bile- 
staining;  in  these  particulars  they  differ  from  what  is  often  seen  in 
advanced  caseous  tubercles.  Tuberculosis  may,  however,  be  implanted 
on  lymphadenoma. 

In  a  boy  aged  sixteen  years,  who  had  extensive  lymphadenomatous  lesions, 
the  liver,  which  was  lardaceous  without  any  definite  cause,  such  as  syphilis  or  sup- 
puration, contained  small  caseous  tubercles  in  which  tubercle  bacilli  were  demon- 
strated (Dickinson  f) . 

The  combined  lesions  of  lymphadenoma  and  tuberculosis  may  be 
found  in  the  liver  (AndrewesJ),  as  is  well  shown  in  a  specimen  (No. 
2223" )  in  St.  Bartholomew's  Hospital  Museum.  Lardaceous  change  maybe 
found  in  a  liver  affected  with  lymphadenoma,  and  from  the  absence  of 
any  recognised  cause,  such  as  suppuration  or  syphilis,  it  would  appear 
that  lymphadenoma,  or  its  underlying  cause,  may  induce  the  lardaceous 
change. 

Microscopical  Appearances. — The  growth  starts  in  the  portal  spaces 
and  extends  outwards,  passing  between  and  eventually  into  the  neighbour- 
ing lobules.  The  margin  of  the  invaded  lobules  has  an  appearance 
like  that  of  intercellular  cirrhosis.  Gradually  the  growth  replaces  the 
lobules,  as  the  result  of  atrophy  of  the  liver  cells  which  may  be  seen  for 
a  time  embedded  in  the  growth.  The  columns  of  deeply  staining  cubical 
cells,  the  so-called  new  bile-ducts,  show  up  prominently  both  in  the 
growth  and  at  its  advancing  margin.  They  are  the  result  of  an  attempt 
at  compensatory  hyperplasia  of  the  liver  cells.  In  an  early  stage  the 
growth  is  composed  of  prohferated  endothelial  cells  which  may  show 

*  Bouvain  and  Ducloux:  La  Presse  M^dicale,  July  13,  1901. 
t  Dickinson,  W.  L.:  Trans.  Path.  Soc,  vol.  liii,  p.  315. 
X  Andrewes,  F.  W.:  Trans.  Path.  Soc,  vol.  liii,  p.  313. 

386 


LYMPHADENOMA    AFFECTING    THE    LIVER.  387 

several  nuclei— lymphadenoma  cells,  leucocytes,  and  young  connective- 
tissue  cells.     A  little  later  there  is  a  distinct  reticulum  to  be  made  out, 


^-.>' 

.   /••  ••'/    ..  ^ 

'         ■  ^ 

« 

• 

« 

f  • 

#     » * 

..  .'*)  ^^ 

.   Fic.   49. — Maiujin   of  Lvau'iiai)kx<)ma.tous  Nodule. 
The  endothelial  and   connective-tissue   cells   forming  the  growth  are  well  seen      Therp  iq  n 

W"  riit^Tir  ''"'  ?""      '"  ""^^  r'  *'^"  fT/V^S'y^J'f-  '^^^"•^  ^tain^nri'seudobile  ca'  aUcull 
Irom  the  Iwer  cells  can  be  seen.     High  power.      (Dr.  H.  Spitta.) 

and  as  time  goes  on  the  netAvork  increases  in  amount  and  the  growth 
becomes  more  and  more  fibrous.     For  a  full  description  of  the  histology 


388  DISEASES   OF   THE   LIVER. 

of  l3^mphadenoma  the  reader  should  consult  Aiidrewes',  Reed's,*  and 
Longcope's  t  papers.J 

There  is  seldom  any  clinical  evidence  that  h'mphadenoma  has  in- 
volved the  hver,  apart  from  slight  enlargement,  and  this  is  not  conmion. 
Exceptionally  the  organ  is  very  considerably  enlarged,  and  if  the  super- 
ficial lymphatic  glands  available  for  clinical  examination  are  but  little 
affected,  the  chnical  aspect  of  the  case,  especially  when  there  is  a  hectic 
temperature,  may  suggest  hepatic  abscess,  as  in  a  case  imder  my  care. 
Suchard  and  Teissier  §  met  with  a  case  suggesting  carcinoma  of  the 
liver. 

Ascites  may  be  present,  but  may  be  due  to  involvement  of  the  intra- 
abdominal lymphatic  glands  and  lymphatic  obstruction;  in  such  cases 
the  effusion  may  be  milkj^  and  resemble  chyle.  Jaundice  does  not  often 
occur,  although  enlarged  glands  in  the  portal  fissure  may  be  so  close 
to  the  bile-duct  as  to  render  it  probable. 

The  treatment  is  the  same  as  in  lymphadenoma,  but  the  prognosis 
is  very  bad  when  the  hver  is  involved. 

*  Johns  Hopkins  Hosp.  Reps.,  vol.  x,  p.  133. 

t  BuU.  Aver  Clin.  Lab.,  Xo.  1,  1903. 

J  Trans.  Path.  Soc,  vol.  liii,  p.  305. 

§  Suchard  and  Teissier:  Bull.  Soc.  Anat.  Paris,  1897,  p.  940. 


HYDATID  CYSTS, 

Hydatids  (udarc-)  of  the  liver  are  the  cystic,  larval,  or  bladder  stage 
of  a  tapeworm  which  in  its  adult  stage  is  found  in  the  intestine  of  the 
dog;  they  also  occur  in  the  wolf,  the  fox,  and  the  jackal. 

Life-history. — This  tapeworm — the  tsenia  echinococcus — is  small,  measuring 
about  4  millimetres,  or  ^  inch,  in  length,  and  composed  of  not  more  than  four  seg- 
ments or  proglottides,  the  last  or  terminal  one  being  larger  than  the  others  put 
together,  and  containing  fully  developed  sexual  organs  and,  when  fecundated,  ova 
to  the  number  of  500.  The  first  segment,  or  head,  has  a  prominent  rostellum  sur- 
rounded by  two  rows  of  hooklets,  there  being  about  20  booklets  in  each  series. 
There  are  also  four  suckers.  When  the  terminal  proglottis  breaks  off  from  the  tape- 
worm and  is  carried  along  mth  the  fseces,  the  contained  ova  become  liberated. 

The  ova  after  their  exit  from  the  bowel  of  the  host  become  scattered  about, 
and  may  find  their  way  into  the  alimentary  canal  of  man,  from  being  eaten  on 
lettuce,  water-cress,  or  other  vegetables,  or  drunk  with  water.  When  the  ova 
get  into  the  stomach,  their  chitinous  envelopes  are  dissolved,  and  an  oval-shaped 
embryo,  with  six  spines  arising  from  one  of  its  poles,  is  set  free.  The  spines  are 
directed  backwards  and  thus  allow  the  embryo  to  bore  its  way  into  the  coats  of  the 
bowel,  but  prevent  it  from  returning  back  along  the  passage  it  has  made.  The 
embryos  get  into  the  portal  vein  and  are  conveyed  to  the  liver.  That  they  pass 
by  the  portal  vein  is  largely  assumed  because  the  liver  is  par  excellence  their  des- 
tination. If  they  simply  bored  their  way  straight  through  opposing  structures, 
it  would  be  natural  to  find  them  equally  distributed  throughout  the  surrounding 
organs.  Possibly,  moreover,  conditions  for  their  further  development  are  more 
favourable  in  the  liver  than  elsewhere,  just  as  in  the  case  of  the  free  embryos  of 
trichina  the  muscles  are  the  place  of  selection. 

It  has  been  thought,  and  very  probably  with  truth,  that  any  blow  or  trauma- 
tism of  the  liver  will  favour  the  evolution  of  an  embryo  into  a  hydatid  cj^st  by 
reducing  the  resistance  of  the  liver  and  so  allo'wang  the  parasite  every  chance  of 
development.  The  passage  of  the  embryo  through  the  walls  of  the  stomach  is  not 
attended  by  any  recognised  symptoms. 

When  the  embryo  reaches  the  liver  and  comes  to  rest,  it  proceeds  to  become 
transformed  into  the  bladder  or  hydatid.  The  embryo  loses  its  hooklets  and  en- 
larges so  as  eventually  to  form  a  small  cyst ;  the  outer  surface  becomes  laminated 
and  is  called  the  ectocyst,  while  more  internally  the  granular  endocyst  is  evolved, 
and  the  contents  undergo  liquefaction.  AVhen  reproductive  changes  leading  to  the 
production  of  daughter  cysts  commence,  the  first  change  is  the  formation  of  brood- 
capsules  in  the  endocyst.  These  are  small  buds,  lined  internally  by  material  resem- 
bling the  ectocyst,  and  externally  by  the  endocyst,  so  that  it  appears  like  an  in- 
vagination of  the  cyst.  The  cavity  of  the  brood-capsule  contains  fluid.  From 
the  outer  surface  of  the  brood-capsule  the  scolices  develop ;  they  are  the  early  stage 
of  the  head  of  the  future  tapeworm  and  are  provided  -Rath  hooklets.  The  scolices 
arising  from  the  outer  surface  of  the  brood-capsule  eventually  become  invaginated 
into  its  interior.  They  readily  become  detached  from  the  wall  of  the  brood-cap- 
sule, and  as  a  result  of  rupture  of  the  brood-capsules  become  free  in  the  cavity  of 
the  cyst.  A  scolex  is  about  0.3  mm.  long  and  consists  of  two  segments;  the  segment 
originally  attached  to  the  wall  of  the  brood-capsule  often  contains  crystals  of  car- 
bonate of  lime,  while  the  free  segment  has  a  crown  of  hooklets  and  four  suckers. 
The  hooklets  measure  0.04  mm.  Should  the  scolex  reach  the  intestine  of  a  dog 
it  develops  into  an  adult  tapeworm  by  lengthening  and  transverse  segmentation  of 
its  posterior  end. 

Daughter  cysts  are  produced  either  inside  the  original  cyst,  endogenous  forma- 
tion, which  is  the  usual  way,  or  more  rarelj^  I)y  external  budding  off,  exogenous 
formation.  The  daughter  cysts  are  derived  from  either  the  scolices  or  brood-cap- 
sules, which  become  vesicular,  or  from  invagination  of  the  parenchymatous  en- 
docyst. The  daughter  cvsts  may  Ijccome  dotacliod  from  tlie  endocyst  and  become 
free  in  the  cavity  of  the  parent   cyst,   and  may   contain  granddaughter  cysts. 

389 


390  DISEASES    OF    THE    LIVER. 

Exogenous  formation  of  daughter  cysts  is  rare  in  man,  though  common  in  sheep. 
Cysts  are  formed  in  the  deeper  layers  of  the  ectocyst,  become  filled  with  fluid,  and 
work  their  way  outwards;  they  finally  project  from  the  surface  of  the  mother  cyst 
and  become  surrounded  by  a  fibrous  adventitious  capsule.  The  mother  cyst  thus 
becomes  knobby  from  the  projection  of  daughter  cysts,  some  of  which  may  become 
disconnected  from  it.  It  is  possible,  however,  that  the  so-called  exogenous  ap- 
pearance is  really  only  due  to  the  cyst  growing  irregularly  and  sending  out  processes 
in  the  lines  of  least  resistance.  Pseudopodial-like  processes  of  a  single  cyst  might 
thus  travel  along  the  portal  spaces  in  the  liver,  there  being  a  continuous  cavity 
throughout.  Later  the  communication  between  the  cyst  and  its  process  might 
become  constricted,  and  in  this  way  the  appearance  of  a  secondary  cyst  attached 
to  the  main  cyst,  but  with  an  independent  cavity,  might  be  produced. 

It  has  been  thought  that  the  extremely  rare  disease,  multilocular  hydatid,  is  a 
form  of  the  exogenous  proliferation  of  the  hydatid  cyst.  In  connexion  with  the 
exogenous  mode  of  growth  it  may  be  pointed  out  that  the  presence  of  two  or  more 
hydatid  cysts  in  the  same  liver  is  probably  due  to  two  distinct  embryos  having 
reached  the  liver  and  not  to  exogenous  formation  of  one  from  the  other. 

Sterile  Hydatid  Cysts. — If  no  multiplication  or  reproductive  changes 
take  place  in  the  cyst,  it  is  spoken  of  as  being  sterile  or  as  an  acephalo- 
cyst,  though  the  latter  term  is  not  often  used  now.  The  fluid  contains 
no  daughter  cysts  or  scolices,  and  the  nature  of  the  cyst,  whether  hydatid 
or  not,  must  be  determined  by  microscopic  examination  of  its  wall. 
Failure  in  reproduction  probably  depends  on  imperfect  nutrition.  Pedun- 
culated hydatid  cysts  that  hang  down  from  the  under  surface  of  the 
liver  are  more  hkely  to  be  sterile  than  those  embedded  in  the  substance 
of  the  liver. 

Warty  ingrowths  from  the  cyst  wall  are  sometimes  observed; 
they  are  probably  abortive  daughter  cysts. 

In  the  museum  of  Surgeons'  HaU,  Edinburgh,  there  is  a  part  of  the  waU  of  a 
hydatid  cyst  showing  extremely  well  this  papillomatous  appearance.  The  cyst 
was  a  large  one  and  contained  many  hundreds  of  small  cysts.     (No.  1885.) 

On  the  other  hand,  it  is  possible  that  in  some  of  the  cases  the  warty 
growths  were  due  to  commencing  degenerative  changes  and  that  the 
process  is  clue  to  involution  and  not  to  imperfect  evolution. 

STRUCTURE  OF  HYDATID  CYSTS. 

The  wall  of  the  true  parasitic  cyst  consists  of  the  outer  cuticle,  or 
ectocyst,  and  an  inner  lining,  or  endocyst.  The  cysts  have  an  opalescent 
whitish-blue  colour,  and  unless  considerably  thickened,  tear  easily.  The 
ectocyst  is  elastic  and  tends  to  curl  up  when  it  is  incised.  Structurally 
it  has  a  very  characteristic  laminated  appearance.  There  are  wavy  bands 
of  homogeneous,  hyaline  material  which,  like  the  wall  of  the  original  ovum, 
is  chitinous. 

The  endocyst  forms  the  parenchymatous  or  granular  internal  hning 
of  the  ectocyst ;  from  it  the  brood  capsules  are  developed.  It  may  contain 
crystals  of  carbonate  of  calcium  like  those  seen  in  the  mature  cestoda 
and  in  the  scohces.  The  fluid  in  a  living  hydatid  cyst  is  clear,  of  a  low 
specific  gravity,  1002  to  1010,  contains  no  albumin,  but  a  considerable 
quantity  of  chloride  of  soda;  for  other  details  see  page  402  (diagnosis 
by  examination  of  fluid).  When  the  cyst  becomes  inflamed  or  dies,  it 
contains  albumin  and  may  be  turbid. 


HYDATID    CYSTS.  391 

Outside  the  parasitic  cyst,  as  a  result  of  compression  and  irritation 
of  the  tissues  of  the  liver,  a  fibrous  capsule  is  produced  which  extends 
for  a  short  distance  into  the  surrounding  liver  substance.  When  a  hyda- 
tid cyst  projects  from  the  surface  of  the  liver,  a  thick  fibrous  covering  of 
the  consistence  of  cartilage  may  develop  over  the  c^^st,  which  resembles 
a  corneal  fibroma  of  the  sjDleen,  and  may  show  calcification.  The  remains 
of  the  hydatid  cyst  may  escape  notice,  and  the  true  nature  of  these  thick- 
walled  cysts  be  overlooked.  AVhen  embedded  in  the  substance  of  the 
liver  the  fibrous  capsule  shows  columns  of  small  cubical  cells,  pseudo-bile 
canaliculi,  due  to  hyperplasia  of  included  liver  cells.  In  addition,  there 
may  be  giant  cells  whose  function  is  to  attempt  absorption  of  the  cyst; 
they  do  not  contain  tubercle  bacilli  and  differ  from  the  giant  cells  of 
tuberculous  granulation  tissue  in  that  their  nuclei  are  in  the  centre  and 
not  at  the  periphery. 

When  two  cysts  arise  in  close  contact  to  each  other,  they  may  be 
enclosed  in  the  same  pseudocyst  or  capsule  derived  from  the  tissues  of 
the  liver  by  ]3ressLire  irritation.  Occasionally  an  hydatid  cyst  is  found 
to  be  divided  into  two  parts  by  a  constriction,  and  thus  to  resemble  an 
hour-glass  or  a  shirt  stud.  This  may  depend  either  on  two  cysts,  origin- 
ally separate,  opening  into  each  other,  or,  as  pointed  out  in  speaking  of 
exogenous  formation  of  daughter  cysts,  on  irregular  gro^vth  due  to 
differences  in  the  resistance  offered  by  the  surrounding  tissues. 

Grange  *  describes  a  suppurating  hydatid  cyst  in  the  Hver  shaped  like  a  shirt 
stud,  with  a  small  superficial  cavity  communicating  by  a  constriction  with  a  larger 
and  more  deeply  seated  cavity. 

Situation  of  Hydatid  Cysts  in  the  Liver. — ^The  cysts  may  be  deeply 
and  entirely  embedded  in  the  liver,  and  are  naturally,  from  the  greater 
size  of  the  right  lobe,  commoner  there  than  in  the  left  lobe.  Cysts  arising 
from  the  upper  and  back  part  of  the  right  lobe  push  the  diaphragm  up 
and  may  imitate  a  pleural  effusion.  When  the  cyst  is  deeply  placed  and 
expands  and  pushes  the  liver  forwards,  the  condition  in  some  ways 
resembles  a  solid  groAvth  of  the  liver.  Not  uncommonly  a  hydatid  cyst 
hangs  down  from  the  under  or  lower  surface  of  the  liver  and  may  resemble 
a  dilated  gall-bladder. 

Number  of  Cysts.— There  may  be  only  one  cyst  in  the  liver,  but  it 
is  not  by  an\'  means  rare  to  find  two  or  three.  Large  numbers  of  small 
cysts  have  been  found  in  the  liver;  forty  (Dolbeau  f)  or  even  a  hundred 
have  been  seen  in  the  same  liver  (Murchison  |). 

Size. — A  single  hydatid  cyst  may  reach  a  very  large  size  indeed.  The. 
largest  hydatid  cyst  of  the  liver  on  record  appears  to  be  one  containing 
36  pints ;  it  occupied  three-cjuarters  of  the  abdomen  and  was  successfully 
operated  upon  by  H;  B.  Robinson;  §  four  years  previously  it  had  been 
tapped  and  40  litres  (70  pints)  removed  with  only  very  temporary  relief. 

Spontaneous   Death. — Inasmuch  as  hydatids  are  most  commonly 

*  Grange:  Lvon  MMical,  tome  xcii,  p.  22,  Sept.  3,  1899. 

t  Dolbeau:  Bull.  Soc.  Anat.  Paris,  1857,  p.  116. 

j  Murchison,  C.:  Diseases  of  the  Liver. 

§  Robinson,  H.  B. :  Trans.  Clinical  Soc,  vol.  xxx,  p.  16. 


392  DISEASES    OF   THE    LIVER. 

present  in  the  liver,  being  found  there  in  57  per  cent,  of  all  the  cases 
of  the  disease,  it  is  natural  that  hydatid  cysts  which  have  become 
latent  and  undergone  involution  changes  ending  in  spontaneous  cure 
are  commoner  in  the  liver  than  elsewhere. 

It  has  also  been  thought  that  they  are  more  often  found  in  the  liver 
because  their  natural  evacuation  is  less  easy  than  in  the  case  of  the  lung 
or  kidney,  from  which  they  may  be  coughed  up  or  passed  into  the  ureter. 
But  with  regard  to  this  it  may  be  said  that  there  is  not  much  difference 
between  the  lumen  of  the  common  bile-duct  and  of  the  ureter,  except  that 
the  larger  end  of  the  ureter,  the  pelvis  of  the  kidney,  is  directed  towards  the 
hydatid  in  the  kidney,  while  the  intra-hepatic  bile-ducts  are  small.  But 
this  explanation  of  the  frequency  of  hepatic  hydatids  is  not  worth  much, 
for  natural  evacuation  is  rare  in  any  organ  and  much  less  common  in 
the  lung  and  kidney  than  in  the  hver. 

Causes  of  Spontaneous  Death. — Possibly  the  cause  may  sometimes  be 
inherent  in  the  individual  parasite,  which,  being  of  poor  vitality,  runs 
its  allotted  course  and  dies  before  having  reached  the  ordinary  size.  For 
death  with  spontaneous  cure  is  most  often  seen  in  small  cysts  which  have 
not  given  rise  to  symptoms  during  life.  This,  however,  is  not  a  universal 
rule,  and  a  large  hydatid,  if  not  operated  on,  may  gradually  undergo 
involution  changes  and  shrivel  up. 

A  remarkable  example  is  recorded  by  Murchison.*  A  patient  had  been  seen 
when  eleven  years  old  by  Sir  Ashley  Cooper,  and  his  liver  was  then  said  to  be  four 
times  its  natural  size  and  was  thought  to  contain  fluid;  there  was  some  question  of 
an  operation,  but  this  was  not  done.  The  tumor  gradually  got  smaller  and  forty- 
five  years  later,  when  Murchison  saw  the  case,  there  was  a  mass  as  hard  as  bone  in 
■connexion  with  the  right  lobe  of  the  Uver. 

The  usual  term  of  life  of  a  hydatid  cyst  is  not  known,  but  it  has  been 
thought  to  be  as  long  as  twenty  years.  Of  the  causes  acting  from  without 
and  impeding  the  growth  or  possibly  poisoning  the  parasite  outright, 
the  most  commonly  recognised  is  the  entrance  of  bile  into  the  cyst.  The 
constant  pressure  exerted  by  the  contents  of  the  tense  cyst  leads  to  atrophy 
of  the  tissues  intervening  between  the  cavity  of  the  cyst  and  an  adjacent 
bile-duct  and  allows  of  the  entry  of  bile  into  the  cyst,  and  sometimes  of 
a  discharge  of  the  contents  of  the  cyst  into  the  bile-duct.  (Vide  Rupture 
of  Hydatid  Cysts  into  Bile-ducts.)  As  evidence  of  the  entrance  of  bile 
into  the  cyst  the  occurrence  of  crystals  of  bilirubin  and  bihverdin  may 
be  forthcoming. 

On  the  other  hand,  dead  cysts  may  not  contain  any  trace  of  bile, 
while  spontaneous  cure  of  hydatid  cysts  may  occur  in  other  organs, 
where,  of  course,  bile  can  play  no  part.  Further,  it  would  appear  that 
the  parasiticidal  action  of  bile  is  slight,  as  Deve  t  finds  that  scolices 
continue  to  grow  in  a  mixture  of  hydatid  fluid  and  bile  even  when  equal 
quantities  of  bile  and  hydatid  fluid  are  used.  Secondary  hydatid 
cysts  can  develop  in  the  peritoneum  when  there  is  a  bile-stained  peri- 
toneal effusion  from  rupture  of  a  hydatid  cyst,  already  communicating 

*  Murchison:  Lectures  on  Diseases  of  the  Liver,  p.  130,  1S77. 
fD^v^:  Soc.  de  biolog.,  Jan.  17,  1903. 


HYDATID    CYSTS.  393 

with  a  bile-duct,  into  the  peritoneal  cavity.  It  therefore  seems  probable 
that  bile  has  little  to  do  with  spontaneous  death  of  hydatid  cysts  in  the 
liver.  In  some  instances  the  entrance  of  bile  is  subsequent  to  the  death 
of  the  parasite. 

Chemical  alterations  in  the  lymph  bathing  the  outside  of  the  cyst 
have  also  been  suggested,  and  it  has  been  thought  that  poisonous  products 
absorbed  from  the  bowel,  such  as  alcohol,  might  play  some  such  part; 
but  the  resistance  of  hydatid  cysts  to  any  form  of  drug  renders  this 
doubtful.  The  entrance  of  fluids,  such  as  blood,  into  the  cavity  of  the 
cyst  may  so  disturb  the  equilibrium  necessary  for  the  continued  life  of 
the  parasite  as  to  lead  to  its  death.  Of  the  occurrence  of  past  haemorrhage 
into  a  hydatid  cyst  there  is  no  very  satisfactory  evidence,  as  the  crystals 
of  hsematoidin  and  bilirubin  are  identical.  It  appears  probable  that  in 
cases  where  "hsematoidin"  is  described  as  being  found  in  cysts  the  crystals 
are  really  bilirubin.*  Absorption  of  the  contained  hydatid  fluid  has 
been  thought  to  be  the  cause  of  spontaneous  death  of  the  parasite; 
this  view  is  supported  by  cure  after  simple  tapping  of  a  cyst,  but,  on 
the  other  hand,  there  is  no  proof  that  under  ordinary  conditions  ab- 
sorption of  the  fluid  can  occur  from  a  living  cyst. 

The  rapid  prohferation  of  the  daughter  cysts  so  that  they  increase 
out  of  all  proportion  to  the  surrounding  fluid  and  produce  heightened 
pressure,  and  so  exert  an  inhibitory  influence  on  the  life  of  the  parasite, 
has  been  put  forward  as  a  cause  of  spontaneous  death. f  That  this  is 
not  a  universal  cause  is  shown  by  the  fact  that  dead  cysts  may  contain 
few  or  even  no  daughter  cysts.  Changes  in  connexion  with  the  fibrous 
capsule  of  the  cyst,  such  as  cicatricial  contraction  and  calcification,  have 
also  been  thought  to  interfere  with  the  nutrition  of  the  parasite,  but  it 
is  difficult  to  prove  the  relationship  between  the  two  processes. 

Changes  Following  the  Death  of  a  Hydatid  Cyst. — The  fluid  of  a 
Hving  h3^datid  cyst  under  ordinary  conditions  is  practicaUy  free  from 
albumin;  after  death,  however,  it  becomes  albuminous.  From  the 
albuminous  fluid  removed  from  a  hydatid  cyst  which  had  previously 
been  killed  by  electrolysis  Boinet}  obtained  crystals  of  a  toxic  body 
analogous  to  myrtilotoxin,  probably  the  result  of  cleavage  of  the  albumin. 
The  albuminous  fluid  in  the  cyst  becomes  turbid  and  cloudy  from  the 
precipitation;  as  time  goes  on  absorption  occurs  and  the  contents  get 
less  fluid  and  more  gelatinous  and  the  parent  cyst  shrinks,  while  fatty 
metamorphosis  of  the  albumin  gives  the  contents  a  buttery,  caseous,  or 
putty-like  character;  various  stages,  from  a  glairy  or  colloid  state  to 
complete  solidity,  may  be  met  with  as  time  goes  on.  The  contents  are 
frequently  yellow  in  colour.  These  changes  in  the  mother  cyst  are  later 
on  repeated  in  the  daughter  cysts.  The  putty  or  gelatiniform  material 
may  contain  crystals  of  cholesterin,  stearin,  bile  pigment,  tyrosin,^  and 
calcification  may  extend  from  the  outer  adventitious  capsule  into  the 
contents  of  the  cyst. 

*  Vide  Dickinson,  W.  L.:  Trans.  Path.  Soc,  vol.  xlv,  p.  259. 
tMurchison:  On  Diseases  of  the  Liver,  1885,  p.  62. 
JBoinet:  Rev.  de  M6d.,  1898,  p.  845. 
§  Carwardine:  Path.  Trans.,  vol.  xlix,  p.  1.32. 


394 


DISEASES    OF   THE    LIVER. 


Contraction  and  shrinking  of  the  outer  fibrous  capsule  lead  to  a 
folding  of  the  cyst  wall  compared  to  the  appearance  of  a  corpus  luteum. 
The  outer  capsule  may  become  extremely  hard  from  infiltration  with 
carbonate  and  phosphate  of  lime.  Good  specimens  of  the  calcified  shells, 
so  to  speak,  of  hydatid  cysts  are  to  be  found  in  most  museums;  there  is 
one  (No.  2234)  in  St.  Bartholomew's  Hospital  Museum  of  multiple  cal- 
cified cysts.  Usually  the  process  of  spontaneous  cure  is  unaccompanied 
by  any  inconvenience  or  clinical  signs. 

In  a  case  recorded  by  Mitchell  Bruce  and  Sheild*  a  very  large  cyst  underwent 
changes  resulting  in  a  gelatiniform  condition  of  its  contents.  The  tumor  was  so 
large,  and  was,  contrary  to  what  would  naturally  be  expected,  increasing  in  size, 
that  laparotomy  was  performed.  The  diagnosis  of  a  solid  hydatid  cyst  had  pre- 
viously been  made  certain  by  aspiration  of  some  of  the  colloid  matter  containing 
booklets. 

In  rare  cases  a  spontaneously  cured  hydatid  may  undergo  suppura- 
tion and,  if  it  communicates  with 
the  bile-ducts,  be  the  cause  of 
suppurative  cholangitis. 

Condition  of  the  Remainder 
of  the  Liver. — -The  pressure  ex- 
erted by  a  large  cyst  causes 
atrophy  of  the  part  of  the  liver 
in  its  immediate  neighbourhood, 
and  in  this  way  a  whole  lobe 
may  become  excavated  and  de- 
stroyed. In  extreme  instances  the 
organ  may  become  so  deformed 
that  its  anatomical  features  are 
quite  obliterated.  Compensatory 
hypertrophy  of  other  parts  of  the 
liver  readily  occurs,  and  the  re- 
sulting hypertrophy  is  often  con- 
siderably in  excess  of  the  normal 
amount  of  hver  substance.  The 
left  lobe  has  been  found  to  weigh 
as  much  as  a  normal  liver.  (Chauffard.f)  The  compensatory  hyper]3lasia 
occurs  with  greater  ease  in  hydatid  disease  of  the  liver  than  in  cirrhosis, 
malignant  disease,  or  abscess.  This  is  probably  because  there  is  no 
depressing  factor,  such  as  the  presence  of  toxines,  to  reduce  the  vitality 
and  health  of  the  liver  cells.  The  compensatory  hypertrophy  is  better 
developed  at  some  distance  from  the  cysts,  and  since  cysts  are  usually  in 
the  right  lobe,  the  left  is  frequently  greatly  hypertrophied,  though  the 
quadrate  and  spigelian  lobes  share  in  the  compensatory  process.  This 
compensation  accounts  for  the  marked  absence  of  constitutional  symp- 
toms in  the  disease.  With  very  rapidly  growing  hydatid  cysts  there  may 
not  be  time  for  compensatory  hjqjertrophy  to  occur,  and  the  amount  of 

*  Mitchell  Bruce  and  Sheild:  Medico-Chirurg.  Trans.,  vol.  Ixxv,  p.  175. 
tChauffard:  Archiv.  Gen.  de  M6d.,  1890. 


Fig.  50. — Drawing   of  an  Obsolete  Hydatid 
Cyst  in  the  Liver. 
From  a  specimen  (series  ix,  No.  179e)  in  the 
Museum   of  St.   George's  Hospital.     (Drawn  by 
Dr.  E.  A.  WUson.) 


HYDATID    CYSTS.  395 

liver  substance  may  for  a  time  be  greatly  diminished.  As  a  coincidence, 
hydatid  cysts  have  been  found  to  be  associated  with  universal  cirrhosis 
of  the  liver  (Cayley,  Weir,  S.  Savage  *),  and  with  malignant  disease.! 
In  a  man  at  forty-nine  who  died  in  St.  George's  Hospital  from  pyloric 
carcinoma  with  extensive  secondary  infection  of  the  Uver,  which  weighed 
10  pounds,  there  was  a  dried-up  hydatid  cyst  in  the  right  lobe  close  to 
the  gall-bladder.  In  a  case  recorded  in  St.  Thomas'  Hospital  Reports 
primary  carcinoma  of  the  liver  was  associated  with  several  calcified 
hydatid  cysts. J  But  there  is  no  reason  to  think  that  these  conditions 
are  secondary  to  the  irritation  exerted  by  the  cyst. 

In  a  case  recorded  by  Pitt§  the  irritation  set  up  by  a  cyst  in  the  left  lobe  of  the 
liver  of  a  man  aged  thirty-nine  years,  who  had  contracted  syphilis  thirteen  years 
before  death,  seemed  to  have  given  rise  to  a  remarkable  syphilitic  growth  enclosing 
the  cyst. 

Relative  Frequency  of  Hepatic  to  Hydatid  Cysts  Elsewhere. — The 
liver  is  more  often  the  site  of  hydatid  cysts  than  the  whole  of  the  re- 
mainder of  the  body.  The  percentage  incidence  of  hydatids  in  the  liver 
is  variously  estimated  at  74  per  cent.  (Lyon  H )  to  44  per  cent.  (Davaine.**) 

In  1897  cases  of  hydatid  disease  Davies  Thomastf  found  the  liver  affected  in 
1084,  or  57  per  cent.,  the  lungs  being  next  with  220,  or  11.6  per  cent.  Finsen 
estimated  the  incidence  of  hydatids  in  the  liver  at  69  per  cent.,  Peiper  JJ  at  66.4  per 
cent.,  Neisser§§  at  50  per  cent.,  and  Cobbold,  on  the  basis  of  his  own  and  Davaine's 
cases,  at  46  per  cent. 

The  great  frequency  with  which  the  liver  is  affected  is  due  to  its 
filtering  the  blood  from  the  intestines  and  thus  arresting  the  embryos 
which  have  got  into  the  portal  vein.  If  the  embryo  is  not  stopped  by 
the  liver,  it  passes  to  the  capillaries  of  the  lung  and  may  come  to 
rest  there. 

ETIOLOGY. 

Geographical  Distribution. — In  England  hydatid  disease  is  said 
to  be  commoner  in  London  than  in  most  country  districts,  but  in  the 
Fen  districts  around  Cambridge  hydatids  are  comparatively  common. 

Murchison  in  2100  postmortem  examinations  at  the  Middlesex  Hospital  records 
13  bodies  in  Avhich  hydatids  were  found,  or  1  in  161;  in  7  of  these,  or  1  in  300,  they 
were  the  cause  of  death.  From  an  examination  of  the  statistics  of  in-patients  at 
St.  Bartholomew's  Hospital  for  thirty  years  Sir.  W.  Church  ||  ||  found  that  one  case  of 
hydatid  disease  was  admitted  in  1100. 

*  Cay  ley,  W.:  Trans.  Path.  Soc,  vol.  xxv,  p.  129.  Savage,  S.:  Brit.  Med. 
Journ.,  1899,  vol.  i,  p.  1030.  Weir:  Medical  Record,  Feb.  4,  1899,  p.  149.  Stevens: 
Brit.  Med.  Jour.,  1901,  vol.  i,  p.  1139. 

t  Habran:  Bull.  Soc.  Anat.  Paris,  1868,  p.  437.     Florand:  Ibid.,  1SS6,  p.  677. 

J  St.  Thomas'  Hospital  Reports,  vol.  xxix,  p.  141. 

§  Pitt,  G.  N.:  Trans.  Path.  Soc,  vol.  xxxvii,  p.  276. 

il  Lyon:  American  Journ.  Med.  Sciences,  vol.  cxxiii,  p.   124. 
**  Davaine:  Trait6   des    Entozoaires,    Paris,    1878. 
tt  Thomas,  Davies:  Hydatid  Disease,  1894. 
tX  Thierische  Parasiten,  S.  158,  1904. 
§§  Neisser:  Echinococcenkranklieitcn,  Berlin,  1877. 
unchurch,  W.  S.:  Clinical  Journal,  March  21,  1900. 


396  DISEASES   OF  THE   LIVER. 

In  Scotland  hydatids  are  very  rare,  but  in  Shetland  they  are  com- 
paratively common.  (H.  Stiles.*)  In  Russia  they  are  rare.  In  Switz- 
erland and  South  Germany  they  are  fairly  frequently  met  mth.  In  Ice- 
land they  are  extremely  common;  estimates  vary  from  one-sixth  to 
one-fifty-eighth  of  the  entire  population,  one-thirtieth  being  the  mean 
and  more  probable  figure.  The  great  frequency  of  hydatid  disease  de- 
pends on  the  enormous  number  of  dogs  and  on  the  fact  that  they  are 
very  frequently  infected  with  tsenia.  Hydatid  cysts  are  rare  in  Africa, 
but  are  becoming  more  frequent  in  Algiers.  In  Australia  they  are  very 
frequent,  being  commonest  in  South  Austraha.  In  1000  postmortem 
examinations  mentioned  by  Stirhng  and  Verco  hydatids  were  found  in 
49,  or  5  per  cent.  In  Victoria  one  case  of  hydatid  occurs  in  every  175 
admitted  to  hospital,  in  New  South  Wales  1  in  380,  while  the  proportion 
in  New  Zealand  and  Tasmania  is  also  very  high.     (Church.) 

In  North  America  hydatid  disease  is  rare,  and  when  it  is  met  with 
is  in  the  bodies  of  foreigners. 

Up  to  July,  1891,  Oslerf  could  only  find  evidence  of  85  cases;  since  the  mi- 
gration of  Icelanders  into  Winnipeg  the  disease  has  become  more  frequent  in  that 
locality.  Ten  years  later  LyonJ  collected  notes  of  241  cases  of  hydatid  disease 
occurring  in  the  United  States  and  Canada  up  to  July  1,  1901.  Most  of  the  cases 
were  either  in  Icelanders  or  in  Germans. 

In  the  Argentine  Republic  hydatid  disease  has  been  becoining  increas- 
ingly common  of  late  years. §  This  depends  on  the  large  number  of 
cattle  and  dogs  there.  Hydatid  disease  is  very  rare  in  India,  and  doubt 
has  been  expressed  as  to  its  origin  there  at  all;||  it  may  be  foimd  in  per- 
sons dying  in  India  who  have  acquired  the  disease  elsewhere.  W.  J. 
Buchanan  **  records  an  undoubted  case  of  hydatid  cyst  of  the  hver  in  a 
native  of  India  who  had  never  been  out  of  the  country. 

There  is  nothing  to  suggest  that  the  natives  of  Iceland  or  Australia, 
where  the  disease  is  most  prevalent,  are  in  the  slightest  degree  immune 
from  hydatid  disease.  Verco  and  Stirhng  ft  state  that  except  for  accident 
and  tuberculosis,  hydatid  disease  was  responsible  for  all  deaths  of  the 
aborigines  in  the  Adelaide  Hospital. 

Method  of  Infection. — The  ova  derived  from  the  dried  and  scattered 
faeces  of  dogs  may  settle  on  vegetables  or  contaminate  drinking-water. 
Lettuce  and  especiaUy  watercress  may,  if  not  carefuUy  washed,  serve 
as  vehicles  for  the  transmission  of  the  disease.  Persons  in  contact  ■\\dth 
dogs  and  other  animals,  the  subjects  of  tsenia  echinococcus,  are  in  danger 
of  becoming  the  hosts  of  the  bladder  stage  of  the  tapeworm.  There  is 
some  risk  in  the  possession  of  pet  dogs,  as  infection  may  be  conveyed 
by  a  dog  licking  the  hands  and  face  of  its  master. 

It  has  been  suggested  as  possible  that  when  portions  of  hydatid  cj'Sts 

*  Stiles,  H.:  Scottish  Med.  and  Surg.  Journ.,  Feb.,  1903. 

t  Osier,  W. :  Practice  of  Medicine,  ed.  ii. 

X  Lyon:  American  Jour.  Med.  Sciences,  vol.  cxxiii,  p.  124. 

§  Vegas  and  Cramwell:  Rev.  de  Chirurg.,  April,  1901. 

II  Chevers:  Diseases  of  India,  p.  624. 
**  Buchanan:  Lancet,  1900,  vol.  ii,  p.  19. 
tt  Verco  and  Stirling:  Allbutt's  System,  vol.  ii,  p.  1114. 


HYDATID    CYSTS,  397 

embedded  in  the  livers  of  sheep  or  oxen  are  eaten,  the  scohces  may- 
develop  in  the  alimentary  canal  of  man  and  give  rise  to  autoinfection. 
This  theory  requires  for  its  confirmation  the  recognition  of  scolices  in 
the  human  alimentary  canal,  and  has  not  yet  been  justified.  Offal  from 
slaughter-houses,  however,  containing  hydatid  cysts  is  a  most  important 
factor  in  the  causation  of  the  tapeworm  in  dogs,  and  so  indirectly  of 
the  cysts  in  man. 

Sex. — The  incidence  of  hydatid  disease  in  the  two  sexes  depends 
on  their  relative  exposure  to  infection,  which  is  generally  more  marked 
for  men.  In  Austraha,  where,  according  to  Stirhng  and  Verco,  the  water- 
supply  in  the  bush  is  the  great  source  of  infection,  the  ratio  is  as  100 
in  men  to  77  in  women.  In  America  Lyon  *  found  the  percentage  in- 
cidence 60  per  cent,  in  man  and  40  per  cent,  in  woman.  In  France 
Davaine  f  found  the  incidence  equal  in  the  two  sexes.  In  Berhn,  how- 
ever, women  were  more  often  affected  than  man  in  the  ratio  of  65  to 
35  (Neisserl),  and  in  Iceland  women  are  twice  as  often  affected  (71  per 
cent.)  as  man  (29  per  cent.)  (Finsen|). 

Age. — ^The  disease  becomes  more  frequent  up  to  about  fifty  years 
of  age  and  then  dechnes.  The  majority  of  cases  occur  between  twenty 
and  forty  years  of  age.  It  is  rare  under  fifteen  years  of  age,  and  it  is 
probable  that  only  5  per  cent,  of  the  total  number  of  cases  occur  under 
ten  years  of  age.  When  children  are  affected,  it  is  said  to  be  less  rare 
in  girls  than  in  boys,  and  to  attract  attention  chiefly  about  eight  years 
of  age. 

Pontou  II  collected  22  cases  in  children  in  1867,  and  a  large  number  have  since 
been  recorded.  In  eight  years  Broca**  operated  upon  nine  cases.  Cases  of  two 
cysts  in  the  hver  of  a  boy  aged  six  years  (H.  B.  Robinson  ft)  and  a  boy  aged  seven 
years  (Cheney  JJ)  have  been  recorded.  In  Cheney's  case  one  of  the  cysts  was  suppu- 
rating. 

CLINICAL  PICTURE. 
Symptoms. — A  hydatid  cyst  of  the  liver  may  remain  entirely  latent, 
so  that  its  presence,  even  when  the  changes  of  involution  or  spontaneous 
cure  have  not  supervened,  may  be  only  revealed  at  the  autopsy,  or  be 
suspected  for  the  first  time  when  the  abdomen  is  examined,  in  the  course 
of  life  insurance  routine  or  in  a  pregnant  or  recently  dehvered  woman. 
Even  when  the  cyst  is  large,  there  may  be  nothing  to  attract  the  patient's 
attention,  except  perhaps  the  increasing  size  of  the  abdomen.  In  some 
instances  there  may  be  a  feeling  of  weight  or  of  dragging  in  the  region 
of  the  liver.  When  the  peritoneal  covering  of  the  liver  is  inflamed,  ten- 
derness and  pain  on  respiration  are  present,  but  acute  perihepatitis  is 
infrequent  in  hydatid  disease  in  the  absence  of  suppuration.  The  con- 
trast between  the  marked  physical  signs  and  the  freedom  from  symptoms 

*  Lyon:  American  Jour.  Med.  Sciences,  vol.  cxxiii,  p.  124. 
t  Davaine:  Traite  de  Entozoaires,  Paris,  1S77. 

i  Neisser:  Die  Echinococcenkrankheiten,  1877.         §  Finsen:  Quoted  by  Lyon. 
II  Pontou:  Thdse  Paris,  1867.     Quoted   in   Traite  des   Maladies  de  I'enfance. 
vol.  iii,  p.  195.  **  Broca:  Sem.  MM.,  1901,  p.  89, 

tt  Robinson,  H.  B.:  Lancet,  1899,  vol.  i,  p.  767. 
it  Cheney:  Archives  of  Pediatrics,  Nov.  1897,  p.  851. 


398  DISEASES    OF   THE    LIVER. 

and  from  constitutional  disturbance  has  already  been  referred  to.  Pres- 
sure symptoms  are,  as  a  rule,  absent ;  this  probably  depends  on  the  slow- 
growth  of  the  cyst. 

Pressure  on  the  stomach  and  intestines,  however,  may  so  embarrass 
these  organs  as  to  give  rise  to  dyspepsia,  vomiting,  and  constipation. 
Obstruction  is  a  most  exceptional  result  of  hydatid  cysts,  but  Reichold  * 
has  recorded  the  case  of  a  woman  in  whom  intussusception  had  been 
diagnosed.  Upward  pressure  on  the  diaphragm  may  greatly  encroach 
on  the  pleural  cavity  and  produce  considerable  dyspnoea.  This  will  be 
more  marked  when  the  abdomen  is  distended  from  some  additional  cause, 
such  as  pregnancy.  The  irritation  of  a  large  hydatid  cyst  may  set  up 
slight  pleurisy  and  give  rise  to  pain  and  cough.  As  in  some  other  hepatic 
conditions,  the  pain  may  be  referred  to  the  right  shoulder.  Epistaxis, 
hsematemesis,  melsena,  and  metrorrhagia  have  been  put  on  record,  but 
are  extremely  rare. 

In  a  case  recorded  by  Hilliert  haemorrhage  took  place  into  a  hydatid  cyst  and 
ran  along  the  hepatic  duct,  which  also  opened  into  the  cyst,  to  the  duodenum.  The 
patient  died  from  the  effects  of  hsematemesis  and  melsena.  At  the  autopsy  the 
cyst  contained  37  ounces  of  blood-clot. 

The  physical  signs  of  hydatid  cysts  are,  unlike  what  occurs  in  many 
diseases,  more  prominent  than  the  symptoms.  In  many  instances  the 
upper  segment  of  the  abdomen  on  the  right  side  and  in  the  epigastrium 
is  prominent  and  firm,  and  there  is  bulging  of  the  costal  arch  on  the 
right  side.  In  great  abdominal  distension  lineae  albicantes  may  be  present. 
Dilated  subcutaneous  veins  are  very  exceptional,  but  a  prominent  "caput 
medusae"  has  been  noted  w^hen  the  inferior  vena  cava  is  compressed  by 
a  large  cyst. 

The  liver  is  enlarged,  its  form  and  outline  varying,  of  course,  with 
the  position  of  the  cyst  or  cysts.  When  the  cyst  is  near  the  convexity 
of  the  liver,  it  tends  to  displace  the  diaphragm  upwards.  A  cyst  in  the 
right  lobe  may  compress  the  lower  lobe  of  the  right  lung  and  imitate 
a  pleural  effusion.  In  rare  instances  a  cyst  in  the  left  lobe  may  simulate 
a  pericardial  effusion. 

When  the  cyst  is  deeply  embedded  in  the  substance  of  the  right  lobe, 
the  liver  is  expanded  and  pushed  forwards  as  if  occupied  by  a  solid 
growth.  When  the  cyst  projects  from  the  under  surface  of  the  right 
lobe,  the  liver  is  pushed  forward,  and  when  it  protrudes  beyond  the  lower 
border  it  may  imitate  an  enlarged  and  distended  gall-bladder,  a  tumor 
of  kidney,  uterus,  or  ovary,  or  a  pancreatic  cyst.  A  pendulous  hydatid 
cyst  may,  like  a  distended  gall-bladder,  be  accompanied  by  a  linguiform 
lobe  of  the  liver.  A  cyst  growing  from  the  anterior  surface  bulges  the 
hypochondrium  out,  or  when  in  the  left  lobe,  the  epigastrium  forwards, 
in  a  remarkable  manner.  In  such  cases  the  enlargement  of  the  liver  is 
not  uniform,  as  it  is  in  cirrhosis,  but  is  localised  and  may  be  manifestly 
due  to  a  tumor,  in  size  varying  from  that  of  an  orange  upw^ards.  The 
hepatic  enlargement  does  not  entirely  depend  on  the  position  of  the  cyst, 

*Reichold:  Munchen.  med.  Wochens.,  April  27,  1897. 
t  Hillier:  Trans.  Path.  Soc,  vol.  vii,  p.  22. 


HYDATID    CYSTS.  399 

though  of  course  it  is  chiefly  ckie  to  the  presence  of  the  cyst.  When  the 
right  lobe  is  occui^iecl  by  a  large  hydatid  cyst,  marked  compensatory 
hypertrophy  of  the  left  lobe  may  occur,  so  that  it  can  easily  be  felt  to 
be  enlarged. 

Chauffard  has  recorded  such  a  case  in  which  the  left  lolie  weighed  aknost  as 
much  as  a  normal  liver.* 

Usually  the  tumor  is  tense  and  elastic;  it  may,  especialty  when 
thick-wallecl  and  covered  by  liver  tissue,  give  the  impression  of  a  hard 
and  solid  tumor,  although  its  contents  are  perfectly  fluid ;  as  has  already 
been  mentioned,  the  contents  may  in  exceptional  cases  undergo  gelat- 
inous change,  although  the  cyst  is  progressively  increasing  in  size.  On 
the  other  hand,  it  may  occasionally  fluctuate  so  as  to  imitate  an  abscess. 
On  percussion  the  cyst  is  practically  always  dull;  the  entrance  of  air  from 
rupture  into  a  hollow  viscus  being  so  rare  as  to  make  it  probable  that 
in  any  case  when  the  cyst  appears  to  be  resonant  it  is  really  covered  by 
stomach  or  intestines.  Gas  has,  however,  been  found  in  suppurating 
hydatid  cysts  without  there  being  any  communication  with  the  intestinal 
tract,  and  can  be  explained  as  the  result  of  infection  with  the  Bacillus 
aerogenes  capsulatus  or  members  of  the  colon  group. 

The  "hydatid  thrill"  is  an  inconstant  sign  and  is,  even  when  present, 
not  pathognomonic,  inasmuch  as  it  may  be  obtained  in  other  cysts. 
It  is  brought  out  by  percussing  the  middle  finger  of  the  outstretched 
left  hand  when  placed  over  the  cyst;  a  peculiar  vibration  is  then  com- 
municated to  the  contiguous  fingers.  This  thrill  was  thought  by  Brian- 
Qonf  (1828)  to  be  due  to  the  impact  of  contained  daughter  cysts,  but 
it  can  be  obtained  in  sterile  hydatid  cysts,  in  tense  cysts  of  other  kinds, 
such  as  hydronephrosis,  and  sometimes  in  encysted  ascites,  or  according 
to  Chauffard, t  even  in  general  ascites  under  certain  conditions,  such  as 
an  elastic  state  of  the  abdominal  walls  in  young  persons.  The  "hydatid 
thrill"  is  not  very  often  obtained,  but  the  conditions  required  for  its 
production  are  more  often  realised  in  hydatid  than  in  other  cysts;  so 
that  its  presence,  though  not  absolute  evidence,  is  strongly  suggestive 
of  the  presence  of  a  hydatid  cyst.  Lancereaux  §  obtained  it  twice  in 
a  personal  experience  of  60  cases;  many  observers  have  never  met  with  it. 

Hydatid  cysts  are  rare  in  early  life,  but  when  they  do  occur,  a  thrill 
is  said  to  be  relatively  less  rare  than  in  adult  patients.  ||  It  has  been 
thought  that  the  occurrence  of  suppuration,  by  altering  the  conditions 
inside  a  hydatid  cyst,  will  remove  the  thrill  (Milian  **). 

When  two  or  more  hydatid  cysts  are  found  either  in  or  in  connexion 
with  the  liver,  the  signs  may  be  very  confusing,  and  from  the  irregularity 
of  the  surface  suggest  cancer,  cirrhosis  with  great  enlargement,  displace- 
ment of  the  liver,  or  affections  of  other  organs. 

*  Chauffard:  Sem.  Med.,  1896,  p.  265.  fBriangon:  Thfee,  Paris,  1828. 

J  Chauffard:  Traits  de  Medicine,  Bouchard  et  Brissaud,  tome  v,  p.  303,  1902. 
§  Lancereaux:  Traits  des  Maladies  du  foie  ct  du  pancreas,  p.  738. 
il  Broca:  Sem.  Med.,  p.  89,  1901. 
**  Milian:  Bull.  Soc.  Anat.  Paris,  1900,  p.  911. 


400  DISEASES    OF   THE   LIVER. 

In  a  case  of  multiple  hydatids  in  the  liver  encroaching  above  on  the  pleural 
cavity  the  do"WTiward  projection  of  two  large  cysts  from  the  right  lobe  of  the  Uver 
left  a  notch  between  them  which  during  life  was  taken  for  the  notch  between  the 
two  lobes  of  the  liver,  the  organ  being  thought  to  be  displaced  doMTiwards 
by  a  pleural  effusion.  Two  hydatid  cysts  in  a  boy  aged  seven  projecting  from  the 
anterior  surface  of  the  right  lobe  gave  rise  to  a  sulcus  which  when  felt  through  the 
abdominal  walls  imitated  the  colon  passing  over  a  tumor  of  the  right  kidney. 
(Cheney.*) 

Pressure  on  the  bile-duct"  producing  jaundice,  on  the  portal  vein  in- 
ducing ascites  or  haemorrhoids,  or  on  the  inferior  vena  cava  causing 
cedema  of  the  legs,  is  very  rarely  seen.  Pressure  symptoms  are  relatively 
less  infrequent  in  children  than  in  adults.  Jaundice  is  almost  constant 
when  an  hydatid  ruptures  into  and  discharges  daughter  cysts  into  the 
ducts,  but  is  rare  apart  from  this. 

Stirling  t  describes  a  large  cyst  with  calcareous  walls  springing  from  the  under 
surface  of  the  left  lobe,  which  pressed  on  the  common  bile-duct  and  thus  produced 
jaundice. 

In  a  man  who  had  had  jaundice  for  eleven  months  and  presented  well-marked 
xanthelasma  multiplex  W.  LeggJ  found  three  hydatid  cysts  in  the  liver;  one  of 
these  projected  into  the  portal  fissure  and  completely  obliterated  the  common 
hepatic  duct. 

A  large  cyst  may  in  rare  cases  compress  the  inferior  vena  cava  and 
produce  oedema  of  the  lower  limbs  and  the  trunk,  and  a  plexus  of  dilated 
veins  over  the  abdomen,  but  complete  obliteration  of  the  inferior  vena 
cava  has  been  recorded  without  any  oedema  of  the  feet  (Deve  §).     A 
pendulous  cyst  is  rather  more  likely  to  exert  pressure  on  the  inferior 
vena  cava  or  right  iliac  veins  than  an  ordinary  hydatid  cyst  embedded 
in  the  substance  of  the  liver.     Ascites  is  practically  always  due  to  some 
comphcation;  thus  it  occurs  when  there  is  leakage  of  the  cyst  after 
aspiration  or  spontaneous  rupture.     When  suppuration  has  supervened 
in  the  cyst  ascites  may  be  due  to  concomitant  local  peritonitis.     The 
large  size  of  some  cysts  naturally  leads  to  considerable  displacement  of 
neighbouring  viscera.     The  amount  of  displacement  depends  on  the  size 
and  situation  of  the  cyst.     The  diaphragm  is  very  frequently  pushed  up 
on  the  right  side,  and  with  a  large  cyst  involving  both  lobes  of  the  hver 
both  sides  of  the  thorax  may  be  greatly  encroached  upon.     In  such  cases 
or  when  the  cyst  is  in  the  left  lobe  the  heart  may  be  greatly  displaced 
upwards.     As  a  remarkable  example,  reference  may  be  made  to  Knaggs'  || 
case,  in  which  the  cardiac  dulness  was  in  the  first  and  second  intercostal 
spaces.     A  large  cyst  may  displace  the  stomach  and  the  other  abdominal 
viscera.     Occasionally  urticaria  may  be  the  first  indication  of  an  hydatid 
cyst,  and  may  be  seen  in  a  case  without  any  proof  that  the  cyst  has 
ruptured  or  leaked.     McMurray**  records  a  case  where  pruritus  and  a 
papular  rash  existed  for  two  years  and  disappeared  the  day  after  an 
unruptured  hydatid  cyst  was  removed.     It  has  been  thought  that  urti- 

*  Cheney:  Archives  of  Pediatrics,  Nov.,  1897,  p.  651. 
t  Stirling:  Intercolonial  Med.  Journal  of  Australasia,  Feb.  20,  1899. 
{Legg,  W.:  Trans.  Path.  Soc,  vol.  xxv,  p.  155. 
§  Dev6:  Bull.  Soc.  Anat.  Paris,  1903,  p.  197. 
II  Knaggs:  Trans.  Chn.  Soc,  vol.  xxiii,  p.  173. 
**  McMurray:  The  Austrahan  Medical  Gaz.,  May,  1896. 


HYDATID    CYSTS.  401 

caria  is  relatively  less  rare  in  children  than  in  adults  affected  with  hydatid 
disease. 

As  a  rule,  there  is  no  change  in  the  blood,  but  in  some  isolated  cases 
an  increase  in  the  proportion  of  eosinophile  cells  has  been  recorded. 
(Minimi,*  Tuffier,  Neusser,  Seligmann  and  Dudgeon, f  Achard,J  Dargein 
and  Tribondeau.§)  In  some  cases  eosinophilia  has  been  slight  in  degree 
and  it  is'  most  exceptional  to  get  such  a  liigh  count  as  in  Seligmann  and 
Dudgeon's  case,  where  the  percentage  was  57  and  fell  after  the  cysts 
were  evacuated.  Eosinophilia  has  been  thought  to  bear  a  very  definite 
relation  to  the  presence  of  animal  parasites  in  the  body  (Milian|l)  and 
to  play  a  part  in  protecting  against  toxines  manufactured  by  the  para- 
sites (Gulland  **).  If  this  is  so,  eosinophilia  would  occur  only  when 
absorption  of  the  contents  of  a  hydatid  cyst  is  going  on.  Eosinophiha 
is  by  no  means  constant,  and  though  its  presence  is  in  favour  of  a 
doubtful  tumor  being  hydatid  in  nature,  its  absence  cannot  be  held 
to  exclude  this  diagnosis. 

The  urine  is  nearly  always  normal  unless  there  is  some  complication. 
A  suppurating  hydatid  may  by  septic  absorjDtion  lead  to  albuminuria  or 
conceivably  to  albumosuria.  The  mechanical  effects  of  a  large  hydatid 
may,  by  pressing  on  the  right  renal  veins,  lead  to  temporary  albuminuria. 

PrEetorius  ft  mentions  a  case  where  albuminuria  disappeared  after  incision  and 
drainage  of  a  hydatid  cyst  of  the  hver. 

In  very  rare  cases  pressure  on  the  inferior  vena  cava  or  on  the  renal  veins 
has  been  thought  to  explain  great  diminution  in  the  excretion  of  urine. 
Davis  If  has  given  an  account  of  a  woman  in  whom  this  sequence  of  events 
was  thought  to  have  occurred. 

As  an  interesting  observation  Girard's  §§  case  of  clubbed  fingers  associated  with 
hydatid  of  the  liver  without  any  pulmonary  changes  may  be  mentioned.  It  was 
probably  an  accidental  coincidence. 

To  sum  up :  the  physical  signs  of  a  hydatid  cyst  in  the  liver  are  out 
of  proportion  to  the  symptoms;  there  may  be  great  enlargement  with 
an  absence  of  constitutional  disturbance.  The  most  marked  clinical 
manifestations  are  produced  when  the  cysts  rupture  into  adjacent  organs 
or  cavities,  or  suppurate — complications  which  will  be  described  later. 

DIAGNOSIS. 

The  diagnostic  features  are  the  presence  of  a  cystic  tumor  in  the  liver, 
which  is  considerably  enlarged,  together  with  a  marked  absence  of  con- 
stitutional disturbance.     The  diagnosis  cannot  be  made  with  absolute 

*  Mimmi:  Rev.  Grit,  de  Glm.  Med.,  April  6,  1901. 

t  Seligmann  and  Dudgeon:  Lancet,  1902,  vol.  i,  p.  1764. 

i  Achard:  Soc.  de  biolog.,  Nov.  16,  1901. 

§  Dargein  et  Tribondeau:  Ibid. 

II  Milian:  Bull.  Soc.  Anat.  Paris,  1901,  p.  323. 
**  Gulland:  Brit.  Med.  Journ.,  1902,  vol.  i,  p.  831. 
tt  Prajtorius :  Berlin,  klin.  Wochensch.,  1898,  S.  312. 
jj  Davis:  Lancet,   1900,  vol.  ii,  p.  1014. 
§§  Girard:  La  Semaine  Medicale,  1903,  p.  32. 
26 


402  DISEASES    OF   THE    LIVER. 

certainty  unless  fragments  of  the  cyst  or  booklets  have  been  obtained 
by  paracentesis  or  as  the  result  of  rupture  of  the  cyst  into  the  alimentary 
tract  or  in  other  positions.  In  the  absence  of  this  criterion  the  diagnosis 
is  largely  one  of  exclusion,  and  will  be  considered  in  the  paragraphs  on 
the  differential  diagnosis. 

Diagnosis  of  a  Hydatid  Cyst  by  Examination  of  Fluid  drawn 
off  by  an  Exploratory  Puncture. — Although  an  exploratory  puncture 
with  a  fine  syringe  is  not  a  proceeding  which  should  be  undertaken,  inas- 
much as  very  severe  symptoms  and  even  death  may  follow  the  escape  of  a 
small  quantity  of  fluid  into  the  peritoneal  cavity,  it  is  often  done  and  a 
diagnosis  made  on  the  characters  of  the  fluid  withdrawn.  At  the  present 
time  an  exploratory  incision  should  always  be  made  and  the  cyst  exposed. 
The  characteristics  of  hydatid  fluid  from  a  living  cyst  are  as  follows: 
It  is  colourless,  slightly  opalescent,  and  neutral  in  reaction,  with  a  specific 
gravity  of  1002  to  1010,  with  about  1  per  cent,  of  solids.  It  contains 
mucin,  but  no  albumin,  small  quantities  of  sugar,  inosite,  succinic  acid,, 
succinate  of  calcium,  and  sometimes  traces  of  cholesterin,  leucin,  and 
tyrosin.  It  contains  a  considerable  quantity  of  chloride  of  sodium. 
Scolices  and  booklets  are  not  free  in  the  living  cysts  and  only  become 
detached  by  the  operation  of  paracentesis  or  when  the  parasite  dies. 
The  detection  of  booklets  is  much  facilitated  by  centrifugalising  the 
fluid;  the  scolices  can  be  seen  as  small  white  dots  by  the  naked 
eye.  When  the  parasite  dies,  the  fluid  becomes  albuminous  and  turbid, 
and  a  toxic  body,  compared  to  myrtilotoxin,  may  make  its  appearance. 
When  suppuration  supervenes,  the  percentage  of  albumin  of  course  in- 
creases. The  laminated  membrane  of  the  ectocyst  may  be  discharged 
from  a  suppurating  hydatid  and  a  section  under  the  microscope  presents 
a  characteristic  and  beautiful  appearance. 

DIFFERENTIAL  DIAGNOSIS. 

There  are  a  large  number  of  conditions,  such  as  tumors  and  cysts 
in  or  close  to  the  liver,  which  may  imitate  a  hydatid  cyst  of  the  liver. 
A  hydatid  cyst  may  (I)  project  from  the  anterior  surface  of  the  liver; 
(II)  be  deeply  seated  in  the  substance  of  the  organ,  (III)  project  up- 
wards towards  the  thorax,  or  (IV)  downwards  into  the  abdomen.  The 
conditions  which  may  be  confused  with  these  four  varieties  will  now  be 
considered  seriatim. 

(I)  When  the  cyst  projects  from  the  anterior  surface  of  the  liver 
diagnosis  is  comparatively  easy.  There  are,  however,  a  number  of  con- 
ditions which  may  possibly  be  confused  with  it.  Simple  cysts  of  the  liver, 
though  hardly  ever  of  such  dimensions  as  to  resemble  a  hydatid,  cannot 
be  accurately  diagnosed  until  their  contents  or  their  walls  are  examined. 
In  multilocular  cystic  disease  of  the  liver  the  concomitant  enlargement 
of  the  kidneys  should  lead  to  a  suspicion  as  to  the  true  nature  of  the 
hepatic  disease.  In  malignant  disease  there  is  usually  cachexia,  while 
in  hydatid  the  general  health  is  good.  In  addition,  multiple  malignant 
growths  often  show  umbilication,  and  there  is  generally  pain,  neither  of 


HYDATID    CYSTS.  403 

which  is  present  in  nncomphcated  hydatid  diseasTe.  The  distinction, 
however,  between  mahgnant  disease  and  hydatid  may  sometimes  be 
very  difficult. 

Thus,  Sargnon*  describes  a  case  in  which  hydatid  was  diagnosed  and  laparotomy 
performed;  the  hver,  when  exposed,  presented  the  appearance  of  multiple  grow^th, 
and  the  abdomen  was  accordingly  closed;  subsequently  at  the  autopsy  the  growths 
were  found  to  be  multiple  hydatid  cysts. 

Cholecystitis. — As  a  rule,  inflammation  of  and  about  the  gall-bladder 
has  no  resemblance  to  a  hydatid  cyst  of  the  liver.  It  is  only  in  the 
presence  of  a  great  deal  of  inflammatory  adhesions  around  the  gall- 
bladder and  of  the  tongue-shaped  elongation  of  the  right  lobe  that  any 
difflculty  is  likely  to  arise.  Pain  is  prominent  in  most  cases  of  chronic 
cholecystitis  and  rare  in  hydatid  disease. 

In  a  woman  aged  fifty  years  who  was  under  my  care  the  liver  was  much  enlarged 
and  extremely  hard,  while  her  general  condition  was  so  good  that  malignant  disease 
seemed  unlikely.  She  was  first  seen  as  an  out-patient  and  was  recommended  to 
come  into  the  hospital.  She  returned  in  a  week's  time  with  a  pad  over  the  liver, 
having  been  tapped  without  any  result  by  a  general  practitioner.  Laparotomy  was 
subsequently  performed  by  my  colleague,  Mr.  Warrington  Haward,  and  a  greatly 
thickened  gall-bladder  containing  a  large  number  of  calculi  found.  The  calculi 
was  removed  and  the  patient  recovered.  Microscopic  examination  of  part  of  the 
wall  of  the  gall-bladder  removed  at  the  operation  only  showed  chronic  inflammation. 

Fro7n  Conditions  in  the  Anterior  Abdominal  Wall. — Suppuration  in 
the  sheath  of  the  rectus  and  in  the  anterior  abdominal  wall  is  more  super- 
ficial than  a  hydatid  and  does  not  move  with  respiration  in  the  same  way, 
while  the  skin  may  be  red  and  oeclematous.  Suppuration  in  the  rectus 
is  not  common,  and  when  it  does  occur,  is  usually  below  the  umbilicus. 
A  hydatid  in  the  anterior  abdominal  wall  is  small  and  can  be  made  out 
to  be  distinct  from  the  liver  and  not  to  move  with  it.  Phantom  tumors 
and  localised  spasm  of  the  right  rectus  abdominis  muscle  disappear 
gradually  under  an  anaesthetic  and  are  resonant  on  percussion.  Localised 
paralysis  of  the  rectus  over  the  liver  has  been  described  by  Potain  f 
as  resulting  from  rheumatism  of  the  vertebral  joints  in  hysterical  sub- 
jects, and  in  cardiac  dilatation  from  local  inflammation  of  the  peritoneal 
covering  of  the  liver;  the  bulging  and  local  distension  which  result 
imitating  a  hydatid  cyst  of  the  liver. 

(II)  When  the  cyst  is  deeply  embedded  in  the  substance  of  the 
liver,  especially  in  the  posterior  part  of  the  right  lobe  of  the  organ,  and 
expands  and  pushes  the  liver  fon^-ards,  the  diagnosis  is  more  difflcidt, 
and  must  be  made  from  a  variety  of  conditions.  Massive  carcinoma  in 
the  substance  of  the  liver  is  a  rare  condition,  and  would  be  accompanied 
by  severe  constitutional  disturbance  and  cachexia,  and  runs  a  rapid 
course.  A  large  cirrhotic  liver,  when  pushed  forwards  by  flatulent  dis- 
tension of  the  stomach,  may  be  sufficiently  prominent  to  imitate  enlarge- 
ment due  to  a  deeply  embedded  hydatid  cyst.  In  cirrhosis  the  enlarge- 
ment is  more  uniform,  affecting  both  lobes,  while  the  surface  is  not  per- 
fectly smooth;   other  signs  of  cirrhosis  may  be  present  and  the  general 

*  Sargnon:  Lyon  Medical,  1S9S,  p.  2.54.  f  Potain:  Sem.  Med.,  1896,  p.  209- 


404  DISEASES    OF   THE    LIVER. 

health  is  not  so  good  as  in  hydatid  disease.  Gummatous  enlargement 
might  imitate  hydatid  disease,  but  it  is  usually  painful,  and  would  prob- 
ably be  accompanied  by  a  history  or  by  other  manifestations  of  syphilis. 
If  any  doubt  exists,  a  course  of  iodide  of  potassium  and  mercury  should 
be  tried. 

The  painless  enlargement  of  lardaceous  disease,  leuksemia,  and 
cardiac  affections  should  be  readily  distinguished  by  signs  of  the 
primary  diseases  and  examination  of  the  urine,  blood,  and  heart.  En- 
largement of  the  spleen  would  militate  against  ordinary,  but  not  against 
multilocular,  hydatid  of  the  liver,  while  it  would  be  greatly  in  favour  of 
lardaceous  disease  and  leuksemia.  The  various  forms  of  suppuration 
in  the  liver,  such  as  a  large  tropical  abscess,  suppurative  pylephlebitis, 
and  cholangitis,  are  practically  always  accompanied  by  fever,  and  often 
by  rigors,  while  the  constitutional  disturbance  is  very  considerable.  The 
history  of  residence  abroad,  dysentery,  appendicitis,  or  cholelithiasis 
would  point  to  suppuration.  But  the  presence  of  fever  and  constitu- 
tional symptoms  indicating  septic  absorption  are  the  points  of  most 
importance.  When  suppuration  occurs  in  a  hydatid  cyst  of  the  liver, 
the  condition  is  the  same  as  a  hepatic  abscess,  and  it  can  only  be  diag- 
nosed by  a  history  of  a  cyst  having  existed  in  the  liver  for  a  considerable 
time.  In  subphrenic  abscess  the  fever  and  constitutional  disturbance, 
the  history  of  acute  onset,  of  symptoms  pointing  to  gastric  ulcer,  §,nd 
in  some  cases  the  presence  of  air  (subphrenic  pyo-pneumothorax),  are 
sufficient  to  distinguish  it  from  an  ordinary  hydatid  cyst.  A  suppurating 
hydatid  may  by  leakage  set  up  a  subphrenic  abscess. 

Aneurysm  of  the  hepatic  artery  is  a  very  rare  condition,  and  is  nearly 
always  accompanied  by  pain  and  jaundice,  and  the  symptoms  are  only 
likely  to  resemble  rupture  of  a  hydatid  cyst  into  one  of  the  bile-ducts. 
In  cases  where  the  aneurysm  is  sufficiently  large  to  be  felt,  there  would 
almost  always  be  pulsation. 

(Ill)  Hydatid  Cyst  Projecting  Upwards  into  the  Thorax. — When 
.a  hydatid  cyst  projects  from  the  convexity  of  the  right  lobe,  or  in  rare 
instances  from  the  upper  surface  of  the  left  lobe,  it  may  be  difficult  to 
distinguish  it  from  a  pleural  effusion,  since  it  may  displace  the  diaphragm 
Tipwards,  lead  to  extensive  collapse  of  the  lung  and  to  dulness  over  the 
greater  part  of  the  right  side  of  the  chest,  without  producing  any  down- 
ward displacement  of  the  liver.  In  such  cases  the  diagnosis  may  only 
be  arrived  at  when  the  contents  of  the  cyst  are  seen;  for  example,  when 
rupture  into  the  lung  leads  to  expectoration  of  pieces  of  hydatid  mem- 
brane or  when  booklets  are  found  in  fluid  drawn  off  by  an  aspirator. 
Skiagraphy,  by  showing  the  upward  displacement  of  the  diaphragm  on 
the  right  side  and  its  relation  to  the  shadow  cast  by  the  heart,  is  more 
likely  to  assist  in  arriving  at  a  correct  diagnosis  than  any  other  means 
short  of  exploration  at  our  disposal.  When  a  hydatid  cyst  gives  rise 
to  the  signs  of  a  small  pleural  effusion  and  to  considerable  enlargement 
of  the  liver,  the  diagnosis  is  easier;  but  in  a  case  with  these  signs  the 
hepatic  enlargement  might  be  due  to  some  other  cause,  such  as  cirrhosis, 
and  the  dulness  in  the  chest  to  a  small  effusion.     The  duhiess  due  to  a 


HYDATID    CYSTS.  405 

pleural  effusion  differs  somewhat  from  that  of  a  hydatid  cyst  in  the  hver^ 
which  displaces  the  diaphragm  upwards.  If  the  line  of  dulness  is  highest 
in  the  axiUa  and  falls  somewhat  both  tow^ards  the  spine  and  sternum,  a 
pleural  effusion  is  more  probable,  w^hile  if  there  is  dulness  at  the  base 
behind  with  a  rounded  summit  there  maybe  a  cyst  in  the  liver.  (Fowler 
and  Godlee.*) 

The  diagnosis  between  a  hydatid  cyst  in  the  upper  and  back  part 
of  the  right  lobe  of  the  liver  and  one  in  the  substance  of  the  right  lung, 
especially  when  near  the  base,  is  very  difficult,  as  the  clinical  signs  and 
symptoms  are  very  much  the  same.  There  is  said  to  be  more  cough  in 
cases  of  pulmonary  hydatid,  and  there  may  be  a  band  of  resonance  below 
the  dulness,  corresponding  to  the  cyst,  owing  to  the  presence  of  some 
resonant  lung  below^  the  hydatid.  Haemoptysis  maybe  an  early  symptom 
in  hydatid  of  the  lung,  while  it  is  not  likely  to  occur  with  a  hydatid  of 
the  liver  except  from  extreme  congestion  of  collapsed  lung;t  it  is  rare 
then,  and  would  only  occur  late  in  the  disease,  when  the  diaphragm,  is 
displaced  upwards  to  a  marked  degree,  viz.,  to  the  level  of  the  second 
rib  or  even  of  the  clavicle.  From  constant  pressure  exerted  by  the  cyst 
the  diaphragm  may  atrophy  so  as  to  allow  the  hydatid  to  project  into 
the  pleural  cavity  or  to  communicate  with  the  lung  without  any  suppura- 
tive or  ulcerative  process. 

What  has  been  said  about  hydatids  in  the  lung  and  the  diagnosis  from 
hydatid  of  the  upper  surface  of  the  liver  applies  in  the  case  of  hydatid 
of  the  pleural  cavity.  As  in  the  case  of  the  lung,  so  here  the  cpiestion 
is  more  likely  to  arise  when  on  the  right  side.  Luff, J  however,  met 
with  a  case  where  a  hydatid  in  the  left  pleura,  containing  six  pints  of 
fluid,  gave  rise  to  signs  of  hydatid  of  the  liver  with  prol^able  extension 
into  the  left  pleura.  It  is  difficult  or  impossible  to  distinguish  between 
a  hydatid  between  the  liver  and  diaphragm  and  a  cyst  projecting  from 
the  convexity  of  the  liver.  In  both  cases  the  liver  is  depressed  and  the 
pleural  cavity  encroached  upon.  When  a  cyst  is  found  between  the 
layers  of  the  suspensory  ligament  of  the  liver,  it  may  have  started  in 
the  superficial  part  of  the  liver  and  grown  up  out  of  it. 

(IV)  When  the  cyst  projects  downwards  into  the  abdomen  it 
is  usually  more  readily  recognised,  but  confusion  may  easily  arise  between 
it  and  other  conditions,  such  as  a  dilated  gall-bladder,  renal  tumor  or 
displacement,  and  various  other  abdominal  tumors.  There  is  also  the 
greater  likelihood  that  cysts  in  this  position  may  press  upon  the  neighbour- 
ing viscera  and  thus  complicate  the  diagnosis.  A  dilated  gall-bladder 
may  closely  resemble  a  hydatid  cyst  hanging  down  from  the  under 
surface  of  the  liver.  It  is  usually,  however,  not  so  prominent.  There 
may  have  been  attacks  of  biliary  colic  or  of  icterus  in  the  past;  though 
both  these  symptoms  may  follow  rupture  of  a  cyst  into  the  bile-ducts. 
A  dilated  gall-bladder  is  pear-shaped  and  much  more  readily  moved 
about  than  a  hydatid  cyst.     During  a  lajiarotomy  a  i)endulous  hydatid 

*  Fowler  and  Godlee:  Tlie  Diseases  of  the  Liingis,  p.  478. 
t  Galliard:  .\rchiv.  ('.('nc'ral.  de  Med.,  tome  clxv,  p.  409,  1890. 
t  Luff,  A.  P.:  Lancet,   1896,  vol.  i,  p.  1134. 


406  DISEASES    OF    THE    LIVER. 

cyst  arising  near  the  gall-bladder  may  be  mistaken  for  that  viscus  even 
b}^  an  experienced  obser\'er. 

Hydronephrosis  of  the  right  kidney  when  it  passes  forv\-ards  towards 
the  abdomhial  wall  ma}'  very  closely  resemble  a  hydatid :  for  the  colon 
need  not  necessarily  he  in  front  of  the  renal  tumor  when  the  latter  is 
large.  A  hydronephrosis  will  project  much  more  into  the  loin,  and 
examination  of  the  urine  may  give  a  clue  by  being  of  a  low  specific  gra^dt}', 
while  the  occurrence  of  inflammation  in  the  kidney  or  the  transition  of 
a  hydronephrosis  into  a  pyonejDhrosis  would  be  shown  by  the  presence 
of  pus  in  the  urine.  The  discharge  of  a  large  quantity  of  urine  associated 
with  cUsappearance  of  the  tumor  is  characteristic  of  an  intermitting 
hydronephrosis.  A  soft  renal  or  suprarenal  gro'o-th  on  the  right  side 
may  imitate  a  hydatid  cyst  projecting  from  the  right  lobe  of  the  hver. 

A  man  aged  twenty-five  had  a  fluctuating  tumor  l^elow  the  hver,  -n-hich  ■n-as  at 
first  thought  to  be  hydatid,  but  puncture  only  brought  blood  away.  I  examined 
him  after  death  in  1S91,  and  found  a  large  cystic  endotheliomatous  grcn-th  arising 
from  the  right  suprarenal  gland  and  in^-ading  the  right  lobe  of  the  hver  bj^  con- 
tinuity. 

Renal  and  suprarenal  groAvths  probalDh'  move  less  on  respiration 
than  those  connected  with  the  liver;  they  aa-III  tend  to  bulge  the  loin 
somewhat,  and  a  careful  bimanual  examination  should  therefore  always 
be  made.  A  floating  kidney  might  give  rise  to  chfficulty  in  diagnosis; 
Potain  has  described  a  form  of  nephroptosis/'' anteversion  of  the  kidney/' 
which  is  especially  hkety  to  resemble  an  hydatid  of  the  hver  unless  a 
careful  bimanual  examination  is  insisted  on. 

Pancreatic  and  Peripancreatic  Cysts. — CH'sts  in  connexion  with  the 
pancreas  or  a  collection  of  fluid  in  the  lesser  sac  of  the  peritoneum  (peri- 
pancreatic cyst)  are  usually  more  prominent  towards  the  left,  and  are 
not  likely  to  be  confused  with  hydatid  cysts,  which  are  only  rarely 
attached  to  the  left  lobe  of  the  liver.  A  hydatid  cyst  dependent 
from  the  left  lobe  of  the  liver  might  imitate  a  pancreatic  cyst. 
Pancreatic  and  other  abdominal  C3'sts  and  tumors  should  be  separated 
from  the  liver  by  a  zone  of  resonance,  while  a  hydatid  cyst  should  be  con- 
tinuous "VAith  it.  Again,  a  pancreatic  cyst  is  more  deeph'  placed  and 
shoifld  he  behind  the  stomach,  while  a  hydatid  cyst  would  be  in  front. 
In  case  of  doubt  the  stomach  should  be  inflated  with  air.  In  the  fol- 
loT^dng  case  a  suppurating  h3'datid  attached  to  the  back  of  the  left  lobe 
of  the  hver  imitated  a  pancreatic  cyst : 

A  woman  aged  forty-nine,  the  mother  of  ten  children,  was  admitted  under  my 
care  at  St.  George's  Hospital  on  November  30,  1901.  Four  months  previously  she 
suddenly  had  an  attack  of  verj'  severe  pain  accompanied  by  rigors  and  followed 
by  jaundice.  The  attacks  were  repeated  at  intervals  of  about  two  weeks.  The 
tumor  was  noticed  after  the  first  attack,  and  was  thought  to  have  varied  in  size 
from  time  to  time.  She  was  a  fat  woman  A\ith  a  large,  tense  tumor  laetween  the 
umbilicus  and  the  ensiform  cartilage;  close  to  the  latter  it  was  dull  on  percussion,  but 
elsewhere  it  was  resonant;  it  could  not  be  separated  from  the  left  lolie  of  the  liver 
and  did  not  bulge  into  the  loin.  This  was  important,  since  when  asked  a  leading 
question  the  patient  said  it  varied  from  time  to  time  according  to  the  amount  of 
water,  sometimes  excessive,  that  she  passed.  There  was  no  jaundice  or  bile  in  the 
urine.  The  diagnosis  lay  l:)etween  a  peripancreatic  cyst,  a  liydronephrosis,  and  a 
hydatid  cyst  dependent  from  the  left  lobe  of  the  liver.     It  was  thought  to  be  a 


HYDATID    CYSTS.  407 

peripancreatic  effusion  into  the  lesser  sac  of  the  peritoneum  folloA\"ing  pancreatitis, 
whicli  possibly  occurred  as  the  result  of  the  passage  of  gall-stones  four  months 
before.  Accordingly  on  December  9  Mr.  Sheild  made  an  incision  over  the  left 
linea  semilunaris  and  came  doT\-n  on  coils  of  intestines  somewhat  matted  together; 
on  separating  them  stinking  pus  wnth  numerous  daughter  cysts  swelled  up  from 
a  cyst  attached  to  the  left  lobe  of  the  liver.  This  cavity  was  drained.  For  a  time 
the  patient  did  well,  but  the  discharge  was  A'ery  copious  and  she  became  very  weak, 
eventually  dj'ing  on  December  21.  At  the  autopsy  there  was  a  large  subphrenic 
abscess  between  the  diaphragm  and  the  right  lobe  of  the  liver.  The  left  lobe  of 
the  liA-er  was  excavated  by  a  suppurating  hydatid  CA'st  which  passed  backwards  and 
was  adherent  to  the  anterior  surface  of  the  pancreas.  The  pancreas  itself  appeared 
healthy.  The  liver  was  fatty  and  swollen  and  weighed  7  pounds.  Both  the 
cystic  and  the  common  bile-ducts  were  much  dilated,  but  there  were  no  gall-stones 
in  the  gall-bladder.     The  spleen,  4  ounces,  was  healthy. 

A  large  hydatid  cyst  should  hardly  be  mistaken  for  ascites  unless  the 
cyst  is  so  large  that  it  actually  fills  the  abdomen,  and  even  then  the 
dulness  'udll  not  reach  to  the  flanks.  In  any  case  chemical  examination 
of  fluid  dra-«Ti  off  by  a  trocar  will  settle  the  question.  A  large  ovarian 
cyst  in  the  abdomen  may  resemble  a  pendulous  hydatid  cyst,  especially 
one  that  has  contracted  secondary'  adhesions  to  the  lower  part  of  the 
abdomen.  The  historv^  of  the  tumor  as  indicating  the  situation  where  it 
was  first  noticed,  whether  near  the  Hver  or  the  pehds,  the  connexion 
of  the  tumor  with  the  liver  or  with  the  uterus,  and  vaginal  examination 
are  points  that  may  assist  in  making  a  diagnosis.  An  ovarian  cyst  under 
ordinar}^  conditions  will  not  move  on  respiration. 


THE  DURATION  AND  PROGNOSIS. 

The  time  during  which  a  hydatid  cyst  may  remain  alive  and  capable 
of  active  growth  is  very  difficult  to  estimate.  But  it  has  been  thought 
to  be  as  long  as  twenty  years,  which  is  quite  in  accord  with  the  history 
of  the  following  case : 

A  man  aged  thirty-five  died  under  the  care  of  my  colleague,  Dr.  Penrose,  in 
St.  George's  Hospital  with  a  large  hydatid,  the  size  of  an  adult's  head  and  full  of 
daughter  cysts,  in  the  right  lobe;  close  to  it  there  was  a  small,  dried-up  cyst.  Nine- 
teen years  before  he  had  been  tapped,  and  presumably  the  small  cyst  had  been  then 
evacuated.  It  is  highly  probable  that  the  two  cysts  were  of  the  same  age  and  due 
to  the  same  infection;  but  even  if  the  larger  cyst  was  due  to  infection  at  the  time 
of  tapping  the  other,  it  must  have  existed  for  nineteen  years. 

The  prognosis  of  a  big  hj^datid  C3'st  really  largely  depends  on  whether 
it  is  operated  upon  or  not.  If  it  is  let  alone  and  not  operated  upon,  it 
may  die,  shrivel  up,  and  give  rise  to  no  further  trouble,  but  there  is  no 
satisfactory  way  of  prophesying  whether  this  will  happen,  and  a  cyst 
which  has  remained  quiescent  or  latent  may  suppurate  without  any  very 
manife.st  cause.  Suppuration  is  a  dangerous  complication,  and  its  possi- 
ble incidence  in  the  remote  future  must  be  faced  in  deciding  not  to  call 
in  surgical  interference. 

The  size,  rate  of  growth,  and  the  possibility  of  rupture  or  suppuration 
supervening  are  points  requiring  consideration.  If  the  cyst  is  sufficiently 
large  to  be  diagnosed  and  is  rapidly  increasing  in  size,  the  danger  of 
rupture  taking  place  is  sufficient  to  make  operation  desirable.  When  a 
cyst  gets  smaller  under  observation,  it  may  be  undergoing  spontaneous 


408  DISEASES   OF  THE   LIVER, 

cure,  and  may  be  left  alone  without  any  immediate  prospect  of  danger, 
but  it  is  safer  to  remove  it,  for  if  suppuration  supervenes,  the  conditions 
are  then  less  favourable  for  successful  operation.  The  situation  of  the 
cyst  makes  a  difference  in  the  prognosis:  if  it  is  deeply  situated  and  in 
the  upper  and  posterior  part  of  the  right  lobe,  it  is  both  more  hkely 
to  encroach  on  the  thorax  and  more  difficult  to  operate  upon.  Another 
point  which  often  cannot  be  determined,  but  which  is  nevertheless  of 
importance  in  the  prognosis,  is  whether  there  is  one  cyst  or  whether  they 
are  multiple. 

If  a  cyst  is  not  growing  rapidly,  and  is  therefore  not  interfered  with, 
there  is  the  possible  danger  of  traumatic  rupture  of  the  cyst,  while  a 
cyst,  though  not  showing  signs  of  enlargement,  may  rupture  into  some 
viscus  to  which  it  has  become  adherent.  Rupture  is  a  complication 
which  always  affects  the  prognosis  and  gives  rise  to  anxiety,  though  the 
gravity  of  the  prognosis  varies  according  to  the  situation  of  the  rupture. 
Thus  rupture  into  the  pericardium  or  inferior  vena  cava  is  nearly  always 
rapidly  fatal.  Deve  *  has  shown  that  death  need  not  always  occur  when 
a  cyst  ruptures  into  the  vena  cava,  if  the  cysts  discharged  are  few  and 
small.  Rupture  into  the  peritoneum  or  even  into  the  pleura  may  prove 
fatal  very  rapidly,  while  if  the  patient  does  survive,  there  is  danger  of 
peritonitis  or  of  empyema.  The  effects  of  escape  of  hydatid  fluid  into 
the  peritoneal  cavity  are  considered  below.  Traumatic  rupture  of  a 
living  cyst  may  give  rise  to  comparatively  little  disturbance,  but  rupture 
of  a  dead  cyst,  the  contents  of  which  have  become  toxic  or  infected  with 
micro-organisms,  is  most  dangerous.  Rupture  into  parts  of  the  peri- 
toneum cut  off  by  adhesions  is,  of  course,  much  less  dangerous,  but  it 
may  then  be  difficult  to  be  sure  that  this  has  occurred.  Gradual  leakage 
into  the  general  peritoneal  cavity  is  not  necessarily  followed  by  such  grave 
symptoms.  Rupture  into  the  bile-ducts  is  very  prone  to  set  up  suppura- 
tive cholangitis,  and  therefore  is  a  grave  complication.  Ruptures  into  the 
lungs,  alimentary  tract,  and  externally  are  less  serious.  Cyrf  estimated 
the  mortality  at  90  per  cent,  when  rupture  occurred  into  the  peritoneum, 
80  per  cent,  into  the  pleura,  70  per  cent,  into  the  bile-ducts,  57  per  cent, 
into  the  bronchi,  40  per  cent,  into  the  stomach,  15  per  cent,  into  the 
intestines,  and  3  per  cent,  onto  the  surface  of  the  body.  Suppuration, 
of  course,  is  also  a  very  grave  complication  and  makes  the  outlook  very 
gloomy. 

If  the  cyst  is  operated  upon,  the  prognosis  depends  on  the  method 
of  operation  adopted,  on  complications  arising  from  the  operation,  while 
there  is,  further,  the  possibility  of  there  being  other  cysts  which,  though 
latent  at  the  time  of  the  operation  and  not  then  attracting  attention, 
may  subsequently  give  rise  to  trouble  and  danger. 

*  Dcve:  Bull.  Soc.  Anat.  Paris,  1903,  p.  185. 

t  Cyr:  Quoted  by  Hoppe-Seyler,  Nothnagel's  Practical  Encyclopa?dia,  Dis- 
eases of  Liver,  p.  802.     English  translation. 


HYDATID    CYSTS.  409 

TREATMENT. 

The  treatment  of  hydatid  cysts  is  essentially  surgical,  and  consists 
in  the  evacuation  or  removal  of  the  cyst.  No  drugs  given  by  the  mouth 
have  any  effect  on  the  parasite.  A  number  of  different  methods  have 
been  employed. 

I.  Simple  puncture  'vsdth  a  trocar  and  removal  of  some  or  all  of  the 
fluid  contents  of  the  cyst.  This  method,  which  is  the  oldest,  has  been 
much  employed,  and  has  naturally  met  with  approval,  as  it  is  simple 
and  easy  to  perform.  After  the  withdrawal  of  the  fluid  the  parasite, 
under  favourable  conditions,  dies  and  the  cyst  shrivels  up. 

Tapping  with  a  trocar  or  an  aspirator  is  adapted  for  superficial  cysts 
close  to  the  abdominal  wall  in  which  there  is  no  danger  of  wounding 
adjacent  structures,  such  as  the  intestines.  It  should  not  be  employed 
for  old,  thick-walled  cysts  or  when  there  is  any  sign  of  suppuration  in 
the  cyst.  Though  in  many  cases  cure  results  from  simple  tapping,  there 
is  an  element  of  risk,  since  severe  symptoms  and  even  death  have  fol- 
lowed this  simple  operation.  The  bad  effects  are  considered  on  page 
410.  Dieulafoy*  considers  that  the  bad  effects  of  simple  tapping  are 
due  to  the  cyst  having  only  been  partially  evacuated,  and  that  as  a 
result  some  of  the  residual  fluid  has  escaped  into  the  peritoneal  cavity; 
he,  therefore,  insists  on  complete  evacuation  of  the  cysts,  and  directs 
that  an  aspirator  should  be  used.  My  own  opinion  is,  however,  that  the 
safest  procedure  is  to  have  the  cyst  fully  exposed  by  a  surgeon  and  then 
treated  as  the  details  of  the  case,  thus  plainly  seen,  show  to  be  the  proper 
course. 

II.  A  modification,  or  rather  an  addition  to  the  simple  procedure  of 
tapping,  consists  in  the  injection  of  antiseptic  fluids  into  the  interior 
of  the  cyst.  In  this  method  a  little  of  the  fluid  is  removed  by  means 
of  a  small  puncture,  and  a  small  quantity  of  some  fluid  is  then  introduced 
with  the  object  of  killing  the  parasite.  This  method,  advocated  by 
Baccelli,  has  been  successfully  put  into  practice  by  B6kay,t  who  injected 
a  solution  of  perchloride  of  mercury,  1  in  1000.  Other  fluids,  such  as 
ox-bile,  so  as  to  imitate  what  has  been  supposed  to  be  one  cause  of  spon- 
taneous cure,  iodine  solution,  carbolic  acid,  alcohol,  formaline,  etc.,  have 
been  used  with  the  same  object.  These  methods  are  dangerous  and  are 
only  mentioned  to  be  avoided.  Suppuration,  or  even  fatal  mercurial 
poisoning,  has  been  recorded. 

III.  Electrolysis. — Hilton    Fagge    and    Durham  t    employed    this 

method  with  success  in  7  or  8  cases.     It  consisted  in  introducing  two 

needles  into  the  cyst  and  then  passing  a  constant  electric  current  through 

the  cyst,  the  needles  being  attached  to  the  negative  pole,  while  the  positive 

pole  of  the  battery  was  connected  with  a  sponge  placed  on  the  skin  of 

the  abdomen  over  the  cyst.     Electrolysis  acts  in  the  same  way  as  simple 

puncture,  and  not,  as  was  at  first  imagined,  by  decomposition  of  the  fluid 

in  the  cyst. 

*Dieulafoy:  Acad,  de  M6d.,  May  30,  1S99. 

t  Bokay:  Archiv  I'.  Kindcrheilk.,  Bd.  xxiii,  S.  310,  1897 

J  Medico-Chirurg.  Trans.,  vol.  liv,  p.  1. 


410  DISEASES    OF   THE    LIVER. 

Accidents  and  Bad  Effects  following  Simple  Tapping. — When  a 
hydatid  cyst  is  tapped  and  the  fluid  is  partially  drawn  off,  some  of  the 
residual  fluid  not  uncommonly  escapes  into  the  peritoneal  cavity,  and 
its  presence  may  be  shown  by  some  shifting  dulness  and  fluctuation  in 
the  flanks  and  lower  part  of  the  abdomen.  There  are  usually  no  bad 
symptoms,  but  intense  itching  followed  by  urticaria  lasting  from  a  few 
hours  to  two  days  may  result;  sometimes  peritonismus,  or  signs  of  false 
peritonitis,  follows  tapping,  and  in  rare  cases  death  preceded  by  convul- 
sions and  collapse  has  occurred.  The  fluid  in  a  living  hydatid  cyst 
contains  no  albumin,  no  hooklets,  and  is  not  capable  of  producing  toxic 
effects  when  injected  into  animals,  and  is  therefore  usually  without  any 
bad  effects  on  the  man. 

Chauffard,*  however,  met  with  a  most  exceptional  case  in  a  man  aged  thirty- 
five  years;  a  hydatid  cyst  was  punctured  and  10  c.c.  of  clear  fluid  dra-mi  off;  epi- 
leptic convulsions  set  in  and  death  followed  within  twenty-five  minutes  from  the 
time  of  puncture  of  the  cyst.  The  cyst  contained  clear  fluid  which  was  -ndthout 
any  poisonous  action  on  animals,  and  did  not  contain  any  alkaloid. 

Vidal,  Kirmisson,  Kornach,  Martini,  Maury,  Boinet  and  Chazouhere 
have  found  that  the  clear  fluid  drawn  off  from  a  living  hydatid  cyst, 
which  contains  neither  albumin  nor  hooklets,  is  not  toxic.  When  the 
hydatid  cyst  dies  and  undergoes  aseptic  necrosis  without  the  introduction 
of  micro-organisms,  its  characters,  both  physical  and  physiological, 
become  changed.  The  fluid  becomes  turbid,  yellow,  syrupy,  contains 
hooklets,  albumin,  and  a  ptomaine.  This  toxic  body  is  analogous  to 
myrtilotoxin  found  in  the  livers  of  poisonous  mussels,  and  gives  rise  to 
the  urticaria  and  other  symptoms  sometimes  manifested  after  the  escape 
of  hydatid  fluid  into  the  tissues.  This  poison  has  been  found  by  Boinet 
and  Chazouhere  t  to  crystallize  in  long,  silky  needles.  Physiologically 
when  injected  into  animals  it  induces  convulsions,  loss  of  motor  and 
sensory  power,  followed  by  slowing  of  the  heart,  rapid  respirations, 
dilated  pupils,  fall  of  blood-pressure,  prostration  and  collapse,  and  in 
larger  doses  death.  VironJ  has  found  a  toxalbumin  in  hydatid  fluid 
from  sheep  which  gives  rise  to  acute  inflammation  of  the  tissues;  this 
throws  light  on  local  suppuration  occurring  in  a  sinus  leading  to  a  hydatid 
that  has  been  aspirated. 

In  a  man  aged  twenty-three  years  with  jaundice,  dangerous  collapse  followed 
exploratory  paracentesis  of  a  hydatid  cyst,  and  subsequently  a  profuse  urticarial 
rash  developed  on  the  abdomen,  legs,  and  extensor  surfaces  of  the  arms,  and  lasted 
for  some  hours  (L.  Humphry  §).  Two  weeks  later  -^\  grain  of  atropine  was  injected 
in  order  to  prevent  a  recurrence  of  these  severe  symptoms  and  paracentesis  was 
successfully  performed.  The  late  Professor  Roy  injected  the  fluid  into  guinea-pigs 
and  a  dog,  and  marked  toxic  symptoms  were  noticed.  Bryant  |1  has  recorded  sudden 
death  five  minutes  after  paracentesis  of  hydatid  of  the  liver;  the  trocar  passed 
through  the  portal  vein,  and  it  is  possible  that  the  hydatid  fluid  may  have  entered 
directly  into  the  circulation. 

*  Chauffard:  Sem.  M6d.,   1896,  p.  265. 

t  Boinet  and  Chazouhere:  Rev.  de  Med.,  1S9S,  p.  S45. 

t  Viron:  Archiv.  de  Med.  experiment,  et  d.  anat.  path.,  1S92,  p.  136. 

§  Humphry:  Lancet,   1887,  vol.  i,  p.   120. 

II  Bryant,  T.:  Chn.  Soc.  Trans.,  vol.  xi,  p.  230. 


HYDATID    CYSTS.  411 

The  toxic  effects  of  hydatid  fluid  are  probably  due  to  the  contained 
alkaloid,  and  need  not  be  regarded  as  the  result  of  the  personal  reaction 
or  idiosyncrasy  of  the  patient,  as  Chauffard  suggests.  The  s3aiiptoms 
may  be  grouped  under  three  headings:  (a)  Cutaneous — i^ruritus  and 
urticaria;  (b)  Cerebrospinal — epileptiform  convulsions;  and  (c)  collapse 
and  cardiac  failure. 

As  mentioned  above,  a  hydatid  rash  has  in  very  rare  instances  been 
seen  without  rupture  or  leakage  of  the  cyst;*  usually  it  is  due  to  one  or 
other  of  these  events.  It  has  been  produced  by  contact  with  the  fluid, 
as  in  the  case  referred  to  by  Achard  of  two  individuals  who  suffered  from 
urticaria  after  making  a  postmortem  on  a  case  of  hydatid  cyst.  A  trocar 
has  also  been  known  to  wound  a  large  branch  of  the  portal  or  hepatic 
vein  and  induce  fatal  haemorrhage.  It  may  be  followed  by  suppuration 
in  the  cyst,  and  thus  not  only  is  time  lost,  but  a  dangerous  complication 
results. 

Surgical  Treatment. — As  already  pointed  out,  the  more  satisfactory 
method  of  dealing  with  hydatid  cysts  of  the  liver  is  by  surgical  means, 
the  abdomen  being  opened  and  the  cyst  exposed.  For  the  various  methods 
of  dealing  with  the  cyst  the  reader  should  refer  to  a  surgical  text-book. 
In  a  few  instances  the  whole  of  the  cj^st,  including  the  external  adventi- 
tious capsule,  has  been  removed.  Generally  the  incision  of  the  cyst  and 
the  removal  of  the  parasite  and  daughter  cysts  are  performed.  There  are 
dangers  connected  with  the  operation,  of  course,  such  as  haemorrhage 
from  veins  in  the  capsule  of  the  cyst,  and  extensive  and  prolonged  leakage 
of  bile  due  to  free  communications  between  the  cyst  and  the  larger  bile- 
ducts.  The  loss  of  bile  from  a  cyst,  if  continued,  may  lead  to  emaciation 
if  it  is  so  extensive  that  all  or  nearly  all  the  bile  escapes  from  the  body 
by  this  channel.  This  result  need  not  occur  if  a  fair  proportion  of  the 
bile  enters  the  duodenum.  As  a  possible  danger  due  to  the  operation, 
long-continued  suppuration  leading  to  lardaceous  disease  may  be  men- 
tioned, but  is  much  less  likely  to  occur  at  the  present  day  than  in 
former  times. 

Prophylaxis. — Raw  vegetables  ought  to  be  carefully  washed,  so  as 
to  prevent  the  possibility  of  ova  being  conveyed  by  them.  As  the  ova 
are  almost  entirely  derived  from  the  faeces  of  dogs,  care  must  be  taken 
by  those  who  keep  dogs  in  the  house.  In  places  where  hj^datid  disease 
is  frequent,  drinking-water,  one  of  the  chief  means  by  which  the  disease 
is  spread,  should  be  filtered  or  boiled,  while  fruit  and  vegetables  should 
not  be  eaten  unless  boiled  or  washed  with  filtered  or  boiled  water. 

A  most  necessary  measure  to  prevent  infection  of  dogs  is  burning  the 
offal  of  sheep  and  oxen  infected  with  hydatid  cysts.  Legislation  should 
make  it  obligatory  on  the  officials  of  slaughter-houses  to  burn  infected 
offal  and  to  prevent  stray  dogs  getting  access  to  this  source  of  infection. 
Strict  measures  of  this  kind  should  be  employed  to  stamp  out  the  disease 
and  prevent  it  obtaining  a  foothold  in  countries  like  America,  where  as 
yet  it  is  not  widespread.  An  additional  measure  that  would  have  a 
beneficial  effect  would  be  the  destruction  of  stray  and  homeless  dogs. 
*McMurray:  Australian  Med.  Gaz.,  May,  1896. 


412  DISEASES    OF   THE   LIVER. 

COMPLICATIONS. 

The  chief  complications  are  rupture  and  suppuration  of  the  cyst. 

Rupture  may  occur  into  the  peritoneum,  into  adjacent  hollow  viscera, 
or  may  perforate  the  diaphragm  and  open  into  the  pleura,  lung,  or  peri- 
cardium. In  order  to  open  into  the  serous  cavities  on  the  other  side  of  the 
diaphragm  the  cyst  must  first  become  adherent  to  the  imder  surface  of 
the  diaphragm  and  then  penetrate  the  muscular  and  serous  coats,  just  as 
a  cyst  has  to  work  its  way  through  the  coats  of  the  stomach  or  intestine 
and  rupture  into  those  organs.  The  process  of  perforation  depends  on 
atrophy,  from  constant  pressure  of  the  tissues  of  the  diaphragm  or  in- 
testine, which  have  become  adherent  to  the  cyst  by  local  adhesive  peri- 
tonitis. When  suppuration  has  occurred,  perforation  and  rupture  occur 
much  more  readily,  and  in  rare  instances  a  suppurating  cyst  may  per- 
forate the  skin  of  the  abdominal  wall. 

Rupture  into  the  peritoneal  cavity  may  be  divided  into  two  categories : 

(a)  Into  the  general  peritoneal  cavity;  the  cyst  may  rupture  freely  or 
merely  leak. 

(b)  Rupture  into  a  localised  part  of  the  abdominal  cavity  which  has 
been  cut  off  by  previous  local  peritonitis.  A  localised  or  subphrenic 
abscess  may  thus  result. 

Rupture  of  a  [hydatid  cyst  into  the  peritoneal  cavity  apart  from 
traumatism  or  suppuration  is  rare,  and,  as  already  pointed  out,  is  more 
readily  produced  in  a  suppurating  cyst  than  in  one  that  is  in  its  ordinary 
condition.  A  hydatid  cyst  which  is  not  suppurating  may  rupture  as 
the  result  of  direct  or  indirect  violence,  or  even  spontaneously  without 
any  manifest  cause.  It  has  been  known  to  occur  in  pregnancy  and  may 
possibly  be  precipitated  by  increased  intra-abdoixdnal  pressure.  Usually, 
however,  there  is  a  history  of  a  blow  on  the  abdomen  immediately  pre- 
ceding the  onset  of  symptoms  of  pain  and  collapse. 

The  escape  of  hydatid  fluid  into  the  general  cavity  of  the  peritoneum 
may  be  rapidly  followed  either  (i)  by  very  severe  symptoms  of  collapse 
succeeded  by  fatal  syncope  or  by  peritonitis,  or  (ii)  by  comparatively 
trivial  symptoms.  The  factor  which  determines  whether  severe  or  com- 
paratively trivial  symptoms  follow  the  escape  of  hydatid  fluid  into  the 
peritoneal  cavity  is  probably  the  state  of  the  cyst  and  its  contents.  If 
the  parasite  is  dead,  the  fluid  becomes  toxic,  while  the  fluid  from  a  hving 
cyst  is  not  toxic.  Rupture  of  a  suppurating  cyst,  or  of  one  in  connexion 
with  an  infected  bile-duct,  into  the  peritoneal  cavity  naturally  sets  up 
acute  peritonitis.  The  sudden  acute  symptoms  might,  in  the  event  of 
the  presence  of  a  hydatid  cyst  in  the  abdomen  being  unknown,  be  mis- 
taken for  irritant  poisoning  or  perforation  of  an  abdominal  viscus.  In 
the  absence  of  an  urticarial  rash  the  real  nature  of  the  condition  would 
probably  only  appear  when  the  abdomen  was  opened.  The  following 
case  illustrates  the  occurrence  of  death  from  peritonitis  and  the  danger 
that  attaches  to  postponing  operative  interference: 

A  woman  aged  thirty-four  had  a  swelling  in  the  upper  part  of  the  abdomen  for 
thirteen  years;     it  began   in  the   epigastrium   and  gradually   enlarged.     She   was 


HYDATID    CYSTS.  413 

admitted  into  St.  George's  Hospital  on  October  19,  1893,  and  a  large  hydatid  was 
diagnosed.  Operation  was  advised,  but  she  was  alarmed  and  left  the  hospital, 
only  to  return  five  days  later  in  a  state  of  collapse  with,  urticaria;  the  tumor  could  no 
longer  be  felt.  Mr.  Turner  performed  laparotomy  and  found  a  ruptured  hydatid 
cyst  which  entirely  replaced  the  left  lobe  of  the  hver.  The  patient  died  next  day. 
There  was  general  peritonitis.     No  other  hydatid  cysts  were  found  in  the  viscera. 

The  leakage  of  a  cyst  into  the  peritoneal  cavity  may  give  rise  to 
collapse  and  symptoms  suggesting  intestinal  obstruction. 

This  condition  of  "  peritonismus "  was  well  shown  in  a  man  aged  thirty  years 
under  my  care,  who  was  operated  upon  for  the  symptoms  of  peritonitis  by  my 
colleague,  Mr.  Sheild,  and  was  found  to  have  a  leaking  hydatid  cyst  of  the  hver. 

Rupture  into  the  general  peritoneal  cavity  is  accompanied  by  sudden 
pain,  but  if  the  contents  are  not  toxic  or  infective,  recovery  may  follow 
with  or  without  the  significant,  but  comparatively  trivial,  incident  of  an 
urticarial  eruption.  {Vide  p.  410.)  If  the  cyst  is  large,  there  may  be 
signs  of  ascites  for  some  time  after  its  rupture.  This  ascites  may  be 
considerable  and  even  reaccumulate  after  tapping.  Debove  and  Sou- 
pault  *  described  such  a  case  where  tuberculous  peritonitis  was  diagnosed. 

The  rupture  of  a  hydatid  cyst  into  the  cavity  of  the  peritoneum  may 
be  complicated  by  the  escape  of  bile  into  the  abdominal  cavity  (chole- 
peritoneum).  The  communication  of  the  hydatid  cyst  with  the  bile-duct 
may  take  place  before  or  after  the  rupture  of  the  cyst  into  the  peritoneum; 
Devef  behoves  that  the  latter  is  most  often  the  case  and  compares  it 
with  the  escape  of  bile  into  a  cyst  after  tapping.  The  effusion  of  bile 
does  not  necessarily  give  rise  to  peritonitis.  In  cases  where  the  bile  is 
sterile  and  there  is  no  peritonitis,  the  abdomen  gradually  swells,  and  after 
days  or  weeks  requires  tapping;  the  effusion  has  a  great  tendency  to  recur. 
It  is  curious  that  there  is  no  jaundice,  for  the  peritoneum  has  great  powers 
of  absorbing  fluid  and  the  quantity  of  bile  in  these  cases  is  often  very 
considerable. 

Two  after  or  remote  effects  of  rupture  of  a  hydatid  cyst  into  the  cavity 
of  the  peritoneum  are:  (I)  Secondary  infection  of  the  peritoneum  wdth 
daughter  cysts;  and  (II)  echinococcal  pseudo-tuberculosis  of  the  peri- 
toneum. 

Secondary  infection  of  the  peritoneum  with  numerous  daughter  cysts 
may  eventually  give  rise  to  very  considerable  trouble.  Doubt  has  been 
thrown  on  the  secondary  infection  of  the  peritoneum  with  daughter  cysts 
from  rupture  of  a  hydatid  cyst  of  the  liver,  and  it  has  been  suggested  that 
what  appear  to  be  secondary  implantations  are  really  independent  cysts,J 
but  this  is  not  in  accordance  with  the  chnical  facts  that  some  years  after 
rupture  of  a  hydatid  cyst  in  the  hver  other  cysts  may  be  found  scattered 
over  the  peritoneum.  The  favourite  situations  for  these  secondary  cysts 
are  the  great  omentum  and  the  pelvis.  It  probably  takes  about  two 
years  for  the  cysts  to  develop  sufficiently  to  give  rise  to  signs  or  symp- 
toms. It  is  a  somewhat  remarkable  fact  that  secondary  infection  of  the 
peritoneum  with  daughter  cysts  may  occur  in  cases  where  the  original 

*  Debove  et  Soupault:  Bull,  et  Mem.  Soc.  M6d.  des  Hop.,  1S92,  p.  855. 

tD6v6:  Rev.  de  Chirurg.,  July,  1902,  p.  67. 

i  Potherat:  Bull,  et  Mem.  Soc.  de  Chirurg.,  1900. 


414  DISEASES    OF   THE    LIVER. 

cyst  has  been  in  communication  with  a  bile-duct  and  the  daughter  cysts 
exposed  to  the  action  of  the  bile. 

Deve*  has  seen  secondary  cysts  develop  in  the  peritoneum  in  cases  where  there 
was  a  bile-stained  peritoneal  effusion  due  to  rupture  of  a  hydatid  cyst,  already  in 
communication  with  a  bile-duct,  into  the  peritoneal  cavity.  He  found  that  scolices 
still  continued  to  grow  in  a  mixture  of  equal  parts  of  hydatid  fluid  and  bile. 

Pseudo-tuberculosis  of  the  peritoneum  f  after  rupture  or  leakage  of 
.  a  hydatid  cyst  is  a  rarely  recognised  though  interesting  condition.  It 
-consists  in  small  granulomata  covered  over  by  the  endothelium  of  the 
peritoneum  and  containing  pieces  of  hydatid  membrane  or  hooklets. 
Histologically  there  are  giant,  endothelioid,  and  small  round  cells.  The 
process  may  be  regarded  as  an  attempt  to  absorb  the  bits  of  membrane 
and  the  hooklets. 

Rupture  into  the  Pleura. — This  is  naturally  more  often  seen  on  the 
right  side.  The  effusions  into  the  pleura  may  be  clear  or  may  become 
purulent;  in  the  latter  case  the  pleural  cavity  may  be  much  like  a 
large  suppurating  hydatid  cyst  with  numerous  daughter  cysts  floating 
in  it.  Such  an  empyema  may  burst  into  the  lung.  In  one  case  under 
my  notice  where  this  occurred  the  patient  was  suffocated.  If,  as  for- 
tunately usually  happens,  the  patient  survives  the  rupture,  a  pyopneumo- 
thorax or  a  bronchobiliary  fistula  may  result.  Rupture  of  a  hydatid 
cyst  into  the  pleura  may  lead  to  an  extravasation  of  bile  into  the  pleural 
cavity.  Deve  J  quotes  two  such  cases  recorded  by  Cruveilhier  and 
Douart. 

Rupture  into  the  Lung. — If  the  lower  part  of  the  pleural  cavity  is 
obliterated  by  adhesions  and  the  cyst  perforates  the  diaphragm,  rupture 
into  the  lung  may  follow  and  set  up  a  pneumonic  or  even  a  gangrenous 
condition  in  the  neighbourhood.  The  hydatid  fluid  may  pass  into  the 
lung  and  give  rise  to  serious  dyspnoea,  and  hydatid  membranes,  which 
may  be  bile-stained,  may  be  coughed  up.  Impaction  of  the  membranes 
or  daughter  cysts  in  the  bronchi  or  trachea  may  give  rise  to  suffocative 
dyspnoea.  Wlien  a  hydatid  cyst  freely  communicates  with  a  bronchus, 
bile  may  pass  into  the  lung  and  a  broncho-biliary  fistula  may  result.  Out  of 
35  cases  of  broncho-biliary  fistula  collected  by  Graham, §  11  were  due 
to  hydatid  cysts  of  the  liver.  These  fistulous  communications  between 
the  lung  and  hydatid  cysts  are  more  likely  to  occur  when  the  hydatid 
projects  from  the  convexity  of  the  liver. 

Jones  II  records  a  case  of  a  suppurating  hydatid  of  the  liver  that  burst  into  a 
bronchus.  The  chest  wall  was  incised  and  the  cyst  eventually  extracted  from  the 
lung.  The  case  was  remarkable  as  occurring  in  a  girl  of  only  eight  j^ears  of  age; 
recovery  followed. 

Rupture  into  the  pericardium  is  very  rare,  and  is  fatal  either  directly 
from  shock  or  later  from  pericarditis. 

*Deve:  Soc.  de  biolog.,  Jan.  17,  1903. 

t  Vide  Deve:  Rev.  de  chirurg.,  Julv,  1902,  p.  79. 

t  D6v6:  Rev.  de  chirurg.,  July,  1902,  p.  67. 

§  Graham,  J.  E.:  Trans.  Association  American  Physicians,  a'oI.  xii,  p.  247. 

II  Jones:  Lancet,  1899,  vol.  ii,  p.  1435 


HYDATID    CYSTS. 


415 


Hj-datid  cy«t  opening  mto 
common  hepatic  duct 


Rupture  into  the  Bile-duds. — The  frequency  Avith  which  this  occurs 
is  difficult  to  estimate,  for  it  often  gives  rise  to  no  cHnical  manifestations, 
or  may  be  mistaken  for  bihary  coUc  clue  to  gall-stones.  In  cases  where 
the  communication  between  the  cyst  and  the  bile-duct  is  small,  the  fluid 
in  the  cyst  may  run  quieth^  away  and  the  cyst  may  shrivel  up ;  on  the 
other  hand,  the  cyst  may  be  infected  from  the  bile-duct  and  suppurate. 
The  characteristic  cases  are  those  in  which  the  communication  between 
the  cyst  and  the  duct  is  sufficiently  large  to  allow  daughter  cysts  to 
escape  into  the  duct  and  pass  along  its  lumen.  This  gives  rise  to  bihary 
obstruction,  jaundice,  cohc,  and  may  easily  be  regarded  as  due  to  gall- 
stones. In  some  cases  there  is  fever  from  infective  or  suppurative 
cholangitis.  In  rare  cases  fragments  of  cysts  or  booklets  have  been 
found  in  the  vomit,  but  are 

more  ofteri    detected    in    the  Cystic  duct  cut  across,  showing  its 

muie   Oiien    ueietLeu    m    lue  opening  into  the  common  bile-duct. 

stools.  The  cysts  may  re- 
main in  the  ducts  and  give 
rise  to  considerable  biliary 
obstruction  and  dilatation 
of  the  ducts.  As  already 
mentioned,  cholangitis  may 
result;  possibly  the  hydatid 
ffiiid  may,  in  the  first  in- 
stance, irritate  the  mucous 
membrane,  in  virtue  of 
toxic  bodies  developed  in 
the  contents  of  dead  cysts, 
and  set  up  a  descending 
cholangitis.  But  in  most 
cases  cholangitis  is  due  to 
microbic  infection,  very 
possibly  ascending  from  the 
duodenum,  wliich  is  fa- 
voured by  the  presence  of 
the  grape-skin-like  mem- 
branes in  the  larger  bile- 
ducts.     Cholangitis  may 

spread  into  the  evacuated  cyst  and  set  up  suppuration.  The  suppurat- 
ing cyst  or  ducts  may  perforate  or  leak  into  the  peritoneal  cavity  and 
give  rise  to  acute  peritonitis  or  a  locahsed  subphrenic  abscess.  The 
hydatid  membranes  may  remain  impacted  in  the  conmion  bile-duct  or 
even  in  the  hepatic  duct  of  one  lobe  of  the  liver. 

In  a  case  under  mj^  care  it  seemed  proI)ablc  that  tliey  had  for  a  considerable 
time  remained  in  the  left  hepatic  duct  and  shortly  before  death  nlo^•cd  into  the  com- 
mon duct,  for  the  ducts  in  the  left  lobe  which  contained  a  small  cyst  were  all  dilated 
and  suppurating,  while  those  in  the  right  lobe  were  normal. 

When  in  the  common  bile-duct  the  membranes  may  project  into  the 
duodenum  through  the  biliary  papilla  and  pass  into  the  intestine  or  they 
may  remain  in  the  duct.     The  cyst  may,  after  rupturing  into  the  bile- 


FiG.  51.^ — The  Commox   Hepatic  Duct   Greatly  Di- 
lated FROM  THE  Presence  of  Part  of  a  Hydatid 
Cyst  which  has  Ruptured  into  it. 
The  cystic  duct  has  been  cut  across  so  as  not  to  ob- 
scure the  view.     From  a  specimen   (Series  ix,  No.  196a) 
in  St.  George's  Hospital   Museum.     (Drawn  by  Dr.  E. 
A.  Wilson.) 


416  DISEASES    OF    THE    LIVER. 

duct,  perforate  the  diaphragm  and  so  give  rise  to  a  broncho-bihary 
fistula. 

Sudden  death  from  rupture  of  a  hydatid  cyst  into  the  left  hepatic  duct  occurred 
in^a  man  aged  forty-four  and  vrSiS  explained  by  Gouraud  and  Rathery  *  as  due  to 
absorption  of  the  hydatid  fluid  by  the  intestines.  This  exceptional  result  is  com- 
parable -R-ith  sudden  death  from  rupture  of  a  hydatid  cyst  into  the  peritoneal  cavity. 
{Vide  p.  412.) 

The  symptoms  of  colic  followed  by  jaundice  so  strongly  suggest  gall- 
stones that  the  true  state  of  affairs  is  not  likely  to  be  suspected  unless 
the  existence  of  a  hydatid  cyst  has  previously  been  recognised,  and 
certainly  cannot  be  diagnosed  unless  pieces  of  bile-stained  hydatid  mem- 
brane are  found  in  the  faeces  or  in  the  vomit. 

Watson, t  Caylej^.t  and  Potain  §  give  accounts  of  cases  of  repeated  biUary  colic 
due  to  the  passage  of  hydatids. 

The  bile-staining  of  hydatid  membranes  is  in  favour  of  their  having 
passed  do\sTi  the  ducts,  but  this  fact  alone  is  not  absolutely  pathogno- 
monic, for  a  cyst  already  in  connexion  w-ith  a  bile-duct  might  discharge 
its  contents  into  the  stomach  or  bowel.  ^'^Tien  suppurative  cholangitis 
has  supervened,  the  underlpng  cause  may  be  thought  to  be  due  to 
cholehthiasis,  or  the  symptoms  of  fever,  rigors,  and  jaundice  might  be 
referred  to  pylephlebitis,  but  pain  and  jaundice  are  less  frequent  in  sup- 
purative pylephlebitis  than  after  rupture  of  a  hydatid  into  the  bile-ducts. 

The  foUowing  case  illustrates  the  impossibiUty  of  diagnosing  the 
presence  of  a  hydatid  c^^st : 

A  man  aged  sixty-four  was  admitted  into  St.  George's  Hospital  on  August  11, 
1897,  under  my  care,  with  a  history  of  constipation  and  abdominal  pain  for  a  week. 
No  vomiting.  He  was  slightly  jaundiced,  thin,  and  somewhat  collapsed.  Nothing 
could  be  felt  in  the  abdomen,  which  moved  freely  and  was  flat  but  somewhat  rigid. 
Left  lumbar  region  bulged,  while  the  right  was  flaccid.  The  temperature  was  not 
raised.  A  provisional  diagnosis  of  malignant  disease  of  colon  was  made;  the  man 
was,  however,  so  bad  that  an  exploratory  operation  was  not  considered  justifiable. 
He  died  two  days  after  admission.  Postmortem  examination  revealed  acute  fibrinous 
peritonitis,  the  tymph  being  deeply  bile-stained;  the  left  lobe  of  liver  contained 
whitish  areas  which  resembled  abscesses  to  the  naked  eye.  They  turned  out  to  be 
dilated  and  suppurating  bile-ducts;  into  the  dilated  bile-duct  of  theleft  lobe  a  thick- 
waUed  cavity  lined  by  granulation  tissue  opened ;  all  the  ducts  in  the  left  lobe  were 
dilated  and  showed  thickening  around  their  walls.  There  were  no  hydatid  cysts  in 
the  cavity  in  the  left  lobe,  but  elongated  hydatid  skins  blocked  the  common  bile- 
duct.  The  liver  was  not  enlarged.  It  seemed  probable  that  one  of  the  dilated 
suppurating  ducts  had  ruptured  or  leaked  into  the  peritoneum. 

As  the  diagnosis  is  difficult  and  is  usually  made  on  the  postmortem 
table,  the  number  of  reliable  published  cases  of  passage  of  hydatid  Cj^sts 
by  the  bile-ducts  in  which  recover}^  has  occurred  is  comparatively  small. 
Without  having  gone  completely  into  the  statistics,  I  have  notes  of  nine 
cases  in  which  complete  recovery  followed.  Cyr  estimated  the  mor- 
tality at  70  per  cent.  It  is  probable  that  as  more  cases  of  jaundice  due 
to  obstruction  of  the  larger  ducts  are  now  being  operated  upon,  more 

*  Gouraud  and  Rathery:  Bull.  Soc.  Anat.  Paris,  1900,  p.  307. 
t  Watson,  Sir  T. :  Lectures  on  Phvsic,  vol.  ii,  p.  631,  ed.  v,  1S71. 
t  Cayley,  W.:  Trans.  Path.  Soc,  Vol.  xxvi,  p.  127. 
§  Potain:  Joum.  de  Med.  et  de  chirurg.  pract.,  Sept.  10,  1900. 


HYDATID    CYSTS.  417 

examples  of  the  collapsed  cysts  obstructing  the  bile-ducts  will  be  forth- 
coming. 

Stirling  *  recently  published  a  case  which  recovered  after  cholecystotomj'  and 
the  subsequent  discharge  of  hydatid  membrane  from  the  wound.  The  first  symptom 
— pain  like  biliary  colic — came  on  suddenly  nine  days  before  the  operation,  and 
was  followed  by  jaundice  and  rigors. 

In  a  woman  aged  forty,  operated  upon  by  F.  T.  Stewart, t  the  hepatic  and  com- 
mon bile-ducts  contained  hydatid  cysts,  while  the  gall-bladder  contained  both  gall- 
stones and  free  hydatid  cysts.  It  is  probable  that  the  previous  passage  of  gall- 
stones through  the  cystic  duct  had  dilated  the  duct  and  thus  enabled  the  cysts  to 
pass  out  of  the  common  hepatic  duct  through  the  cy.stic  duct  into  the  gall-bladder. 
Under  ordinary  conditions  hydatid  membranes  would  never  be  able  to  work  their 
way  up  a  normal  cystic  duct. 

Rupture  into  the  stomach  is  rare.  This  viscus  is  more  likely  to  be 
penetrated  when  the  cyst  is  in  the  left  lobe  of  the  liver.  Of  11  cases 
referred  to  by  Davaine,  6  were  fatal.  When  rupture  has  taken  place, 
the  cyst  may  become  tympanitic  from  the  entry  of  air,  and  pieces  of 
hydatid  membrane,  which  may  be  bile-stained,  may  be  recognised  in 
the  vomit  or  in  the  faeces. 

Rupture  into  the  intestines  is  also  rare.  The  prognosis  seems  to  be 
better  than  when  rupture  occurs  into  other  hollow  viscera,  for  in  15 
of  Davaine's  J  cases  only  one  died.  Rupture  into  the  duodenum  is  very 
rare,  and  an  exact  diagnosis  during  life  is  hardly  possible. 

In  a  case  reported  by  Hale  White  §  a  hydatid  in  the  left  lobe  was 
opened  during  life,  the  patient  eventually  died,  and  a  second,  suppurating,  hydatid 
cyst  was  found  in  the  right  lobe.  The  cyst  in  the  left  lobe  was  found  to  com- 
municate by  a  rather  long  passage  with  the  duodenum.  In  a  man  aged  twenty- 
six  years  who  died  jaundiced  and  emaciated  there  were  two  cysts,  one  containing 
bile,  which  was  opened  during  life.  After  death  a  hydatid  cyst  of  large  size  was 
found  in  the  right  lobe,  which  had  opened  into  the  duodenum.  || 

When  rujjture  into  the  colon  occurs,  the  prognosis  would  seem  to  be 
very  good,  since  in  21  cases  collected  by  Letanneur  **  no  deaths  took 
place.  On  the  other  hand,  the  diagnosis  of  these  cases,  unless  confirmed 
by  an  autopsy,  is  open  to  doubt;  some  of  them  may  be  cases  of  rupture 
into  the  bile-duct. ft 

Rupture  into  the  inferior  vena  cava  or  the  hepatic  veins  is  very  rare. 
In  11  cases  collected  by  Deve  Xt  the  cyst  opened  in  7  into  the  inferior 
vena  cava,  and  in  4  into  the  hepatic  veins.  In  8  of  these  cases  death 
occurred  very  rapidly;  this  may  be  due  to  cysts  becoming  impacted 
in  the  right  side  of  the  heart  or  to  pulmonary  embolism,  the  branches  of 
the  pulmonary  artery  being  blocked  with  large  fragments  of  membrane 
or  cysts;  Init  in  some  cases  there  is  no  evidence  of  embolism  and  death 
may  have  been  due  to  toxic  bodies  in  the  hydatid  fluid.     Rupture  into 

*  Stirling:  Intercolonial  Medical  Journal  of  Australasia,  Feb.  20,  1899,  p.  98. 

t  Stewart:    Philadelphia  Med.  Journ.,  Sept.  2,  1899,  p.  433. 

t  Davaine:    Traite  des  Entozoaires,  Paris,  1877. 

§  Hale  White:    Trans.  Path.  Soc,  vol.  xxxvi,  p.  252. 

II  St.  Bartholomew's  Hosp.  Reports,  vol.  xxxv,  Registrar's  report,  p.  214. 
**  Letanneur:    Quoted  by  Potain,  Journ.  de  Med.  ct  C'liirurg.,  Sept.   10,  1900. 
tt  (Compare  a  case  recorded  bv  F.  J.  Smitli:    Lancet,  1901,  vol.  i,  p.  400. 
Xt  D<5vo:    Bull.  Soc.  Anat.  Paris,  1903,  p.  185. 
27 


418  DISEASES    OF   THE    LIVER. 

these  veins  need  not  necessarily  give  rise  to  sudden  death  if  the  daughter 
cysts  discharged  into  the  blood-stream  are  few  and  quite  small. 

There  is  a  specimen  (No.  1371)  in  the  museum  of  the  London  Hospital  of  rup- 
ture of  a  hydatid  cyst  in  the  right  lobe  of  the  liver  into  the  inferior  vena  cava. 

In  very  rare  cases  (Seidel,  Vegas  and  Cranwell  *)  fatal  pulmonary 
embolism  has  been  due  to  thrombosis  of  the  inferior  vena  cava,  set  up 
by  compression  of  the  vein  by  a  cyst.  In  most  exceptional  instances  a 
hydatid  cyst  has  ruptured  into  the  pelvis  of  the  kidney,  the  gall-bladder, 
or  the  portal  vein.  Rupture  through  the  abdominal  wall  is  very  much 
rarer  than  in  former  days,  as  a  cyst  would  be  now  treated  surgicalh" 
long  before  it  had  penetrated  the  abdominal  wall.  It  is  the  most  favour- 
able place  for  spontaneous  rupture;  of  21  cases  collected  by  Murchison, 
13  recovered. 

Suppuration. — Suppuration  in  a  hydatid  is  a  serious  complication, 
as  it  practically  converts  the  case  into  one  of  hepatic  abscess.  The 
symptoms  are  much  the  same  in  both  cases,  but  in  hydatid  there  is  a 
marked  tendency  to  perforate  or  rupture  into  adjacent  organs  or  cavities ; 
but  from  the  fact  that  adhesions  are  less  frequent  around  ordinary  hydatid 
cysts,  a  suppurating  one  is  not  so  likely  to  point  through  the  skin  as  an 
ordinary  hepatic  abscess. 

Mechanism  of  Suppuration  in  a  Hydatid  Cyst. — Suppuration  may  be 
set  up  in  several  ways:  It  may  be  due  to  direct  infection  from  without 
after  paracentesis  or  incision.  It  may  be  due  to  rupture  of  the  cyst 
into  the  ducts  or  may  follow  injury  to  the  liver.  In  the  latter  instance 
the  resistance  of  the  tissues  around  the  cyst  is  so  reduced  that  any  micro- 
organisms in  the  neighbourhood  are  able  to  multiply  and  set  up  inflam- 
mation. Suppuration  may  be  due  to  infection  of  the  liver  itself  or  of 
th6  bile-ducts.  Petit  f  has  described  the  spread  of  infection  from  the 
pleura,  but  in  most  cases  of  associated  empyema  and  suppurating  hydatid 
cysts  the  pleura  is  secondarily  involved.  Suppuration  may  occur  as  the 
result  of  hsemic  infections ;  for  example,  in  typhoid  fever,  infective  endo- 
carditis, and  the  puerperal  state.  When  there  are  several  cysts  in  the 
liver,  suppuration  may  be  limited  to  one  or  may  extend  to  the  others. J 
Suppurative  inflammation  usually  attacks  a  living  or  a  dying  hydatid 
cyst,  but  has  occurred  in  one  which  appeared  to  have  undergone  spon- 
taneous cure. 

The  results  of  bacteriological  examination  of  suppurating  hydatid 
cysts  are  somewhat  divergent.  In  some  instances  no  micro-organisms 
have  been  found,  and  it  has  been  thought  by  Chauffard  and  Widal  ^ 
that  suppuration  is  not  dependent  on  the  presence  of  bacteria,  but  due 
to  chemical  poisons.  That  toxic  bodies  may  develop  in  hydatid  fluid  is 
well  estabhshed,  and  Viron  1|  has  found  a  toxalbumin  in  the  hydatid 
fluid  from  a  sheep  which  set  up  acute  inflammation.     Possibly  in  some 

*  Quoted  by  Deve:    Bull.  Soc.  Anat.  Paris,  1903,  p.  196. 
t  Petit:    Rev.  Mens,  de  MM.  et  de  Chirurg.,  1877,  t.  i,  p.  678. 
j  For   illustrative  case,  vide  Sinclair  White:    Brit.  Med.  Journ.,  1897,  vol.  ii, 
p.  398.  §  Chauffard,  Widal:    Soc.  MM.  des  Hop.,  April  7,  1891. 

II  Viron:    Archiv  de  mcd.  exper.  et  d'anat.  path.,  1892,  p.  136. 


HYDATID    CYSTS.  419 

instances  suppuration  is  non-microbic.  In  other  instances  micro-organ- 
isms have  been  isolated  and  in  some  cases  mixed  infections  have  been 
found.  The  micro-organisms  observed  are  streptococci,  Staphylococcus 
pyogenes  aureus  and  citreus,  pneumococcus,  and  Bacterium  coli  com- 
mune. The  extremely  foetid  character  of  the  pus  may  depend  on  the 
presence  of  strictly  anaerobic  micro-organisms. 

In  a  foetid  suppurating  hydatid  cyst  in  a  boy  aged,  eleven  years  Halle  and  Bac- 
aloglu*  found,  in  addition  to  B.  coli  and  streptococci,  two  strictly  anaerobic  microbes 
— Staphylococcus  parvulus  and  Bacillus  fragilis. 

When  suppuration  takes  place  in  a  hydatid  cyst,  haemorrhage  not 
uncommonly  follows,  and  as  a  result  the  contents  have  a  dark  pur^Dhsh- 
red  colour  not  unlike  that  seen  in  some  cases  of  tropical  abscess.  A  very 
rare  event  is  the  production  of  gas  in  a  suppurating  hydatid  cyst;  this 
is  probably  due  to  the  Bacillas  aerogenes  capsulatus  or  to  infection 
with  other  members  of  the  colon  group.  In  a  case  at  St.  Bartholomew's 
Hospital  the  presence  of  gas  gave  rise  to  an  amphoric  note  on  percussion 
over  the  cyst  during  iife,t  and  in  Habershon'sJ  case  there  was  a  well- 
marked  bell  note. 

A  suppurating  hydatid  cyst  by  leaking  may  give  rise  to  a  subphrenic 
abscess,  or  exceptionally  to  a  subphrenic  pyopneumothorax. 

Tuffier  and  Barbarin§  describe  the  case  of  a  woman  who  was  operated  upon  for 
a  subphrenic  abscess  on  the  right  side  containing  air,  which  displaced  the  liver  back- 
wards. After  death  it  was  found  that  this  depended  on  a  suppurating  hydatid 
cyst  which  had  also  set  up  general  peritonitis. 

For  the  general  clinical  features,  etc.,  of  suppurating  hydatid  cysts 
the  reader  should  refer  to  the  description  of  hepatic  abscess. 


MULTILOCULAR  OR  ALVEOLAR  HYDATID. 

History. — Cases  of  this  rare  disease  were  formerly  regarded  as  ex- 
amples of  colloid  carcinoma  of  the  liver,  until  Virchow,  in  1856,  demon- 
strated their  parasitic  nature. 

Incidence. — The  disease  is  very  rare,  though  possibly  it  is  occasion- 
ally overlooked  or  regarded  as  malignant  disease  or  multiple  hydatids 
of  the  ordinary  kind.  It  is  met  with  in  the  south  of  Germany,  Bavaria 
and  Wurtemburg,  Hannover,  Switzerland,  Austria,  and,  according  to 
Posselt,  II  is  beginning  to  appear  in  the  Tyrol.  Dieulafoy  **  is  only  able 
to  refer  to  two  cases  of  multilocular  hydatid  disease  in  France — one  of 
the  liver  (Bniyantft))  the  other  of  the  lung  and  pleura  (R^nonJJ).  It 
was  formerly  regarded  as  rare  in  Russia,  but  recent  1}'  63  cases  ha\'e  been 

*  Hall6  et  Bacaloglu:  Archiv  de  med.  experiment,  et  d'anat.  path.,  Sept.,  1900, 
p.  689. 

t  St.  Bartholomew's  Hospital  Journal,  Jan.,  1899,  p.  64. 

j  Habershon,  S.  H.:    Practitioner,  Feb.,  1902,  p.   178. 

§  Tuffier  et  Barbarin:    Bull.  Soc.  Anat.  Paris,  Nov.,  1898,  p.  689. 

II  Posselt:    Deutsches  Archiv  f.  khn.  Med.,  Bd.  Lxiii,  1899. 
**  Dieulafoy:    Manuel  do  Pathologic  Intern.,  tome  ii,  p.  773. 
tt  Bruvant:    Bull.  hist,  et  scientif  de  1'  Auvergne,  1899. 
JtRenon:    Soc.  biolog.,  Feb.  12,  1900. 


420  DISEASES    OF   THE    LIVEE. 

collected  by  Melnikow-Rozvedenkow,*  who  considers  that    it  is  more 
often  met  with  there  than  elsewhere. 

It  is  generally  stated  that  no  case  has  been  recognised  in  England. 
There  are  specimens  of  this  disease  in  the  Army  Medical  Museum  at 
Netley  (Nos.  1230,  1239). 

Hilton  Fagge  f  examined  a  specimen  of  colloid  cancer  in  the  museum  of  Guy's 
Hospital  which  Frerichs  had  suggested  might  be  alveolar  hydatid,  but  found  nothing 
to  svipport  this  view. 

In  America  two  cases  have  been  reported,  both  in  natives  of  Germany 
(Osier  I).  Its  geographical  distribution  differs  from  that  of  the  common 
echinococcus,  and  it  is  noteworthy  that  it  is  not  met  with  in  Australia 
or  Iceland,  w^here  the  ordinary  hydatid  is  specially  common.  It  has 
been  described  in  cows  and  other  domesticated  animals,  and  it  has  been 
thought  that  the  infection  is  thus  conveyed  to  man.     (Posselt.) 

Nature.— A  good  deal  of  discussion  has  taken  place  as  to  the  nature 
of  multilocular  or  alveolar  hydatid  disease,  i.  e.,  whether  it  is  merely 
an  exogenous  form  of  the  ordinary  echinococcus  or  an  entirely  distinct 
parasite.  Klemm  §  found  the  ordinary  taenia  echinococcus  in  the  intes- 
tine of  a  dog  fed  on  the  multilocular  hydatid,  but  it  is  possible  that  the 
taenia  was  present  in  the  dog  previously;  for  Mangold,  ||  and  subsequently 
Miiller,**  by  giving  the  scolices  to  animals,  obtained  a  tsenia  different 
from  that  of  the  ordinary  echinococcus.  The  geographical  distribution 
of  the  two  forms  does  not  correspond,  as  it  should  do,  on  the  supposition 
that  multilocular  hydatid  is  merely  the  result  of  exogenous  multiplication 
of  the  ordinary  echinococcus.  Melnikow-Rozvedenkow,  from  careful 
and  exhaustive  researches,  comes  to  the  conclusion  that  the  alveolar 
hydatid  is  quite  distinct  from  the  ordinary  echinococcal  cyst.  According 
to  his  views,  it  should  be  regarded  as  belonging  to  the  class  of  the  infective 
granulomata  and  be  compared  with  tuberculosis,  actinomycosis,  and 
syphilis,  since  it  manufactures  a  special  irritative  toxine  which  leads  to 
inflammation  followed  by  coagulation  necrosis. 

The  embryo  reaches  the  liver  by  the  portal  vein  and  becomes  em- 
bedded in  one  of  the  portal  spaces  and  develops  into  a  chytinous  multi- 
locular mass  which  becomes  encysted.  The  parasite  produces  ova  which 
are  spherical  or  OA^al,  and  measure  from  170  to  1000  f-  in  diameter;  an 
embryo  encysted  in  the  liver  may  produce  15  to  60  ova.  In  the 'pro- 
duction of  ova  when  in  the  human  body  this  cestode  resembles  the 
trematode  worms,  such  as  the  liver  fluke  (Distomum  hepaticum).  The 
embryos,  being  endowed  with  amoeboid  movement,  invade  the  tissues, 
set  up  inflammatory  and  degenerative  changes,  and  may  be  destroyed 
by  phagocytosis.  When  the  embryos  get  into  the  hepatic  ^Tins,  they 
may  set  up  metastases  in  the  lungs,  brain,  etc. 

*  Melnikow-Rozvedenkow:   Studien  liber  den  Echinococcus  alveolaris,  1901. 
t  A  Text-book  of  Medicine,  by  Fagge  and  Pye  Smith,  vol.  ii,  p.  459. 
X  Osier:    Practice  of  Medicine,  p.  375,  ed.  iv. 
§  Klemm:    Dissert.,  Miinchen,  18S3. 
II  Mangold:    Berlin,  klin.  Wochen.,  1892,8.50. 
**Miiller:    Miinchen.  med.  Wochen.,  1893,  S.  225. 


HYDATID    CYSTS.  421 

As  already  pointed  out,  alveolar  hydatid  leads  to  an  exogenous 
formation  of  cysts,  and  thus  contrasts  with  the  endogenous  production 
of  daughter  cysts  inside  the  parent  C5''st  which  characterises  the  ordinary 
echinococcus  in  man. 

Morbid  Anatomy. — ^The  liver  is  enlarged  and  may  show  no  external 
signs  of  disease;  it  may  be  nodular  from  the  projection  of  the  parasite, 
and  from  perihepatitis  be  adherent  to  the  diaphragm  or  to  surrounding 
parts.  According  to  Posselt's  statistics,  the  right  lobe  is  affected  alone 
in  65  per  cent,  of  the  cases,  while  the  left  lobe  is  exclusively  involved  in 
10  per  cent.  The  posterior  part  of  the  right  lobe  is  the  seat  of  election. 
The  tumor  is  surrounded  by  a  fibrous  capsule  containing  an  alveolar 
arrangement  of  irregular  cavities,  some  of  which  are  occupied  by  the 
gelatinous  hydatid  cysts,  others  by  caseous,  purulent,  or  bile-stained 
debris.  The  appearance  is  much  like  that  of  colloid  carcinoma.  The 
contents  of  degenerated  cysts  may  eventually  resemble  mortar  from 
admixture  with  lime  salts.  The  hver  is  hard  from  fibrosis,  which  may 
involve  more  distant  parts  of  the  organ,  and  may  grate  under  the  knife 
from  calcareous  infiltration.  Occasionally  large  cystic  spaces  may  form. 
The  bile-ducts  are  often  compressed,  and  inflammation  may  spread  to 
the  vessels  in  the  portal  spaces  and  set  up  endophlebitis,  lymphangitis, 
and  obstruction  and  obliteration.  The  naked-eye  appearances  may 
suggest  colloid  carcinoma,  or,  from  the  sponge-like  structure,  actino- 
mycosis.* 

Histology. — The  parasite  shows  a  structureless  wavy  membrane  with 
a  granular  endocyst.  Scolices  and  hooklets  are  not  always  forthcoming. 
In  the  debris  of  older  cysts  calcareous  granules,  cholesterin,  and  hsema- 
toidin  crystals  may  be  seen.  The  walls  of  the  cavities  show  active  pro- 
liferation of  the  connective-tissue  cells  with  the  production  of  fibroblasts 
and  giant  cells;  this  is  followed  by  coagulation  necrosis  and  caseation 
like  that  seen  in  tuberculosis.     The  liver  cells  may  show  fatty  change. 

Clinical  Features. — ^The  disease  is  usually  seen  in  persons  between 
twenty-five  and  fifty  years  of  age,  and  occurs  rather  more  often  in  men 
than  in  women.  According  to  Vierordt,  its  incidence  in  the  sexes  is  in 
the  proportion  of  3  (males)  to  2  (females).  The  onset  is  very  gradual, 
and  usually  the  first  symptoms  are  referred  to  the  region  of  the  liA-er, 
and  consist  of  pain,  weight,  and  discomfort.  On  examination  the  liver 
is  enlarged  and  feels  hard  and  resistant  and  its  edge  firm;  the  surface 
may  be  smooth,  or  nodular  when  the  parasite  involves  the  capsule.  In 
the  latter  event  it  will  be  tender,  and  pain  may  be  set  up  by  perihepatitis. 
In  rare  cases  fluctuation  and  softening  may  be  made  out  in  the  hepatic 
tumor. 

The  spleen  is  said  to  be  enlarged  in  90  per  cent,  of  the  cases.  Jaundice 
is  common  and  occurs  in  four-fifths  of  the  cases.  It  may  be  the  first 
thing  noticed  and  tends  to  become  deep.  As  a  result  choltemia  with 
multiple  haemorrhages  may  develop.  In  rare  instances  the  jaundice 
intermits  and  varies  from  time  to  time.  As  jaundice  may  depend  on 
obstruction  inside  the  liver,  bile  may  still  pass  into  the  duodenum  and 
*  Compare  Wynne:   St.  Bartholomew's  Hosp.  Reports,  vol.  xxv,  p.  159. 


422  DISEASES    OF   THE    LIVER. 

appear  in  the  faeces.  Ascites  is  much  less  freciuent  than  jaundice;  it 
may  be  due  to  pressure  on  the  portal  vein,  or  to  chronic  inflammation  of 
the  peritoneum,  ffidema  of  the  legs  may  occur  in  the  late  stages  of 
the  disease,  and  in  rare  instances  depends  on  pressure  on  the  inferior 
vena  cava.  The  urine  may  be  of  low  specific  gravity  and  so  copious  as 
to  imitate  diabetes  insipidus.  In  some  cases  there  are  irregular  fever  and 
excessive  perspiration;  in  this  connexion  it  should  be  remembered  that 
tuberculosis  is  said  to  super\'ene  in  3  per  cent,  of  the  cases.  (Posselt.*) 
Emaciation  is  a  late  event,  and  thus  contrasts  with  the  course  of  events 
in  mahgnant  disease  of  the  liver.  Digestive  disturbances  are  not  un- 
common, su_ch  as  dyspepsia,  nausea,  vomiting,  cUarrhoea,  or  constipation. 
In  some  instances  there  is  thirst  or  a  voracious  appetite,  and  in  these 
cases  the  bodily  weight  may  increase. 

Course  and  Duration. — The  disease  runs  a  very  chronic  course  and 
may  last  as  long  as  ten  3^ears.  Death  may  be  due  to  increasing  weakness 
or  to  cholsemia  and  continued  jaundice. 

Diagnosis  is  extremely  difficult,  and  the  disease  will  probably  be 
regarded  as  malignant  until  the  liver  is  carefully  examined.  This  mistake 
has  been  made  even  when  the  hver  has  been  ex|Dosed  by  laparotomy. 
The  slow  course  of  the  disease  may  arouse  a  suspicion  as  to  its  real  nature. 
Ilemo^^al  of  a  fragment  of  the  gro-v^i:h  at  a  laparotomy  and  microscopic 
examination  have  estabhshed  the  diagnosis,  but  mere  puncture  is  of  no 
value.  It  may  also  be  mistaken  for  h}^3ertrophic  biliary  cirrhosis  or 
cysts  of  the  pancreas.  If  the  liver  is.  enlarged  and  no  localised  tumor 
is  paljDable,  the  presence  of  jaundice  and  of  splenic  enlargement  may 
suggest  bihary  cirrhosis.  Bat  jaundice,  when  present  in  multilobular 
hydatid,  is  much  deeper  than  in  biliary  cirrhosis,  and  the  enlargement  of 
the  spleen  comes  on  later  in  the  course  of  the  disease. 

Prognosis. — The  difficulty  of  diagnosis  accounts  for  the  fact  that 
most  cases  are  recognised  after  death,  and  that,  as  far  as  our  knowledge 
goes,  the  prognosis  is  bad.  But  it  is  to  be  hoped  that  comparatively 
early  operation  and  excision  of  the  grovi;h  will  give  good  results. 

Treatment. — The  only  efficient  means  of  treatment  is  excision  of 
the  affected  parts  of  the  liver,  which  should  be  undertaken  as  early  as 
possible.  Bruns  f  has  successfully  treated  a  case  by  excision  of  the 
parasite.     Merely  tapping  has  not  been  found  to  be  successful. 

*  Posselt:    Deutsches  Archiv  f.  klin.  Med.,  1899. 

t  Bruns:    Bruns'  Beitrage  z.  klin.  Chirurgie,  Bd.  xvii. 


FATTY  LIVER. 

Under  the  heading  of  "fatty  hver"  it  will  be  convenient  to  consider 
together  the  changes  described  separately  by  many  writers  as  fatty  infil- 
tration and  fatty  degeneration.  It  mil  be  well,  however,  at  the  outset 
to  state  briefly  what  is  meant  by  the  two  terms. 

Fatty  infiltration  or  accumulation  is  an  exaggeration  of  the  physio- 
logical storage  of  fat  in  the  hepatic  cells;  thus  it  is  normally  present  in 
young  children,  sometimes  in  healthy  adults  who  have  died  suddenly 
from  accidents,  and  constantly  in  obesity. 

Fatty  degeneration  is  a  pathological  production  of  fat  at  the  expense 
of  the  protoplasm  of  the  liver  cells,  and  is  the  result  of  a  retrograde 
metabolism. 

The  histological  differences  between  the  two  conditions  are  described 
on  page  426,  but  in  practice  they  run  into  each  other,  and  it  is  difficult 
to  draw  a  hard-and-fast  line  between  them.  It  is  better,  therefore,  to 
speak  of  pathological  fatty  change  in  the  liver. 

Etiology. — Pathological  fatty  change  in  the  liver  is  met  with  in  a 
number  of  conditions  which  have  in  common  the  presence  of  toxines 
or  poisons  in  the  blood.  Thus  a  fatty  state  of  the  liver  cells  is  the  most 
constant  change  found  in  the  bodies  of  alcoholic  persons,  and  experiment 
shows  that  this  must  be  regarded  as  due  to  the  effect  of  alcohol  as  a 
protoplasmic  poison.  Numerous  other  poisons  lead  to  the  same  change, 
e.  g.,  phosphorus,  arsenic,  antimony,  chloroform,  iodoform,  sulphuric, 
oxalic,  carbolic,  tartaric,  and  other  acids,  sulphonal.* 

Experimentally  Rosenfeldf  finds  that  phloridzin  gi^-es  rise  to  fatty  change  in 
the  liver  which  is  an  infiltration  and  not  a  degeneration,  as  shown  by  the  fact  that 
if  the  animal  is  kept  without  food  for  twenty-four  hours  no  accumulation  of  fat 
occurs  in  the  liver. 

A  certain  amount  of  fatty  change  is  induced  by  numerous  bacterial 
toxines,  and  may  occur  in  typhoid  fever,  pneumonia,  puerperal  fever, 
cholera,  diphtheria,  smallpox, J  scarlet  fever,  erysipelas,  and  streptococcal 
infections.^  Fatty  change  in  the  liver  is  very  frequent  in  ]nilmonary 
tuberculosis.  Louis  found  it  in  40  out  of  120  fatal  cases.  It  is  thought 
to  be  more  frequent  in  female  than  in  male  patients.  (Budd.  ||)  It  is 
very  striking  to  find  extensive  fatty  change  in  the  liver  of  an  emaciated 
patient  who  has  little  or  no  subcutaneous  fat.     Frerichs**  regarded  the' 

*  Taylor  and  Sailer:   Contributions  from  the  William  Pepper  Laboratory,  Phila- 
delphia, 1900,  p.  120;    and  Garrod:    Lancet,  1900,  vol.  ii,    1323. 
t  Rosenfeld:    Zeit.  f.  klin.  Med.,  Bd.  xxviii,  S.  256. 

I  Arnaud:    Marseille  Medical,  1899,  p.  39. 

§  Roger  et  Garnier:    Rev.  de  Mt'-d.,  t.  xxi,  p.  97,  March,  1901. 

II  Budd,  G.:    Diseases  of  the  Liver,  p.  304,  ed.  iii,  1857. 

**  Frerichs:   I^iseases  of  Liver,  vol.  i,  pp.  285,  301.     Translation  by  New  Syden- 
ham See. 

423 


424  DISEASES    OF   THE    LIVER. 

fatty  condition  of  the  liver  as  due  to  the  absorption  of  fat  from  the  sul?- 
cutaneous  and  other  parts  of  the  body  and  sometimes  to  imperfect 
secretion  of  bile.  This  theory  will  not  stand  against  the  facts  that  in 
cases  of  emaciation  and  jaundice,  as,  for  example,  carcinoma  of  the  head 
of  the  pancreas  compressing  the  bile-duct,  there  is  often  no  fatty  change 
at  all  in  the  liver.  The  administration  of  fatty  food  and  cod-liver  oil 
can  hardly  account  for  the  change,  inasmuch  as  cod-liver  oil  was  not 
used  in  Louis'  time.  (Wilson  Fox.*)  Insufficient  oxidation  depending 
on  the  condition  of  the  blood  cannot  be  an  exclusive  or  a  very  essential 
cause,  since  fatty  change  in  the  liver  is  much  less  marked  in  emphysema, 
chronic  bronchitis,  and  congenital  morbus  cordis  than  in  pulmonary 
tuberculosis. 

The  fatty  liver  in  tuberculosis  is  at  the  present  time  referred  to  retro- 
gressive or  degenerative  changes  set  up  by  poisons  reaching  the  liver. 
Whether  this  is  due  to  the  tuberculous  toxine  alone  seems  doubtful. 

Peronf  found  that  intravenous  injections  of  virulent  cultures  of  tubercle  bacilli 
lead  to  extensive  fatty  degeneration  of  the  liver,  an  effect  which  was  prevented  if 
the  cultures  had  previously  been  raised  to  100°  C.  for  five  minutes;  but  CarriereJ 
as  a  result  of  injection  of  tubercuUn  produced  cloudy  sweUing,  vacuolation,  and 
necrosis  of  the  liver  cells,  but  never  any  fatty  or  lardaceous  degeneration.  The 
latter  experiments  suggest  that  the  fatty  degeneration  is  due  to  the  effects  of  toxines 
other  than  those  of  the  tubercle  bacillus,  such  as  might  result  from  secondary 
streptococcal  infections. 

Fatty  change  in  the  liver  cells  is  met  with  in  intestinal  diseases,  such 
as  dysentery,  diarrhoea,  etc.,  and  would  therefore  appear  to  be  due  to 
the  action  of  poisons  absorbed  from  the  alimentary  canal. 

Thus  in  32  cases  of  gastro-enteritis  in  children  Thiemich§  found  fatty  change 
in  23,  Freeborn  II  found  a  similar  condition  in  50  per  cent,  of  cases  of  diarrhoea  in 
children  under  three  years  of  age.  Freeman**  found  that  in  496  cases  of  children 
dying  of  various  diseases  the  hver  was  fatty  to  the  naked  eye  in  202,  or  41  per  cent., 
and  that  this  change  was  common  in  acute  infectious  disease  and  in  disease  of  the 
aUmentary  tract,  but  rare  in  other  chronic  wasting  disorders.  Menetrierft  has  de- 
scribed fatty  liver  due  to  a  grave  infection  of  appendicular  origin. 

Fatty  change  is  also  met  with  in  grave  anaemia,  and  is  probably  due 
to  the  poisons  giving  rise  to  the  ansemia.  It  is  also  well  marked  in  cases 
fatal  from  the  status  epilepticus  (MottJt),  in  diabetic  coma,  and  in  some 
fatal  cases  of  acidosis  after  anaesthesia  in  children, §§  all  of  which  are 
toxic  conditions. 

Fatty  change  in  the  liver  is  frequently  present  in  the  bodies  of  preg- 
nant women,  and  is  very  probably  due  to  the  diseases  or  morbid  condi- 
tions responsible  for  death.     It  has,  however,  been  thought  that  a  fatty 

*  Wilson  Fox:   Treatise  on  Diseases  of  the  Lungs  and  Pleura;,  p.  620. 

t  Peron:  Soc.  biolog.,  April  23,  1898. 

j  Carriere:    Archiv  Exper.  et  d'anat.  path.  Med.,  Jan.,   1897. 

§  Thiemich:    Beitr.  z.  path.  Anat.,  Bd  xx,  S.  179. 

li  Freeborn:    Acad.  Med.  New  York,  Jan.,   1897. 
**  Freeman:    Archives  of  Pediatrics,  1900,  p.  81. 
tt  Soc.  Med.  d.  Hop.  Paris,  Oct.  30,  1903. 
ilMott:    Archives  of  Clavbury  Asvlum,   1899. 

§§  Brackett,  Stone,  and  Low:  Boston  Med.  and  Surg.  Jour.,  vol.  cli,  p.  2,  July 
2,  1904. 


FATTY    LIVER.  425 

change  is  constant  in  pregnanc5^  During  lactation  fatty  change  occurs 
in  the  cells  around  the  intralobular  vein  and  has  been  regarded  as  showing 
that  the  hver  manufactures  fat  to  be  utihsed  in  the  niilk  (Ranvier,* 
Sinety  f)  as  an  internal  secretion  of  fat. 

Fatty  change  is  frequently  found  in  association  with  other  lesions 
of  the  hver,  such  as  cirrhosis,  lardaceous  disease,  and  chronic  venous 
engorgement.  It  is  then  due  either  to  some  poison,  to  impaired  nutrition, 
or  to  both  factors.  In  some  instances  acute  fatty  transformation  of  the 
liver  ceUs  occurs  and  proves  fatal  with  much  the  same  clinical  mani- 
festations as  acute  yellow  atrophy.  In  some  cases  there  is  no  clear  evi- 
dence as  to  the  nature  of  the  toxic  or  infective  cause.  It  has  been  noted 
after  operations, J  and  has  been  thought  to  l^e  due  to  iodoform,  carbolic 
acid,  chloroform,  or  to  a  combined  action  of  toxines  due  to  disease  and 
of  chloroform. 

Morbid  Anatomy. — In  cases  where  the  liver  cells  rapidly  undergo 
•fatty  metabolism  the  organ  is  much  enlarged,  for  example,  in  phosphorus 
poisoning,  and  in  extreme  cases  a  weight  of  as  much  as  12  pounds  has 
been  reached. 

In  1890  a  woman  aged  sixty-seA^en,  who  for  years  had  been  a  heavy  drinker 
and  lately  had  consumed  a  bottle  of  whiskey  a  day,  was  admitted  into  St.  George's 
Hospital  deeply  jaundiced,  unconscious,  and  with  scarcely  audible  heart  sounds; 
the  urine  did  not  contain  leucin  or  tyrosin.  At  the  autopsy,  which  I  performed,  the 
liver  weighed  lOf  pounds  and  floated  in  water;  microscopically,  besides  very  ex- 
tensive fatty  change,  there  was  some  apparent  increase  in  the  amount  of  the  fibrous 
tissue — probably  a  replacement  fibrosis.  The  heart,  16  ounces,  showed  fatty  degen- 
eration. The  degenerative  process  was  probably  acute,  though  less  so  than  in  acute 
yellow  atrophy.  It  is  possible  that  such  cases  should  be  called  acute  yellow  hyper- 
trophy. 

The  enlargement  affects  all  parts  equally  and  the  normal  shape  of 
the  liver  is  retained,  the  edges  becoming  rounded  and  thicker.  "When 
the  fatty  change  comes  on  slowly,  enlargement  is  much  less  marked  and 
some  fatty  livers  are  of  a  normal  size  or  occasionally  small.  A  fatty  liver 
is  usually  uniformly  smooth  on  the  surface,  and  as  seen  after  death, 
anaemic.  The  consistency  varies,  being  sometimes  firm,  and  this  without 
an}^  fibrosis;  sometimes  soft  and  friable. 

In  a  boy  aged  three  years  who  died  as  the  result  of  poisoning  from  the  absorp- 
tion of  iodoform  from  a  wound  the  liver  weighed  .30  ounces  and  was  remarkaljlv 
firm,  keeping  its  shape  and  impressions  like  His'  model.  Microscopically  there 
was  marked  fatty  change  but  no  fibrosis  or  lardaceous  disease.  During  life  there 
were  high  temperature,  delirium,  and  wasting. 

These  differences  in  the  consistency  of  a  fatty  liver  may  depend  on 
conditions  preceding  death,  such  as  septic  agencies  leading  to  acute 
changes,  or  may  be  the  result  of  postmortem  decomposition.  On  section 
the  lobules  are  often  very  distincth'  mapped  out  so  that  the  surface  has 
a  granular  appearance  exactly  like  that  of  fine  cirrhosis  of  the  mono- 
lobular  type.     It  is  often  impossible  to  be  certain  as  to  the  existence  of 

*  Ranvier:    Soc.  de  biolog.  Paris,  April,  1S72. 

t  Sinety:    de  I'etat  des  foie  chez  les  femelles  en  lactation,  Paris,  1873. 
X  Compare  cases  and  remarks  by  L.  G.  Guthrie:    Lancet,  1S94,  vol.  i,  pp.  193, 
257;    and  1903,  vol.  i,  p.  10.    Brackett,  Stone,  and  Low,  loc.  cit. 


426 


DISEASES   OF   THE   LIVER. 


cirrhosis  or  not  until  microscopic  sections  have  been  made.  In  other 
cases  where  the  fatty  change  affects  the  cells  of  the  lobules  universally 
the  cut  section  is  uniform  and  has  no  resemblance  to  cirrhosis.  The 
specific  gravity  of  the  liver  is  diminished  and  the  organ  may  float  in 
water.  When  cut  into,  the  surface  of  the  section  may  be  soft  and 
yielding,  or  in  some  instances  firm.  The  dry  blade  of  a  knife  is  rendered 
greasy  by  the  exuding  oil  when  the  organ  is  soft.  If  put  into  a  flame, 
the  fat  melts,  may  burn  in  a  spluttering  manner,  and  if  allowed  to  drop 
on  paper,  leaves  an  oily  stain.  Local  haemorrhages  and  focal  bile-staining 
may  be  found  due  to  extravasation,  depending  on  fatty  degeneration 
and  rupture  of  these  vessels.  Local  areas  of  fatty  change  are  not  un- 
commonly seen  in  the  liver  in  cases  of  a  septic  nature;  they  are  due  to 
the  local  action  of  toxines  produced  on  the  spot  by  micro-organisms  in  the 
vessels  of  the  Uver. 

Histologically  the  liver  ceUs  contain  globules  of  fat  of  varying  sizes 

which  are  refractive  and 
stain  black  with  osixiic  acid. 
The  fat  is  found  especially 
in  the  peripheral  part  of  the 
lobule,  but  by  no  means 
exclusively  there. 

A  distinction  has  been 
drawn  between  fatty  degen- 
eration and  fatty  infiltra- 
tion of  the  hver  ceUs.  Thus 
in  fatty  infiltration  the  ceUs 
at  the  periphery  of  the 
hepatic  lobules  are  chiefly 
occupied  by  globules  of  fat 
of  considerable  size,  whereas 
in  fatty  degeneration  the 
globules  are,  as  a  rule, 
smaller  and  may  occur  in 
any  part  of  the  lobules,  the 
process  often  beginning  in 
the  central  zone.  In  fatty  infiltration  the  protoplasm  of  the  liver  cells  is 
mechanically  displaced  by  the  fat  deposited  in  it,  to  the  side  of  the  cell, 
while  in  fatty  degeneration  the  protoplasm  is  chemically  altered  and 
by  retrograde  metabohsm  has  produced  the  fat;  the  cells  therefore  are 
shrunken,  the  protoplasm  granular,  and  the  nucleus  fragmentary,  but 
in  its  ordinary  position.  After  removal  of  the  fat  in  cases  of  infiltra- 
tion the  cells  return  to  their  normal  state,  whereas  in  degeneration  they 
break  up. 

No  hard-and-fast  line  can  be  drawn  between  fatty  infiltration  and  de- 
generation of  the  liver  cells;  the  infiltration  is  an  exaggeration  of  the 
normal  storage  of  fat,  but  it  passes  into  a  pathological  condition  without 
any  corresponding  and  sharp  distinction.  Strictly  speaking,  fatty  infiltra- 
tion should  concern  the  connective-tissue  cells  of  the  liver  (Kupffer's  cells) 


Fig.  52. — Extensive  Fatty  Change  in  the  Liver 
Cells,  the  Result  of  Acute  Degenerativi: 
Changes.    (Photomicrograph  by  S.  G.  Penny,  Esq.) 


Plate  5. 


1.    SURFACK  OF   LlVlSll  WITH  NODULAR  CIRRHOSIS. 

The  liobnails  look  like  masses  of  secondary  new-growth. 


'2.  Section  ok  the  Livior  ok  Above. 

Sliowing   engorgonioMt  of  lUirons  tissue  and   white  colour,  dui;  lo  fatty   dcgenerati d"  the  liver 

in  the  hobnails.     Drawn  by  Dr.  10.  A.  Wilson. 


FATTY    LIVER. 


427 


and  fatty  degeneration  the  secreting  cells  of  the  hver.  Although  experi- 
mentally fatty  change  can  be  induced  in  Kupffer's  cells  by  the  injection 
of  toxines,  this  is  not  noticeable  in  ordinary  cases  of  fatty  hver,  whether 
associated  with  obesity  or  with  disease.  It  is  better  to  speak  of  fatty 
change  in  the  liver  rather  than  of  fatty  infiltration  or  degeneration. 

From  a  review  of  the  pathology  of  fatty  degeneration  and  infiltration  Herx- 
heimer  and  Walker  Hall*  conclude  that  there  are  no  reliable  facts  to  show  that  fat 
arises  directly  from  degeneration  of  tht^  proteid  molecule.  The  factors  which  lead 
to  so-called  "fatty  degeneration"  lower  the  A'itality  of  the  cells  and  thus  favour 
increased  deposit'  of  fat  in  the  cell.  The  term  fatty  degeneration  should  be  re- 
placed by  degenerative  fatty  infiltration. 


i*-,- 


Fig.  53. — Microscopic  Section  of  Liver,  Showing  Extensive  Fatty  Change  in  the  Liver 

Cells. 
Some  groups  of  cells  are  free  from  any  change,  while  in  others  hardly  any  protoplasm  is  left. 
There  is  an  increase  in  the  amount  of  the  interlobular  fibrous  tissue,  suggesting  slight  multi- 
lobular cirrhosis.     X72. 


The  fibrous  tissue  of  the  portal  spaces  shows  up  so  as  to  suggest  some 
old  fibrosis,  and  freciuently  there  is  some  small-cell  infiltration  in  and 
around  the  portal  spaces.  This  is  due  to  wasting  and  atrophy  of  the 
essential  liver  parenchyma,  and  may  be  called  a  ''replacement  fibrosis." 
Though  in  miniature  much  the  same  as  hepatic  cirrhosis,  it  is  unimpor- 
tant, and  unless  very  marked,  the  condition  should  be  regarded  as  de- 
pendent on  the  fatty  change  and  should  not  be  spoken  of  as  fatty  cirrhosis, 
but  rather  as  fatty  liver.  In  this  way  any  confusion  between  this 
condition  and  genuine  cirrhosis  with  superadded  fatty  change  is  avoided. 

Clinical  Picture. — Signs. — In  cases  where  there  is  general  obesity 
the  li\-er  may  be  made  out  by  percussion  to  be  enlarged,  but  it  may 
*  Medical  Chronicle,  vol.  xl,  July,  1904. 


428  DISEASES    OF   THE    LIVER. 

be  difficult  to  feel  the  edge  distinctly,  both  because  the  abdominal  walls 
are  overloaded  with  fat  and  because  during  hfe  the  enlarged  fatty  hver 
is  often  soft.  Fatty  ]iver  is  indeed  ver\^  often  latent  and  unsuspected. 
The  skin  may  be  greasy,  the  tension  of  the  pulse  is  usually  low,  and  the 
heart  sounds  distant  or  feeble.  Fat  women  often  have  remarkably  small 
chests,  and  in  the  dead-house  the  contrast  between  the  enormous  fatty 
covering  and  the  size  of  the  thorax  is  often  most  striking. 

In  cases  where  a  fatty  hver  is  associated  with  definite  disease,  such 
as  pulmonar}^  tuberculosis,  the  lii^er  is  enlarged  and  smooth,  but  is  less 
firm  than  in  lardaceous  disease  or  cirrhosis,  and  therefore  not  so  easily 
felt.  The  spleen  is  not  enlarged,  and  there  is  no  ascites  or  jaundice. 
Addison  *  laid  stress  on  the  condition  of  the  skin  accompamdng  fatty 
Hver — ^bloodless,  looking  like  fine  polished  ivor}^,  almost  semitransparent, 
and  exquisitely  smooth,  hke  satin.  This  change  was  earhest  seen  and 
best  marked  on  the  backs  of  the  hands .  Addison  also  referred  to  recurring 
attacks  of  oedema  in  cases  of  fatty  liver,  especially  when  the  patients 
were  alcohohc.  Possibly  the  oedema  .was  due  to  peripheral  neuritis  or 
cardiac  dilatation. 

The  ammonia  in  the  urine  may  be  increased  at  the  expense  of  the 
urea.  This  should  be  regarded  not  as  evidence  of  failure  in  the  urea- 
forming  power  of  the  hver  cells,  but  as  eA'idence  that  the  morbid  process 
underMng  the  fatty  change,  for  example,  phosphonis  poisoning,  leads 
to  the  formation  of  organic  acids  which  seize  hold  of  the  armnonia  and 
prevent  its  conversion  into  urea. 

Lepine  and  Eymonnetf  describe  an  excess  of  glycero-phosphoric  acid  in  the 
urine;  this  is  derived  from  lecithin,  -^'hicli  they  showed  to  be  present  in  excess  in 
fatty  Hvers.  Hsematoporphyrinuria  is  often  seen  in  cases  where  the  liver  is  fatty ,_+ 
and'  may  be  due  to  the  liveV  being  unable  to  arrest  the  urobihn  which  reaches  it 
from  the  alimentary  canal. 

The  symptoms  are  those  of  the  condition  or  disease  responsible  for 
the  secondary  change  in  the  hver.  Xo  doubt  the  various  functions  of 
the  hver  are  not  so  well  performed  as  they  would  be  if  the  cells  were 
healthy,  but  there  is  no  constant  or  preeminent  failure  of  function. 
When  the  degeneration  is  \ery  acute  and  at  the  same  time  extensive, 
the  symptoms  approach  those  of  acute  atrophy,  although  actually  the 
hver  is  much  larger  than  normal.  But  the  condition  then  ceases  to  be 
one  of  ordinary  fatty  liver. 

The  stools  are  hght,  and  the  biliary  secretion,  though  it  does  not  fail, 
is  probably  deficient.  Jaundice  does  not  occur  in  uncomphcated  cases, 
and  there  is  no  portal  obstruction,  so  that  there  is  no  ascites  or  enlarge- 
ment of  the  subcutaneous  abdominal  veins.  Piles  have  been  said  to 
occur,  but  this  is  probably  a  coincidence.  The  diarrhcea  formerly  thought 
to  depend  on  fatty  liver  is  probably  the  cause  rather  than  the  effect. 
There  is  no  pain  associated  with  fatty  liver. 

As  a  result  of  severe  traumatism  fat  from  the  hver  might  pass  into 

*  Addison,  T.:    Guy's  Hosp.  Reports,  vol.  i.  p.  476,  1S36. 
t  Lepine  et  Evmonnet:    Lvon  Medical,  tome  xU,  p.  15. 
t  Garrod:    Lancet,  1900,  vol.  ii,  p.  1323. 


FATTY    LIVER.  429 

the  hepatic  veins  and  give  rise  to  fat  embohsm  of  the  hmgs.     This  has 
actually  been  shown  to  have  occurred  by  Engel.* 

Diagnosis. — Painless  enlargement  of  the  liver,  ^nth  a  smooth,  com- 
paratively soft  surface,  in  an  individual  in  whom  one  of  the  known 
causes  of  a  fatty  liver,  such  as  alcoholism  or  pulmonary  tuberculosis, 
is  active  should  suggest  its  presence.  It  must  be  diagnosed  by  exclusion 
of  the  following  conditions : 

(1)  Leuksemic  infiltration  of  the  liver  leads  to  a  firmer  condition 
and  can  be  at  once  recognised  by  examination  of  the  blood. 

(2)  Lardaceous  disease.  The  liver  is  much  firmer  than  in  fatty  liver, 
and  there  may  be  signs  of  lardaceous  disease  of  the  kidneys  (albuminuria), 
splenic  enlargement,  or  diarrhoea. 

(3)  Cirrhosis,  especially  an  enlarged  cirrhotic  liver  with  latency 
of  the  symptoms.  When  there  are  no  symptoms,  the  diagnosis  is  very 
difficult  and  turns  chiefly  on  the  surface  of  the  liver;  if  it  is  smooth, 
fatty  change  is  probable,  while  if  irregular,  cirrhosis  is  indicated.  In 
numerous  instances  fatty  change  is  associated  with  cirrhosis. 

(4)  A  displaced  liver  if  movable  is  at  once  recognised,  but  if  displaced 
by  some  undetected  cause,  such  as  a  pleural  effusion  or  pneumothorax, 
a  further  ixiistake  is  not  improbable,  and  it  might  be  regarded  as  a  large 
fatty  liver. 

(5)  Enlargement  of  the  liver  due  to  a  deep-seated  hydatid  cyst  or 
abscess.  Here  the  liver  is  much  more  prominent  and  more  easily  felt 
and  mapped  out,  while  there  may  be  signs  of  pressure,  pain,  or  fever. 

Prognosis. — Patients  with  fatty  livers  are  very  frec{uently  addicted 
to  chronic  alcoholism,  and  are  bad  subjects  for  operation  and  bear  severe 
illness,  such  as  pneumonia,  erysipelas,  and  accidents,  very  badly.  Sy- 
monds,t  Verneuil,t  and  L.  Guthrie  §  have  insisted  on  the  danger  of 
operations  on  these  patients;  and  Guthrie,  who  has  pointed  out  that 
chloroform  narcosis  is  specially  dangerous  in  patients  with  fatty  livers, 
has  recorded  a  series  of  cases  in  children  in  which  symptoms  suggesting 
acute  yellow  atrophy  followed  operations,  and  in  which  a  fatty  liver  was 
found  after  death.  Gilbert  and  LerebouUet  ||  have  drawn  attention  to 
the  frequency  with  which  pneumonia  proves  fatal  in  cases  where  the  liver 
is  fatty,  and  lay  stress  on  the  view  that  death  results  in  such  cases  not, 
from  hepatic  disease,  but  because  of  it.  Apart  from  the  dangers  attend- 
ing operations  and  acute  illness  the  prognosis  of  fatt}^  liver  is  that  of 
the  accompanying  disease  or  condition. 

The  treatment  of  fatty  liver  is  that  of  the  primary  cause,  such  as 
obesity  or  pulmonary  tuberculosis.  In  cases  such  as  those  reported  by 
Guthrie,  where  symptoms  suggesting  acute  yellow  atrophy  came  on 
after  chloroform  narcosis,  the  treatment  is  the  same  as  in  acute  yellow 
atrophy.  If  there  is  evidence  of  acidosis  large  doses  of  bicarbonate  of 
soda  should  be  given,  or  it  sliould  be  admiiiistored  !)>'  intramuscular 
transfusion. 

*  Engel,  H.:    Muncliener  med.  Woclicn.,  Rd.  xlviii,  S.  104G,  1901. 

t  Symonds:    Med.  Times  :ind  Gaz.,  ISGO,  vol.  ii,  p.  351. 

t  Verneuil:    Gaz.  des  Hop.,  March  3,   1881. 

§  Guthrie,  L.:    Lancet,  1903,  vol.  i,  p.  10. 

II  Gilbert  and  LerebouUet:   Mem.  et  Bull.  Soc.  M6d.  des  Hop.,  1902,  p.  .577. 


LARDACEOUS  DISEASE  OF  THE  LIVER. 

Synonym:  Amyloid,  Waxy  Disease  of  the  Liver. 

Hope  figures  an  undoubted  case  of  lardaceous  disease  in  his  work 
on  "Morbid  Anatomy"  published  in  1834  as  "hypertrophy  of  the  red 
substance  of  the  liver."  In  his  book  on  diseases  of  the  liver  in  1857 
Budd  *  described  the  condition  as  "scrofulous  disease  of  the  liver." 

INCIDENCE  AND  ETIOLOGY. 

The  liver  is  not  so  often  affected  as  the  spleen  and  kidneys.  In  the 
combined  statistics  of  Birch-Hirschfeld,  Loomis,  Dickinson,  Goodhart, 
and  Turner,  there  are  795  cases  of  lardaceous  disease,  in  which  the  spleen 
was  affected  585  times,  the  kidney  539  times,  and  the  liver  in  387. 

The  causes  of  lardaceous  change  in  the  liver  are  the  same  as  those 
of  lardaceous  disease  generally,  viz.,  prolonged  suppuration  and  syphilis 
without  necessarily  any  associated  production  of  pus ;  while  grave  cachec- 
tic conditions  due  to  chronic  and  severe  toxaemias  occasionally  appear 
to  be  responsible  for  it.  Tuberculosis  jper  se  does  not  give  rise  to  the 
lardaceous  change,  but  when  a  tuberculous  lesion,  for  example,  in  the 
lung,  or  in  connexion  with  bone,  becomes  secondarily  infected,  lardaceous 
disease  may  develop.  This  is  seen  in  chronic  pulmonary  tuberculosis, 
hip-joint  disease,  or  caries  of  the  spine  with  psoas  abscess. 

Incidence  in  chronic  pulmonary  tuberculosis.  In  326  cases  tabulated  by  Westt 
lardaceous  disease  was  met  with  in  20,  or  6.2  per  cent.;  in  Wilson  Fox's  series  of  91 
cases  the  percentage  was  as  high  as  15. 

The  lardaceous  change  is  usually  produced  slowly  after  months  of 
suppuration,  but  it  has  been  found  in  the  liver  one  month  after  the  onset 
of  osteomyelitis  (Soyka).  This  acute  production  of  lardaceous  change 
has  also  been  produced  experimentally  in  animals.  (Krawkow,|  A.  B. 
Green.  §) 

Prolonged  suppuration  is  now  so  comparatively  infrequent  that 
lardaceous  disease  is  less  common,  and  relatively  more  often  due  to 
syphilis,  than  formerly.  As  a  result  of  congenital  syphilis,  lardaceous 
change  is  seen  as  a  late  result,  but  hardly  ever  occurs  in  association  with 
the  pericellular  cirrhosis.  In  tardive  hereditary  syphilis  it  may  be  com- 
bined with  gummata  or  with  parasyphilitic  multilobular  cirrhosis.  (Vide 
p.  378.)  It  is  interesting  to  note  that  the  lardaceous  change  may  be 
local  in  the  liver  around  a  gumma,  an  abscess,  or  a  suppurating  hydatid. 
This  points  to  the  conclusion  that  the  change  is  due  to  the  action  of  a 
toxine  which  is  derived  from  the  abscess  or  gumma.  Lardaceous  disease 
is  occasionally  seen  in  other  infective  conditions. 

*  Budd,  G.:  Diseases  of  the  Liver,  p.  312,  ed.  iii,  1S57. 
t  West:    Diseases  of  Respiratory  Organs,  vol.  ii,  p.  426. 
i  Krawkow:    Archiv  de  Med.  experim.  et  d'anat.  path.,  tome  viii,  1896. 
§  Green:   Journ.  Path,  and  Bact.,  vol.  vii,  p.  184. 

430 


LARDACEOUS    DISEASE    OF   THE    LIVER.  431 

Comba  and  Malenchini*  observed  lardaceous  change  in  a  child,  previously 
healthy,  who  died  with  hseniorrhagic  diphtheria;  in  this  case  the  change  was  prob- 
ably due  to  the  toxines  of  associated  streptococci,  and  need  not  be  referred,  as  the 
authors  inchne  to  do,  to  the  diphtheria  toxine. 

Lardaceous  change  may  be  associated  with  lynjphadenoma  in  the 
Hver  without  any  other  cause, f  and  I  have  seen  it  in  chronic  lymphatic 
leukaemia. 

Pathogeny. — Lardaceous  change  is  allied  to  hyaline  degeneration;  they  are 
different  stages  in  degenerative  modifications  of  protoplasm,  the  hyaline  change 
being  the  earlier.  The  change  consists  in  the  production  of  an  abnormal  albumin- 
ous body  and  is  apparently  due  to  the  action  of  a  poison  or  poisons  on  protoplasm. 
This  body  may  be  produced  either  in  the  circulation  or  in  the  tissues.  CzernyJ 
believed  that  the  change  began  in  the  leucocytes,  since  in  artificial  suppuration 
the  white  corpuscles  when  stained  with  iodine  showed  granules  of  a  brown  colour 
(iodophilia),  which  further  turned  to  a  blue  colour  on  adding  sulphuric  acid.  This 
prelardaceous  substance,  according  to  Czerny's  view,  passed  into  the  tissues  and 
became  lardaceous  material;  according  to  this  theory,  the  process  is  an  infiltration, 
analogous  to  calcareous  infiltration  and  not  a  local  degeneration.  Krawkow§  con- 
sidered that  microbic  infection  was  absolutely  necessary  and  that  the  amyloid  or 
lardaceous  change  did  not  follow  aseptic  suppuration  such  as  is  set  up  by  turpen- 
tine. He  regarded  the  change  as  due  to  the  absorption  of  the  poisons  produced 
by  microbes,  and,  like  Czerny,  looked  upon  lardaceous  disease  as  an  infiltration 
rather  than  a  local  degeneration.     These  results  require  further  confirmation. 


MORBID  ANATOMY. 
The  liver  is  enlarged  and  may  weigh  more  than  twice  its  normal 
amount;  it  has  been  known  to  weigh  14  pounds.  The  surface  is  smooth, 
usually  anaemic,  and  may  show  a  few  stellate  veins.  The  enlargement 
is  uniform  and  the  shape  of  the  organ  is  so  well  preserved  that  the  im- 
pressions of  adjacent  viscera  recall  His'  anatomical  model.  The  margins 
of  the  liver  are  firm  and  rounded.  It  is  extremely  firm  and  can  be  cut 
into  thinner  slices  than  a  healthy  organ.  Its  consistency  is  much  in- 
creased and  it  is  less  elastic  than  normal,  but  is  not  so  resistant  to  the 
knife  as  a  cirrhotic  liver.  The  specific  gravity  of  the  liver  substance  is 
higher  than  in  health  and  has  been  said  to  be  1080  (Wilks||).  The  liver 
substance  is  anaeiTiic,  but  its  colour  varies  with  the  degree  of  anaemia; 
it  may  resemble  the  fat  of  bacon  or,  when  less  anaemic,  look  like  smoked 
salmon.  The  lobular  arrangement  is  accentuated.  The  glands  in  the 
portal  fissure  may  be  considerably  enlarged,  but  do  not  exert  pressure 
on  the  bile-ducts  or  portal  vein.  As  in  other  organs,  the  lardaceous 
change,  when  slight,  may  not  be  manifest  to  the  naked  eye,  and  micro- 
scopic exaiTiination  or  staining  with  iodine  may  be  necessary. 

Iodine  Stain. — The  existence  of  lardaceous  disease  of  the  liver  should  be  tested 
for  in  the  postmortem  room  by  the  iodine  reaction.  A  solution  of  iodine  in  water, 
containing  a  little  iodide  of  potassium  to  dissolve  it,  the  diluted  liquor  iodici  of  the 
Pharmacopoeia  U.  S.  A.,  or  Lugol's  solution  (iodine  1  part,  iodide  of  potassium  2  parts, 

*  Comba  and  Malenchini:    Lo  Sperimentale,  1901. 

t  Buchanan:  Glasgow  Med.  Journ.,  1889,  vol.  ii,  p.  117.  Fagge  and  Pye  Smith's 
Text-book  of  Medicine,  vol.  ii,  p.  647,  ed.  iv. 

X  Czerny:   Archiv  f.  experiment.  Patholog.  u.  Pharmak.,  Bd.  xxxi,  S.  209,  1893. 

§  Krawkow:    Centr.  f.  allg.  Path,  und  path.  Anat.,  vol.  iv,  p.  338. 

II  Wilks,  S.:  Quoted  l)y  Hilton  Fagge,  Principles  and  Practice  of  Medicine,  vol. 
ii,  p.  312. 


432  DISEASES    OF   THE    LIVER. 

water  200  parts) ,  should  be  used.  The  tincture  of  iodine  should  not  be  employed,  since 
the  spirit  it  contains  partially  coagulates  any  albumin  there  may  be  on  the  surface 
of  the  hver  and  thus  obscures  the  reaction.  The  cut  section  should  first  be  washed 
to  remove  any  blood,  and  since  alkali  interferes  with  the  reaction,  should  be  treated 
with  a  dilute  solution  of  acetic  acid.  The  solution  of  iodine  should  then  be  poured 
upon  it,  or,  better,  a  thin  slice  of  the  liver  should  be  placed  in  a  beaker  of  the  watery 
solution  of  iodine.  The  selective  action  of  iodine  is  then  well  shown;  the  healthy 
parts  are  coloured  yellow,  while  the  lardaceous  parts  become  of  a  dark  mahogany. 
The  intermediate  zone  of  the  lobules  stands  up  as  brown  rings  on  a  yellow  ground. 
The  colour  changes  if  H2  SO4  is  added,  but  does  not  actually  turn  blue,  as  was 
originally  described,  but  becomes  a  dark  violet  or  allied  tint. 

Microscopic  Examination. — ^The  chief  brunt  of  the  disease  falls  on 
the  capillaries  in  the  intermediate  zone  of  the  lobules  of  the  Uver,  which 
appear  swollen,  homogeneous;  and  tortuous.  They  compress  and  to  a 
great  extent  conceal  the  hepatic  cells,  while  the  narrowing  of  the  lumen 
of  the  capillaries  impedes  the  flow  of  blood  through  them,  and  as  a  result 
the  liver  cells  atrophy  and  degenerate.  On  section  the  swollen  homo- 
geneous curves  of  the  capillaries  imitate  the  appearance  that  would  be 
presented  by  swollen  hepatic  cells,  but  the  latter  can  be  made  out  in 
appropriately  stained  specimens  between  the  enlarged  capillaries,  and 
it  is  then  seen  that  they  never  undergo  lardaceous  change.  The  lar- 
daceous transformation  of  the  capillaries  eventually  spreads  throughout 
the  lobule,  and  may  then  invade  the  walls  of  the  intralobular  vein. 
The  fibrous  tissue  of  the  portal  space  remains  healthy,  as  is  well  seen 
in  sections  stained  by  Van  Gieson's  method. 

While  the  capillaries  are  the  part  of  the  hepatic  vascular  system 
chiefly  attacked  by  the  lardaceous  change,  exainination  of  livers  in  which 
the  change  is  just  commencing  shows  that  the  first  part  to  be  affected 
is  the  middle  coat  of  the  small  arteries;  later  it  attacks  the  capillaries, 
and  eventually,  if  the  change  is  excessive,  it  may  attack  the  walls  of 
the  portal  and  hepatic  veins.  When  an  early  case  of  lardaceous  change 
is  exainined  and  the  change  is  entirely  limited  to  the  small  arterioles,  a 
condition  which  can  be  well  studied  around  a  gumma,  the  middle  coat 
is  seen  to  be  irregularly  affected.  The  lardaceous  material  is  found  to 
lie  between  the  muscular  fibres  of  the  media  and  not  in  them;  it  spreads 
inwards  to  the  intima,  but  neither  in  the  arterioles  nor  capillaries  does  it 
involve  the  lining  endothelium,  which  maybe  found  to  show  fatty  change. 

It  is  noteworthy  that  the  atrophy  and  degeneration  of  the  hepatic 
cells  are  not  accompanied  by  fibrous  replacement.  It  is  possible  that  this 
failure  of  reaction  on  the  part  of  the  connective  tissue  in  the  lardaceous 
liver  is  due  to  the  very  low  state  of  nutrition  of  the  fibrous  tissue.  (Kant- 
hack.*)  Microscopic  sections  may  be  examined  fresh,  with  iodine  solu- 
tion, or  preferably  with  methyl-aniline  violet. 

Staining  Reactions. — With  methyl-aniline  violet  in  watery  solution  the  larda- 
ceous capillaries  are  stained  red,  while  the  healthy  tissues  are  coloured  violet;  this 
stain  is  better  shown  if  the  sections  are  washed  in  water  acidulated  with  acetic  or 
hydrochloric  acid.  It  is  a  much  more  delicate  stain  than  the  iodine  one,  and  it 
seems  probable  that  it  reacts  to  an  earlier  stage  of  lardaceous  change  than  iodine. 
When  the  lardaceous  change  is  very  far  advanced,  the  methyl-aniline  violet  reaction 
may  fail,  while  the  iodine  reaction  continues  to  be  marked.  Other  substances,  such 
as  colloid  or  hyalin,  occasionally  stain  like  lardaceous  tissue.     Krawkow  considers 

*  Kanthack,  A.  A.:    St.  Bartholomew's  Hosp.  Journ.,  Nov.,  1S96. 


LARDACEOUS   DISEASE    OF  THE   LIVER.  433 

that  the  reaction  is  more  easily  obtained  in  fresh  sections,  and  that  shght  degrees 
of  it  may  not  be  shown  if  the  tissues  are  previously  hardened.  Gentian  violet  may 
also  be  employed;    it  has  the  same  selective  staining  effect. 

A  lardaceous  liver,  if  kept  for  a  long  time,  may  lose  the  power  of 
staining. 

Hadley*  has  described  under  the  title  "achroo-amyloid  liver"  an  appearance 
exactly  like  the  lardaceous  change,  which  would  not  react  to  any  of  the  selective 
stains.  It  does  not  appear  that  the  tissues  were  kept  for  a  long  period  before  being 
examined;    indeed,  even  at  the  autopsy  the  liver  showed  no  reaction  with  iodine. 

CLINICAL  PICTURE. 

Symptoms. — Lardaceous  disease  of  the  liver  is  usually  subordinate 
either  to  the  primary  condition  to  which  it  is  due  or  to  the  general 
manifestations  of  widespread  lardaceous  disease,  for  it  is  rare  for  the 
liver  to  be  the  only  organ  affected.  There  are  no  symptoms  pathogno- 
monic of  lardaceous  disease  affecting  the  Uver  to  the  exclusion  of  the 
other  viscera.  Jaundice  does  not  occur  unless  there  is  some  other  factor, 
such  as  a  gumma.  Ascites  if  present  is  in  all  probability  due  to  con- 
comitant cirrhosis,  gumma,  chronic  peritonitis,  or  renal  disease. 

Tirard  f  met  with  oedema  of  legs  and  ascites  in  a  child  with  a  lardaceous  liver 
secondary  to  tuberculous  ostitis  of  the  spine,  but  the  inferior  vena  cava  was  ob- 
literated by  the  spinal  abscess. 

Ascites  does,  however,  occasionally  occur  in  uncomplicated  instances 
of  lardaceous  Uver.  It  may  be  part  of  general  oedema,  or  terminal  and 
due  to  extreme  cachexia.  It  is  remarkable  that  although  the  hver  is 
almost  universally  lardaceous,  it  shows  little  clinical  evidence  of  func- 
tional inadequacy.  It  has,  it  is  true,  been  thought  that  the  bile  is 
diminished  in  amount,  and  that  the  fseces  become  pale.  The  liver  is 
free  from  pain  or  tenderness  unless  there  is  some  complication,  such  as 
abscess,  perihepatitis,  growth,  or  gumma. 

Signs. — The  only  real  evidence  of  the  presence  of  lardaceous  disease 
of  the  liver  is  its  enlargement,  which  is  uniform,  smooth,  and  painless. 
It  is  only  when  combined  with  gummata,  cirrhosis,  perihepatitis,  or  in 
the  rare  event  of  a  secondary  growth  occurring  in  a  previously  lardaceous 
liver  that  the  surface  becomes  rough  and  nodular.  The  left  lobe  of  the 
liver  may  be  prominent  in  the  epigastrium  and  has  sometimes  given  rise 
to  a  suspicion  of  primary  malignant  disease  (Musser|),  or  been  indis- 
tinguishable from  an  enlarged  spleen. 

In  a  case  recorded  by  Affleck  §  no  cause  for  lardaceous  disease  was  forthcoming, 
and  what  turned  out  to  be  great  enlargement  of  the  left  lobe  in  a  lardaceous  liver 
simulated  the  spleen  of  splenic  anaemia. 

DIAGNOSIS. 

Under  this  heading  the  other  forms  of  painless  enlargement  of  the 
liver  must  be  mentioned.     In  every  case  it  is  important  to  determine 

*  Hadley:    Trans.  Path.  Soc,  vol.  1,  p.  134. 
t  Tirard,  N.:    Medical  Treatment,  1900,  p.  338. 
t  Musser,  J.  H.:    Philadelphia  Med.  Journ.,  May,  1899. 
§  Affleck,  J.  O.:    Edinburgh  Med.-Chir.  Soc,  Dec.  21,  1897. 
28 


434  DISEASES   OP  THE   LIVER. 

whether  the  causes  for  lardaceous  disease  are  or  have  been  present,  and 
whether  there  are  any  signs  of  renal  or  intestinal  disease  of  the  same 
nature. 

In  the  absence  of  ansemia  and  some  degree  of  wasting  the  probabiUties 
are  against  any  known  case  of  hepatic  enlargement  being  due  to  the 
lardaceous  change.  In  leukaemia  the  liver  is  enlarged,  but  a  blood 
examination  will  settle  any  question,  if  such  arise.  When,  as  compara- 
tively rarely  happens,  lymphadenoma  attacks  the  liver,  there  will  almost 
certainly  be  enlarged  glands  elsewhere.  Simple  fatty  liver  is  less  readily 
felt  and,  as  a  rule,  is  associated  with  obesity.  In  cases  of  phthisis  an 
enlarged  liver  may  be  due  to  fatty  change  or  to  lardaceous  disease,  and 
to  settle  the  question  the  other  signs  of  lardaceous  disease  must  be  looked 
for;  if  all  of  them,  such  as  albuminuria,  dropsy,  diarrhoea,  enlarged 
spleen,  are  absent,  it  may  be  assumed  that  the  hver  is  fatty. 

A  hydatid  cyst  deep  in  the  substance  of  the  organ  may  so  displace  the 
liver  forwards  as  to  imitate  the  physical  signs  of  a  lardaceous  Hver,  but 
the  other  symptoms  and  causes  of  lardaceous  disease  are  wanting,  and 
the  patient's  general  health  is  usually  so  good  that  it  puts  lardaceous 
disease  out  of  court.  A  large  cirrhotic  liver  may,  from  its  size  and 
firmness,  imitate  a  lardaceous  liver.  In  both  diseases  the  spleen  may 
be  enlarged,  and  when  ascites  occurs  in  lardaceous  disease,  the  condition 
may  easily  be  regarded  as  cirrhosis.  A  history  of  past  suppuration  and 
the  presence  of  albuminuria,  and  to  a  lesser  degree  past  syphilis,  are  in 
favour  of  lardaceous  disease,  while  a  history  of  alcoholism  and  hsemat- 
emesis  point  to  cirrhosis.  The  following  case  illustrates  the  difficulties 
which  may  arise  in  correctly  diagnosing  between  these  two  conditions : 

A  woman  aged  forty-seven  was  under  my  care  in  St.  George's  Hospital  in  June- 
July,  1900,  with  ascites,  oedema  of  the  legs,  albuminuria,  and  signs  of  pulmonary 
tuberculosis  at  both  apices.  There  was  a  history  of  hjematemesis,  and  the  facial 
aspect  was  that  of  cirrhosis.  She  was  tapped  twice  and  then  passed  into  a  drowsy 
•condition  from  which  she  rallied  temporarily  after  transfusion.  At  the  autopsy 
-there  was  lardaceous  disease  of  the  liver  (53  ounces)  and  kidneys  due  to  chronic 
phthisis.  Microscopically  there  was  no  fibrosis  of  the  liver.  There  was  slight 
thickening  of  the  capsule  of  the  liver  and  opacity  of  the  peritoneum,  but  not  enough 
chronic  peritonitis  to  account  for  the  ascites.  It  is  possible  that  the  lardaceous 
condition  of  the  liver,  together  with  the  slight  peritoneal  change,  was  responsible 
for  the  ascites.  It  is  probable  that  what  was  described  as  hsematemesis  was  in 
reality  haemoptysis. 

PROGNOSIS. 

When  the  liver  is  enlarged  so  that  it  is  readily  felt,  and  there  is  reason, 
from  the  history,  to  believe  that  it  is  due  to  lardaceous  disease,  the  prog- 
nosis is  bad,  since  the  disease  is  likely  to  attack  the  kidneys  and  the 
intestines.  The  affection  of  the  liver  itself  does  not  make  so  much 
difference,  but  it  is  evidence  that  the  disease  is  present  and  may  affect 
more  important  organs. 

Under  appropriate  treatment  a  lardaceous  liver  may  diminish  in  size. 
Sir  D.  Duckworth  *  recorded  a  case  where  it  diminished  by  half  before 
death  occurred,  and  previously  Graves  f  described  great  improvement 

*  St.  Bartholomew's  Hosp.  Reports,  vol.  x,  p.  57. 
t  Graves:    Clinical  Medicine,   p.   568. 


PIGMENTATION   OF  THE   LIVER.  435 

in  cases  which  were  probably  of  the  same  nature.  Experimentally  it 
has  been  shown  by  Lubarsch*  that  lardaceous  disease  may  pass  away; 
he  excised  a  piece  of  a  lardaceous  spleen  from  an  animal  some  weeks  be- 
fore death  and  after  death  no  evidence  of  lardaceous  change  was  present. 

TREATMENT. 

The  first  step  is  to  remove  the  primary  cause  of  lardaceous  disease, 
if  it  is  still  progressing.  Any  suppuration  should  if  possible  be  sub- 
mitted to  surgical  treatment  so  as  to  bring  it  to  a  rapid  and  satisfactory 
termination.  When  syphilis  is  the  cause,  iodide  of  potassium  should  be 
given,  while  good  results  have  also  been  obtained  from  iodide  of  iron. 
If  there  be  concomitant  renal  disease,  the  effect  of  iodide  must  be  care- 
fully watched,  as  an  iodide  eruption  is  then  more  readily  produced.  I 
have  seen  an  eruption  so  produced  closely  resemble  a  uraemic  rash.  The 
general  health  requires  careful  attention  and  sea  air,  good  food,  and 
hygienic  surroundings  are  required,  while  bitter  tonics,  iron,  and  acids 
do  good.  Alkalis  have  been  recommended,  chiefly  on  theoretical  grounds, 
but  do  not  succeed  any  better,  if  so  well,  as  acids.  Budd  and  Warburton 
Begbie  have  recommended  the  administration  of  chloride  of  anunonium, 
but  its  utility  is  very  doubtful.  Constipation  may  require  attention,  but 
mild  laxatives  should  be  given,  otherwise  severe  diarrhoea  may  be  set 
up;  in  fact,  the  treatment  of  constipation  in  tuberculous  enteritis  and 
in  lardaceous  disease  is  ahke  in  the  caution  that  is  necessary  for  fear  of 
setting  up  an  uncontrollable  diarrhoea.  Diarrhoea  may  be  very  trouble- 
some, and  by  exhausting  the  patient  lead  to  a  fatal  issue.  It  may 
alternate  with  constipation,  and  should  be  treated  by  astringents,  and 
if  necessary  with  opium.  General  dropsy  requires  cardiac  tonics,  iron, 
and  diuretics,  while  the  skin  should  be  made  to  act  freely  by  diaphoretics 
and  hot-air  baths,  or  the  amount  of  fluid  should  be  restricted. 

PIGMENTATION  OF  THE  LIVER. 

The  subject  of  pigmentation  in  association  with  cirrhosis  is  described 
under  the  head  of  Pigmented  Cirrhosis  (p.  299).  It  is  merely  necessary 
here  to  mention  the  various  conditions  in  which  the  liver  cells  contain 
pigment.  The  pigments  may  be  divided  into:  (I)  Intrinsic,  or  those 
produced  in  the  body  and  derived  from  the  blood  or  bile;  and  (II) 
extraneous  pigments  introduced  into  the  body;  these  are  of  compara- 
tively little  importance. 

INTRINSIC  PIGMENTS. 

These  include  pigments  derived  from  the  blood,  viz.,  haemosiderin, 
which  contains  iron;  hsematoidin,  an  iron-free  body;  and  the  bile  pigment. 

Haemosiderin.— The  cells  of  the  hver  may  contain  haemosiderin— 
an  iron-containing  pigment  derived  from  the  destruction  of  red  blood- 
corpuscles  and  the  haemoglobin  thus  liberated— in  a  number  of  condi- 
tions.    In  a  systematic  examination  of  the  liver  in  300  cases  Castaignef 

*  Lubarsch:    Virchow's  Archiv,  Bd.  cl,  S.  471.  ,  n  ■ 

tCastaigne:  Quoted  bv  Chauffard,  Traits  de  Medecine  (Bouchard-Bnssaud), 
tome  V,  p.  240,  ed.  ii,  1902.' 


436  DISEASES   OF  THE    LIVER. 

found  that  in  31,  or  more  than  10  per  cent.,  the  hver  cells  contained 
hsemosiderin.  This  subject  has  been  very  ably  dealt  with  by  Abbott.* 
The  characteristic  reaction  (Perl's  test)  for  hsemosiderin  consists  in 
placing  microscopic  sections  in  a  2  per  cent,  solution  of  ferro cyanide 
of  potassium  for  three  minutes,  transferring  to  a  1  per  cent,  solution  of 
hydrochloric  acid  for  two  to  five  minutes,  and  washing  in  distilled  water; 
the  pigment  granules  take  a  bluish-green  colour.  This  blue  colouration  is 
well  seen  in  the  ceUs  in  the  periphery  of  the  lobule  in  pernicious  anaemia. 
It  also  occurs  in  leukaemia,  in  some  cases  of  enteric  fever,  and  in  cases 
of  chronic  intestinal  disorder.  Adami  f  considers  that  hsemosiderin  is 
deposited  around  the  diplococcal  form  of  the  colon  bacillus,  described 
by  him,  in  the  liver  cells.  Haemolysis  of  bacterial  origin  has  been  thought 
to  account  for  hsemosiderosis  of  the  liver  cells  in  ordinary  cirrhosis  {vide 
p.  208)  and  in  hsemochromatosis  (vide  p.  300).  Hsemosiderosis  of  the 
liver  is  also  seen  after  haemorrhage  into  the  peritoneal  cavity,  in  fatal 
cases  of  purpura,  and  has  been  produced  by  experimental  haemolysis; 
for  example,  by  toluylendiamine.  (Meunier.J)  In  some  cases  of  new- 
growth  in  the  Uver  the  hepatic  cells  in  the  neighbourhood  of  the  growth 
show  haemosiderin.  I  have  also  seen  it  in  lymphadenoma.  In  malaria 
the  hver  cells  may  contain  haemosiderin,  and  it  has  also  been  described 
in  association  with  suppuration.     (Abbott.  |) 

Haematoidin. — This  iron-free  pigment  is  seen  in  and  between  the 
liver  cells  around  the  intralobular  vein  in  chronic  venous  engorgement 
of  the  liver.  (Vide  p.  89.)  It  may  also  occur  in  the  neighbourhood  of 
haemorrhages,  innocent  nsevi  ('' melanotic  angioma"),  scars  of  old  ab- 
scesses, gummata,  etc. 

In  the  various  forms  of  biliary  obstruction  the  liver  cells  are  degen- 
erated and  occupied  by  granules  of  bile  pigment. 

EXTRINSIC  PIGMENTATION. 

In  Anthracosis,  Silicosis,  etc. — In  rather  rare  instances  particles 
of  carbon  or  of  other  foreign  substances  have  been  found  in  otherwise 
normal  livers ;  the  liver  of  cirrhosis  (vide  p.  300)  may  show  im- 
pregnation with  particles  of  carbon — cirrhosis  anthracotica  (Welch  H ) ; 
Lancereaux**  describes  this  condition  in  copper- workers;  of  stone 
(Adami  jf ),  and  with  silver  after  its  medicinal  use  for  epilepsy  (From- 
mannJJ).  Reference  has  been  made  elsewhere  (p.  300)  to  a  case  of  cir- 
rhosis in  a  sweep  with  pigmentation,  probably  due  to  soot,  of  the  fibrous 
tissue.  It  is  very  possible  that  the  livers  of  sweeps  and  other  persons 
exposed  to  soot-laden  atmospheres  frequently  contain  soot.  These 
conditions  are  interesting  curiosities  but  have  no  clinical  significance. 

*  Abbott,  M.:   Journ.  Path,  and  Bacteriology,  vol.  vii,  p.  55. 
t  Adami:    Journ.  American  Med.  Assoc,  Dec.  23,  1899. 
t  Meunier:   Th^se  Paris,  1897-8,    No.  171. 

I  Abbott,  M.:   Journ.  of  Path,  and  Bacteriology,  vol.  vii,  p.  55. 

II  Welch:   Johns  Hopkins  Hosp.  Bull.,  1891,  32. 

**  Lancereaux:    Traits  des  Maladies  du  foie  et  du  pancreas,  p.  380. 

tt  Adami:   Sajous'  Annual,  1898,  vol.  ii,  p.  313. 

it  Frommann:    Archiv  f.  Anat.  u.  Physiol.,  Berlin,  1860. 


CALCIFICATION  OF  THE  LIVER. 

This  condition,  which  is  a  pathological  curiosity,  occurs  in  two 
forms — primary  and  secondary. 

Primary  calcification  is  very  rare;  it  may  occur  in  the  hver  cells,  as 
in  Bristowe's  and  Mihel's  cases  or  in  the  walls  of  the  vessels.  In  three 
cases  this  calcification  was  associated  with  chronic  nephritis. 

In  a  boy  aged  sixteen  years  who  died  with  scarlatinal  dropsy  Bristowe*  found  in- 
filtration of  the  liver  cells  with  an  earthy  salt  which  dissolved  in  acetic  acid. 

In  a  boy  aged  seventeen  years  who  died  from  chronic  pulmonary  tuberculosis  and 
parenchymatous  nephritis  Mihel  f  found  that  the  liver,  which  grated  under  the 
knife  and  had  the  aspect  of  chronic  venous  engorgement,  showed  calcareous  in- 
filtration of  the  liver  cells  around  the  intralobular  veins.  The  infiltration  appeared 
to  be  due  to  calcium  phosphate.  In  a  girl  aged  fourteen  years  who  died  with  ad- 
vanced interstitial  nephritis  the  liver  was  found  by  Brill  and  LibmanJ  to  show 
calcification  with  calcium  phosphate  around  the  branches  of  the  hepatic  artery, 
which  showed  endarteritis  obliterans.  The  liver  showed  chronic  perihepatitis  and 
chronic  venous  engorgement. 

Babes  ^  refers  to  a  case  where  death  occurred  from  tuberculous  disease 
of  the  hip ;  the  liver  showed  areas  of  calcification  regarded  as  due  to  the 
deposit  of  salts  absorbed  from  the  affected  bones.  In  a  curious  instance 
of  widespread  calcification  affecting  the  heart  and  arteries  in  a  man  aged 
twenty-five  years  Bramwell  ||  and  Gulland  found  the  liver  healthy. 

Though  calcification  of  arteries  in  the  hver  is  extremely  uncommon 
in  man,  it  is  said  not  to  be  very  rare  in  horses;  it  is  apparently  a  primary- 
change  and  analogous  to,  if  not  identical  with,  senile  calcification  of  the 
muscular  coats  of  arteries.  In  the  Royal  College  of  Surgeons  of  England 
there  is  a  Hunterian  specimen  of  a  branching  piece  of  bone  from  the  hver 
of  a  sheep  (No.  2803),  which  was  thought  to  have  been  formed  in  ob- 
literated blood-vessels;  it  is  probably  a  calcified  clot  in  the  portal  vein. 
The  occurrence  of  calcification  more  commonly  in  these  animals  is  proba- 
bly related  to  their  food;  thus  actinomycosis  in  herbivora  may  undergo 
calcification,  which  it  does  not  do  in  man. 

In  secondary  calcification  a  deposit  of  calcareous  salts  occurs  in 
inflammatory  products  of  considerable  age,  such  as  gummata,  the  scars 
of  cured  abscesses,  the  walls  of  hydatid  cysts,  and  in  the  walls  of  the 
gaU-bladder  as  the  result  of  past  or  chronic  inflammation.  A  remarkable 
example  of  diffuse  calcareous  infiltration  of  the  hver  recorded  by  Targett** 
was  probably  secondary  to  syphihtic  inflammation.     {Vide  Fig.  44.) 

*  Bristowe,  J.  S.:   Trans.  Path.  Soc,  vol.  viii,  p.  233. 

t  Mihel:  Srpsi  Arhiv  za  Celokupno  lekarstvo.,  1900.  Quoted  Philadelphia 
Med.  Journal,  1901,  p.  199. 

t  Brill  and  Libman:   Jour.  Experiment.  Med.,  vol.  iv,  p.  541,  1899. 
§  Babes:   Virchow's  Archiv,  Bd.  cv,  S.  511. 
II  Bramwell,  B.:    Edinburgh  Hosp.  Reports,  vol.  iv,  p    175. 
**  Targett:  Trans.  Path.  Soc,  vol.  xl,  p.  123. 

437 


438  DISEASES   OF  THE  LIVER. 

Carrel*  has  put  on  record  a  case  where  a  tumor  of  the  ILver  due  to  psorospermosis 
underwent  calcification.  The  tumor  was  removed  in  a  laparotomy  undertaken 
with  the  view  that  it  was  a  calcified  gall-bladder.  Chemically  the  salts  chiefly 
present  were  carbonate  and  phosphate  of  calcium. 

Sometimes  hard,  coral-like  masses,  of  about  the  size  of  a  marble,  are 
found  embedded  in  the  liver.  They  are  probably  the  dried-up  remains 
of  biliary  cysts  or,  in  other  words,  intra-hepatic  calculi.  Small  bile  cysts 
without  any  general  bihary  obstruction  are  occasionally  seen;  as  time 
goes  on  their  contents  become  more  viscid  and  eventually  solid. 
*  Carrel:   Lyon  Medical,  tome  xciii,  p.  S9. 


LEUK.EMIC  INFILTRATION  OF  THE  LIVER. 

Synonym:  LeucocythEemic  Infiltration. 

The  liver  may  be  very  greatly  enlarged  from  leuksemic  infiltration, 
especially  in  the  rarer  form  of  the  disease,  lymphatic  leukaemia.  In 
splenomedullary  or  myelogenous  leukaemia  there  is  not  necessarily  any 
enlargement,  though  it  may  be  very  considerable. 

Murchison*  describes  a  case  which,  from  the  illustration  given  of  the  blood,  was 
evidently  splenomedullary  leukaemia,  with  a  liver  that  was  smaller  than  natural, 
weighing  35  ounces.  On  the  other  hand,  in  the  two  following  cases  of  splenomedul- 
lary leukaemia  examined  after  death  at  St.  George's  Hospital  the  liver  was  greatly 
enlarged.  The  liver  of  a  man  aged  twenty-six  weighed  7|  pounds,  while  the  spleen 
weighed  6  pounds;  both  these  organs  showed  scattered  through  their  substance 
white  spots  resembling  miliary  tubercles  but  due  to  dense  infiltration  with  leuco- 
cytes. 

The  liver  of  a  woman  aged  twenty-seven  weighed  10  pounds  and  the  spleen  76 
ounces.  Together  these  two  viscera  occupied  almost  the  whole  of  the  front  of  the 
abdomen,  a  few  coils  of  intestine  only  appearing  above  the  pubes.  There  was 
no  ascites.  The  enlargement  of  the  liver  was,  contrary  to  what  is  usually  seen, 
almost  entirely  of  the  right  lobe  and  not  of  both  lobes. 

The  liver  not  uncommonly  weighs  5  or  6  pounds  instead  of  2J,  and 
may  weigh  much  more. 

Morbid  Anatomy. — The  surface  of  the  liver  is  pale  and  smooth.  On 
section  it  is  pale  and  sometimes  may  show  naked-eye  evidences  of  accu- 
mulations of  white  blood-corpuscles  either  in  the  larger  portal  spaces 
or  in  the  substance  of  the  liver.  In  rare  instances  there  are  pink- 
ish white  masses  around  the  portal  spaces ;  less  rarely  there  are  white 
spots  exactly  like  miliary  tubercles  embedded  in  the  liver  substance. 
Microscopic  exaixdnation  shows  that  these  are  areas  of  dense  leucocytic 
infiltration  and  not  tuberculous  granulation  tissue.  In  the  condition 
described  as  chloroma,  which  is  really  lymphatic  leukaemia,  the  portal 
canals  have  been  found  to  be  marked  out  as  green  tracks. 

Microscopically,  the  appearances  are  not  always  exactly  alike.  There 
may  be  a  general  and  diffuse  crowding  of  the  capillaries  with  leucocytes 
with  some  increase  at  the  periphery  of  the  lobules,  or  there  may  be 
intense  leucocytic  infiltration  around  the  portal  spaces  at  the  periphery 
of  the  lobules,  with  comparatively  little  blocking  of  the  intralobular  capil- 
laries. When  there  is  marked  infiltration  at  the  margin  of  the  lobules 
the  lobulation  is  clearly  seen  with  the  naked  eye,  and  the  microscopic 
appearances  are  at  first  sight  suggestive  of  interlobular  inflammation, 
e.  g.,  suppurative  pylephlebitis.  The  leucocytes  are  chiefly  large  or  small 
mononuclears;  in  splenomedullary  leukaemia  myelocytes  are  seen  in  the 
capillaries.  The  liver  cells,  especially  in  the  centres  of  the  lobules,  may 
stain  imperfectly  from  degeneration,  depending  on  impaired  nutrition, 
and  may  be  fatty  or  atrophied.     At  the  periphery  of  the  lobule  the 

*  Murchison:    Diseases  of  the  Liver,  cd.  ii,  p.  308. 
439 


440 


DISEASES    OF  THE   LIYEK. 


hepatic  cells  are  sometimes  pigmented  -^"itli  hi^mosiderin  and  resemble 
the  appearances  in  pernicious  anaemia.  Cirrhosis  does  not  develop  as 
the  result  of  leuksemic  infiltration. 

Clinical  Features. — There  is  really  nothing  wliich  can  be  specially 
correlated  with  leuksemic  infiltration  of  the  hver  in  a  case  of  leukaemia 
except  the  painless  enlargement  of  the  hver.  In  the  latter  stages  of 
leukaemia  ascites  is  not  uncommonly  present :  it  has  been  suggested  that 
this  may  be  due  to  pressure  of  leucocj-tic  infiltration  on  the  intra-hepatic 
branches  of  the  portal  vein,  or  to  pressure  of  enlarged  glands  in  the 
portal  fissure  in  the  portal  vein.  But  it  seems  more  probable  that  it  is 
due  to  some  concomitant  chronic  peritonitis  and  to  the  cardiac  debihty 
and  altered  blood-state.     It  is  conceivable  that  ascites  might  be  in  some 


Fig.  54. — Photomicrograph  of  Liter  ix  Leukemic  Infiltration-. 
There  is  dense  leucocji:ic  massing  around  a  vein  and  an  excessive  number  of  white  blood-cor- 
puscles in  the  capillaries.     The  liver  cells  stain  badly.     (Taken  by  S.  G.  Penny,  Esq.) 


degree  determined  by  thrombosis  in  the  terminal  branches  of  the  portal 
vein  in  the  hver.  The  mine  in  a  case  of  leuksemic  infiltration  of  the 
hver  was  found  to  contain  hsematoporphyrin  by  Garrod.*  who  was  in- 
clined to  regard  this  pigment  as  specially  related  to  the  hepatic  change. 
In  other  respects,  such  as  the  excess  of  uric  acid,  the  urine  shows  the 
characters  due  to  leukaemia. 

The  diagnosis  of  leukaemic  infiltration  of  the  hver  depends  on  an 
examination  of  the  blood.  This  shotild  be  done  in  a  doubtful  case  of 
painless  hepatic  and  splenic  enlargement  in  order  to  prevent  the 
disease  being  regarded  as  lardaceous  or  s}-philitic  and  treated  with 
iodide  of  potassium. 

The  prognosis  and  treatment  are,  of  course,  those  of  leukaemia. 
*GaiTod,  A.  E.:  Lancet,  1900.  vol.  ii.  p.  132,3. 


SIMPLE  CYSTS  OF  THE  LIVER. 

Various  forms  of  cysts  may  occur  in  the  liver,  and  may  be  conven- 
iently classified  as  follows : 

1.  Parasitic  cysts.     Echinococcal  or  hydatid  cysts.     (Vide  p.  389.) 

2.  Cysts  manifestly  due  to  biliary  obstruction.  There  may  be  wide- 
spread dilatation  of  the  bile-ducts  in  the  hver  in  cases  of  long-standing 
bihary  obstruction.  The  ducts  stand  out  under  the  capsule  and  contain 
mucous  fluid.  This  change  is  entirely  secondary  to  the  cause  of  the 
obstructive  jaundice,  such  as  carcinoma  of  the  head  of  the  pancreas,  etc., 
and  will  not  be  further  discussed  here.  The  effects  of  bihary  obstruction 
may  be  more  locahsed  and  give  rise  to  definite  cysts,  which  in  exceptional 
instances  may  be  of  very  considerable  size;  in  North's  *  case  a  cyst  con- 
taining five  pints  of  coffee-coloured  fluid  was  associated  with  a  calculus 
impacted  in  the  common  bile-duct. 

In  a  man  aged  thirty-nine  who  died  in  St.  George's  Hospital  with  jaundice 
supervening  in  the  course  of  pancreatic  diabetes  compUcated  with  rapid  pulmonary 
tuberculosis,  there  were  remarkably  large  intra-hepatic  calculi  composed  of  bih- 
rubin.f  There  were  bihary  cysts  on  the  surface  of  the  liver,  with  inflamed  walls  and 
fibrosis  spreading  outwards  into  the  surrounding  hver  substance.     (Vide  Fig.  95.) 

A  few  words  may  be  said  about  cysts  occurring  in  cirrhosis  of  the 
liver.  They  are  very  rare  and  may  arise  in  two  distinct  ways:  (1)  By 
biliary  retention,  and  then  resemble  those  just  described;  (2)  by  the 
softening  down  of  the  adenomatous  masses  seen  in  nodular  cirrhosis. 

These  cysts  are  small,  sometimes  microscopic,  and  are  only  of 
pathological  interest.     The  following  is  an  example  of  macroscopic  cysts : 

A  woman  aged  forty-four  years  died  with  ascites  and  cirrhosis  in  St.  George's 
Hospital.  The  liver,  41  ounces,  was  finely  granular  and  showed  microscopically 
multilobular  cirrhosis,  sometimes  passing  into  unUobular  cirrhosis.  On  the  con- 
vexity of  the  right  IoIdc  near  the  falciform  ligament  there  was  a  cyst  the  size  of  a 
hazel-nut  with  clear  contents.  Near  it  was  a  dried-up  cyst  with  thick  walls  and 
almost  calcareous  contents.  This  transformation  of  cysts  into  solid  formations 
is  often  seen  in  the  kidney.  The  dried-up  and  calcareous  contents  of  these  hepatic 
cysts  may  imitate  intra-hepatic  calculi.  This  liver,  which  also  showed  the  effects 
of  tight  lacing,  is  depicted  in  Fig.  6. 

Mcroscopic  cysts  or  dilatations  of  the  small  bile-ducts  are  occasionally 
seen. 

In  making  microscopic  sections  of  a  hobnailed  liver  weighing  41  ounces,  dilata- 
tion of  the  bile-ducts  in  the  portal  spaces  was  found.  There  was  perihepatitis 
and  chronic  peritonitis  in  this  case  and  small  calculi  in  the  gall-bladder,  but  there 
was  no  history  or  evidence  of  past  biliary  obstruction. 

The  adenomatous  formations  seen  in  nodular  cirrhosis  may  soften 
down  and  form  false  cysts  resembhng  those  seen  in  degenerating  new- 

*  North:  Medical  Record  (N.  Y.),  vol.  xxii,  p.  344,  1882. 
t  Vide  Trans.  Path.  Soc,  vol.  xhx,  p.  133. 
441 


442  DISEASES   OF   THE   LIVER. 

growths.     Cysts  due  to  degenerative  changes  in  carcinoma  and  sarcoma 
of  the  liver  are  described  on  page  489. 


SIMPLE  CYSTS. 

They  are  usually  single  or  present  in  very  small  numbers;  when 
there  are  a  large  number,  the  condition  becomes  that  of  cystic  disease. 
(Vide  p.  445.)  As  a  rule,  the  cysts  are  small  and  of  no  clinical  impor- 
tance. Large  simple  cysts  are  sometimes  met  with.  Probably  some  of 
those  recorded  are  sterile  hydatid  cysts ;  microscopic  exaixdnation  of  the 
cyst  wall  should  decide  the  point.  Cysts  sufficiently  large  to  contain 
many  pints  have  been  described. 

In  Bayer's*  and  Winckler'sf  cases  there  were  thirteen  and  a  haK  pints,  and  in 
North's  J  case  five  pints,  of  fluid.  Doran  §  has  written  a  most  valuable  paper  on 
these  cysts. 

In  some  instances,  such  as  Sharkey's,  |1  single  cysts  containing  a  pint 
of  fluid  have  been  found.     Usually  they  are  much  smaller. 

Mode  of  Formation. — Simple  cysts  are  usually  regarded  as  retention 
cysts  due  to  local  obstruction  of  the  bile-ducts.  Although  in  a  fully 
developed  stage  they  do  not  contain  bile,  they  may  do  so  in  an  early 
stage. 

Thus  in  a  woman  aged  thirty-five  years  who  died  in  St.  George's  Hospital  in 
1892,  with  peripheral  neuritis  and  puhnonary  tuberculosis,  there  was  a  small  cyst 
containing  bile  in  the  left  lobe  of  the  liver. 

The  bile  disappears  from  the  cyst  probably  in  the  same  way  that  it 
does  in  general  biliary  obstruction  of  long  standing,  and  becomes  replaced 
by  clear  albuminous  fluid.  It  has  been  suggested  that  a  bile-containing 
cyst  may  be  due  to  nipture  of  aij  intra-hepatic  bile-duct.  (Doran.) 
Other  methods  of  origin  have  been  suggested  for  simple  cysts  of  the 
liver,  such  as  dilatation  of  the  glands  of  the  larger  bile-ducts  or  dilatation 
of  aberrant  bile-ducts.  Again,  some  of  the  small  single  cysts  with  blood- 
stained contents  may,  as  in  the  spleen,  be  the  result  of  degenerative 
changes  in  nsevi.  A  large  single  cyst  may  be  due  to  cystic  change  in 
an  adenoma  of  the  bile-duct,  the  papillomatous  growth  softening  down 
in  the  same  way  as  adenomata  of  the  thyroid  gland. 

Shattuck  **  reports  a  case  in  point  where  the  cyst  contained  a  gallon  of  clear 
fluid. 

Morbid  Anatomy. — ^The  cysts  are  commoner  on  the  surface  of  the 
liver  than  deeply  embedded  in  its  substance,  but  they  are  very  seldom 
pedunculated;  Doran  refers  to  three  large  pedunculated  CA'-sts.  Thej- 
are  usually  surrounded  by  a  firm,  fibrous  capsule  which  often  contains 

*  Bayer,  K.:  Prag.  med.  Wochen.,  1892,  S.  637. 
t  Winckler:  Quoted  by  Doran. 

t  North:  Medical  Record  (N.  Y.),  vol.  xxii,  p.  344,  1882. 
§  Doran,  A.:  Medico-Chirurg.  Trans.,  vol.  Ixxxvii. 
II  Sharkey,  S.  J.:  Trans.  Path.  Soc,  vol.  xxxiii,  p.  168. 
**  Shattuck:  Boston  Med.  and  Surg.  Journ.,  April  26,  1900,  p.  427. 


SIMPLE    CYSTS    OF  THE   LIVER.  443 

numerous  blood-vessels,  and  in  cases  of  old  standing  may  show  some 
calcareous  infiltration.  In  recent  cysts  the  walls  are  thin.  The  ioner 
surface  is  smooth,  but  is  often  ridged,  possibly  from  the  remains  of  par- 
titions between  originally  separate  cysts,  and  may  resemble  the  inside 
of  the  auricles  of  the  heart.  It  has  an  opaque  white  colour,  except 
in  cases  where  the  cysts  are  very  thin- walled. 

A  typical  specimen  occurred  in  the  liver  of  a  man  aged  sixty-three  who  died 
of  a  thoracic  aneurysm;  on  the  surface  of  the  convexity  of  the  Mver,  near  the  falci- 
form ligament,  there  was  a  cyst  the  size  of  a  hazel-nut,  with  traces  of  partitions  but 
not  completely  multilocular.  In  the  liver  of  a  man  aged  seventy-eight,  who  had 
granular  kidneys  with  a  few  minute  cysts,  the  liver,  which  otherwise  appeared 
natural,  contained  four  cysts;  three  of  them  were  on  the  surface  of  the  liver,  the 
other  was  deeply  embedded  on  the  substance  of  the  right  lobe;  it  was  the  largest, 
and  measured  |  of  an  inch  across.  The  contained  fluid  was  straw-coloured  and  the 
walls  were  smooth. 

The  larger  simple  cysts  must  be  distinguished  from  hydatid  cysts  by 
examination  for  booklets  and  for  laminated  membrane,  while  during  an 
operation  the  relations  of  the  cyst  must  be  noted  in  order  to  differentiate 
it  from  idiopathic  dilatation  of  the  extra-hepatic  bile-ducts.  The 
nature  of  the  contents  of  these  cysts  varies  considerably.  The  con- 
tents are  usually  clear  and  colourless,  but  may  be  bile-  or  blood-stained, 
green,  reddish,  or  bro"ViTi.  From  degenerative  changes  in  the  lining 
epithelium  the  contents  may  become  syrupy,  hke  some  renal  cysts,  and 
so  tend  to  dry  up  and  form  solid  white  encapsulated  masses  of  small 
size.  The  fluid  is  albuminous  and  may  contain  blood  or  epithelial  cells, 
hsematoidin,  bile  pigment,  cholesterin,  tyrosin.*  In  Doran's  case  the 
cyst  contained  two  and  a  half  pints  of  bile.  It  is  probable  that  as  the 
result  of  injury  extravasation  of  blood  or  of  bile  may  take  place  into  a 
cyst  with  clear  serous  contents. 

Microscopic  Appearances. — -The  capsule  is  composed  of  laminated 
fibrous  tissue  which  may  contain  bile-ducts,  sometimes  dilated.  Occa- 
sionally blood  pigment  is  found  between  the  bundles  of  fibrous  tissue. 
The  fibrous  tissue  invades  the  liver  tissue  for  a  very  short  distance  and 
is  fined  internally  by  a  layer  of  epithelial  cells  which  may  be  columnar, 
cubical,  or  polyhedral  in  the  small  cysts.  In  exceptional  instances  the 
epithelium  may  be  ciliated.  (Friedreich,!  Hanot  and  Gilbert. |)  In  the 
larger  cysts  the  cells  are  absent  or  much  flattened. 

Clinical  Features. — Simple  serous  cysts  are  very  rarely  large  enough 
to  give  rise  to  signs  or  symptoms.  When  they  do,  the  signs  are  usually 
like  those  of  hydatid  cysts,  or  occasionally  of  an  ovarian  cyst,  and  the 
treatment  is  the  same.  Rupture  into  the  peritoneal  cavity  may  occur, 
and  when  large,  induce  shock  and  collapse.  In  rare  instances  severe 
haemorrhage  may  occur  into  a  large  cyst  and  even  give  rise  to  a  fatal 
result. 

Kilvington§  mentions  a  case  which  died  with  symptoms  like  those  of  rupture 
of  a  large  internal  aneurysm,  from  haemorrhage  into  a  large  simple  cyst  of  the  li'V'^er. 

*  Campbell  McDonnell:  Lancet,  1900,  vol.  i,  p.  45.3. 

t  Friedreich:  Archiv,f.  path.  Anat.,  Bd.  xi,  S.  466,  1857. 

t  Hanot  et  Gilbert:  Etudes  Sur  les  Maladies  de  foie,  p.  301. 

§  Kilvington:  Intercolonial  Medical  Journ.  of  Australasia,  vol.  vii,  p.  557,  1902. 


444  DISEASES   OF  THE   LIVER. 

In  Doran's*  case,  where  the  cyst  contained  two  and  a  half  pints  of 
bile-stained  fluid,  the  patient  was  markedly  jaundiced. 

Usually  simple  serous  cysts  are  found  accidentally  at  the  autopsy, 
and  more  often  in  middle-aged  persons.  Durante  f  has  met  with  one 
in  an  infant  in  whom  there  was  no  evidence  of  general  cystic  disease  of 
the  Hver. 

Diagnosis. — When  of  such  a  size  as  to  be  palpable,  they  can  only 
be  distinguished  from  hydatid  cysts  by  examination  of  fluid  obtained 
from  aspiration.  The  fluid  is  albuminous  and  does  not,  of  course,  contain 
booklets. 

The  treatment  is  excision  of  as  much  of  the  cyst  wall  as  is  possible; 
this  can  be  carried  out  most  successfully  in  cases  where  the  cyst  is  pedun- 
culated. In  cases  where  the  cyst  is  embedded  in  the  hver  it  should  be 
dealt  with  on  the  same  lines  as  hydatid  cysts. 

*  Doran,  A.:  Medico-Chirurg.  Trans.,  vol.  Ixxxvii. 
t  Durante:  Bull.  Soc.  Anat.  Paris,  1902,  p.  953. 


CYSTIC  DISEASE  OF  THE  LIVER. 

The  liver  may  be  occupied  by  a  large  number  of  cysts  of  varying 
sizes,  and  thus  presents  a  contrast  to  the  single  or  isolated  cysts  already 
referred  to.     This  condition  is  spoken  of  as  cystic  disease  of  the  Uver. 

Incidence. — From  their  age-incidence  the  cases  may  for  convenience 
be  divided  into  two  categories — those  seen  in  adult  life  and  those 
found  in  the  newly  bom;  though  it  is  very  probable  that  those  seen  in 
adult  life  are  also  congenital,  but,  being  less  marked,  have  survived. 

Only  a  few  cases  have  been  reported  in  newly  horn  infants;  there 
are  probably  not  more  than  fifteen  published  cases.  But  it  is  likely  that 
the  disease  is  doubtless  often  overlooked,  as  it  may  not  be  manifest  until 
the  liver  is  examined  ixiicroscopically.  I  have  seen  two  cases  myself,  in 
both  of  which  the  naked-eye  appearances  were  rather  those  of  fibrosis  than 
of  cystic  disease.  Asalargeproportionof  thecasesof  cystic  fivers  in  infants 
have  been  associated  with  deformities,  such  as  polydactylism,  etc.,  it  is 
probable  that  if  the  livers  of  monsters  and  still-bom  children  were  sys- 
tematically examined  microscopically,  congenital  cystic  disease  of  the 
liver  would  be  found  in  a  comparatively  larger  number. 

Cases  have  been  reported  by  Kanthack  and  myself,*  Still  (2),t  Bar  and  Renon,  J 
Couvelaire,§  Couvelaire  and  Porak,||  Carr6,**  Brindeau  and  Mac6,tt  Kilvington.ji 
In  all  these  cases  the  kidneys  were  also  markedly  cystic.  Borst§§  recorded  a 
case  in  a  child  seven  months  old  Dudgeon  ||  ||  a  case  which  was  probably  of  this 
nature  in  a  child  of  nine  months  in  which  the  kidneys  were  normal;  W.  Miiller*** 
a  case  in  a  female  child  two  years  of  age  whose  abdomen  began  to  swell  at  ten 
months,  and  Batty  Shawftt  a  case  in  a  child  aged  seven  years  in  which  the  kidneys 
were  not  involved.  These  cases  tend  to  support  the  view  that  the  less  marked 
congenital  cases  may  -persist  into  adult  life. 

Possibly  the  case  of  a  full-term  child  the  subject  of  many  abnormalities,  in- 
cluding cystic  kidneys,  obliteration  of  the  bile-duct  and  communicating  cysts,  one 
in  each  lobe  of  the  liver,  belongs  to  this  group;  no  microscopic  examination,  how- 
ever, was  made  (Witzel  ttt)-  Gueniot's§§§  case  may  also  belong  to  this  category.  A 
fuU-term  foetus  had  6  fingers  and  6  toes,  anencephaly,  absence  of  external  genitals, 
kidneys  three  times  the  normal  size,  and  a  cyst  in  each  lobe  of  the  liver;  the  cyst 
in  the  left  lobe  contained  40  grammes  and  that  in  the  right  lobe  80  grammes  of  clear 
fluid.  This  was  the  eighth  child  of  a  woman  who  married  her  nephew;  none  of  the 
children  survived;    some  of  them  showed  abnormalities. 

*  Kanthack  and  RoUeston:  Virchow's  Archiv,  Bd.  cxxx,  S.  4SS. 
t  Still:  Trans.  Path.  Soc,  vol.  xlix,  p.  155. 
i  Bar  and  Renon:  C.  R.  Soc.  de  biolog.,  1894,  p.  835. 
§  Couvelaire:    Annal  de  Gyn.  et  d'obstet.,  Nov.,  1899. 

II  Couvelaire  and  Porak:  C.  R.  de  la  Soc.  d'obstet.  et  de  Gvnec.  et  de  Pediat., 
Paris,  Jan.,  1901,  p.  26. 

**  Carre:    These  Paris,  1901,  No.  232. 
tt  Brindeau  and  Mace:   Gaz.  Hebdom.,  Feb.,  1899. 

it  Kilvington:   Intercolonial  Med.  Journ.  of  Australasia,  vol.  vii,  p.  557,  1902. 
§§  Borst:    Festschrift  der  phys.  med.  Gesellschaft,  Wiirzburg,  1899. 
nil  Dudgeon,  L.:    Trans.  Path.  Soc,  vol.  liv,  p.  296. 
***Muller,  W.:    Virchow's  Archiv,  Bd.  clxiv.  S.  270. 
ttt  Shaw,  H.  B.:    Lancet,  1903,  vol.  i,  p.  1447. 
ttt  Witzel:    Centralblatt  f.  Gviuik.,  1880,  S.  561. 
§§§Gueniot:    Bull,  de  I'Acad.  de  MM.  Paris,  tome  xxv,  p.  169,  1891. 

445 


446  DISEASES    OF   THE    LIVER. 

Association  with  Cystic  Disease  of  the  Kidneys. — Real  cystic  disease 

of  the  liver  is  practically  always  accompanied  by  a  similar  and  almost 

always  more  advanced  change  in  the  kidneys.     This  association  was 

first  noted  by  Bristowe."^    A  few  accidental  cysts  may  occur  in  the  Hver 

without  any  similar  change  in  the  kidney,  but  this  hardly  constitutes 

cystic  disease. 

Two  cases  of  probable  cystic  disease  of  the  liver  -^-ithout  similar  change  in  the 
kidneys  have  been  referred  to  (Dudgeon  and  Batty  Shaw).  Dr.  Lazarus-Barlow 
has  told  me  of  a  case  of  cystic  disease  of  the  liver  in  a  young  adult  in  which  the 
kidneys  were  normal. 

Cystic  kidneys  not  uncommonly  occur  without  cystic  disease  of  the 

Hver. 

In  63  cases  of  cystic  kidneys  collected  by  Lezarsf  46,  or  73  per  cent.,  were  free 
from  cystic  change  in  the  liver.  In  90  cases  of  congenital  cystic  disease  of  the  kid- 
neys LuzzatoJ  found  five  in  which  the  liver  was  similarly  affected.  Still§  collected 
35"  cases  of  combined  cj'stic  change  in  the  liver  and  kidney,  of  which  3  were  in  in- 
fants. 

Concomitant  cysts  in  other  organs  have  been  described,  but  it  is 
doubtful  whether  any  importance  should  be  attached  to  the  obsen^ation. 

Age. — Multilobular  cystic  disease  is  usually  obser^-ed  comparatively 
late  in  life,  apart  from  the  rare  cases  seen  in  infants.  In  26  cases  collected 
by  StiU,  17  were  over  fifty,  and  4  over  seventy,  years  of  age;  the  youngest 
adult  case  was  thirty-nine. 

Sex. — ^The  female  sex  is  more  often  affected  than  the  male — according 
to  Still,  in  the  proportion  of  3  to  1 ;  21  of  his  28  cases  being  females. 

MORBID  ANATOMY. 

In  congenital  cystic  disease  in  infants  the  hver  is  in  a  majority  of 
the  few  recorded  cases  little  if  at  all  enlarged,  and  does  not  present  any 
manifest  naked-eye  evidence  of  cystic  change,  except  perhaps  a  few 
minute  cysts  on  the  surface  of  the  organ.  In  Porak  and  Couvelaire's  || 
remarkable  case  the  hver  was  so  large  that  it  impeded  dehvery  and  had 
to  be  tapped  before  the  foetus,  which  was  greatly  deformed,  could  be 
extracted.  On  section  the  fibrous  tissue  in  the  portal  spaces  is  consider- 
ably increased  in  amount ;  a  few  cystic  dilatations  may  appear,  but  most 
of  them  are  microscopic.  The  naked-eye  appearances  are  usually  more 
suggestive  of  fibrosis  than  of  cystic  change.  The  larger  bile-ducts  and 
the  gall-bladder  are  healthy. 

Probably  the  existence  of  combined  cystic  disease  of  the  kidney  and 
liver  is  sometimes  overlooked ;  the  kidney  change  is  well  marked,  while 
that  in  the  liver  may,  unless  examined  microscopically,  escape  detection. 
It  is  therefore  desirable  that  the  liver  should  always  be  examined  micro- 
scopically in  cases  of  cystic  disease  of  the  kidney.  The  contents  of  the 
cysts  are  clear  and  do  not  contain  bile. 

*  Bristowe,  J.  S.:    Trans.  Path.  Soc,  vol.  vii,  p.  229. 
t  Lezars:    These  Paris,  1888. 

I  Luzzato:   Quoted  bv  Boinet  and  Ravbaud,  Rev.  de  Med.,  Jan.  10,  1903. 
§  Still,  G.  F.:   Trans. "Path.  Soc,  vol.  xlix,  p.  155. 

II  Porak  and  Couvelaire:    Loc.  cit. 


CYSTIC   DISEASE   OF  THE   LIVER. 


447 


In  adult  cases  of  cystic  disease  the  liver  may  be  A-ery  greatly  en- 
larged, though  this  is  not  alwaj^s  the  case. 

A  cystic  liver  in  the  College  of  Surgeons  Museum  weighed  13  pounds  7  ounces, 
and  in  Roberts'*  case  Hi  pounds. 

A  cystic  liver  from  an  adult  woman  may  show  the  deformity  of  tight 
lacing.     (Vide  St.  Bartholomew's  Hosp.  Museum,  No.  2204  d.) 

The  degree  of  cystic  transformation  is  nearly  always  nmch  less  in 
the  hver  than  it  is  in  the  kidneys.  The 
kidneys  are  usually  megalocystic,  while  the 
cystic  hver  is  smaller  in  proportion.  The 
cj^sts  are,  however,  bigger  than  those  seen  in 
babies,  probably  from  the  fact  that  several 
cysts,  originally  separate,  have  united  to- 
gether. Their  size  varies  very  considerably; 
there  may  be  a  number  of  quite  small  ones, 
with  one  or  more  larger  ones.  In  cases 
where  the  hver  is  considerabh'  enlarged 
there  may  be  a  number  as  big  as  a  walnut. 
In  exceptional  instances  a  very  large  cyst 
may  be  formed.  • 

In  Cleaver' sf  case  there  were  many  small  cysts 
and  a  single  large  one  measuring  7  J  inches  in  cir- 
cumference. 

The  cysts  appear  on  the  surface  of  the 
organ  and  may  thus  give  rise  to  considerable 
deformity.  They  are  surrounded  by  a  cap- 
sule of  well-formed  fibrous  tissue.  On  sec- 
tion the  hver  is  more  or  less  honey-combed 
by  numbers  of  independent  cavities.  The 
C3"sts  usually  contain  clear  albuminous  fluid, 
which  is  sometimes  brovm,  probably  from 
haemorrhage.  They  contain  abundant  pro- 
teids,  urea,  chlorides,  and  sometimes  blood 
and  epithelial  cells,  cholesterin,  oxalate  of 
calcium,  leucin,  and  creatinin,J  but  not  bile. 
There  is  a  considerable  increase  in  the 
amount  of  fibrous  tissue  in  the  liver.  The 
large  bile-ducts  and  the  gall-bladder  are  free 
from  any  special  change. 

Microscopical  Appearances. — In  the  cystic  livers  of  newly  born 
infants  there  are  a  numl^er  of  tubules  in  the  portal  spaces  which  are 
lined  with  subcolumnar  pjiitlieliuin  and  are  somewhat  dilated.  They 
closely  resem])le  dilated   ])ile-ducts,   but   are  far  more    prominent  and 

*  Roberts:    Annals  of  Surgerv,  vol.  xix,'p.  251. 

t  Cleaver:    Philadelphia  Medical  .lourn.,' 1901,  p.  1139. 

J  Forbes,  J.  G.:   St.  Bartholomew'.^  Hospital  Reports,  vol.  xxxiii,  p.  207. 


V 


Fig.  55. — Sectiox  of  Cystic  Dis- 
ease   OF   THE    Liver   in   an 
Adult. 
The     liver     also     showed    a 

furrow     due      to     tight      lacing. 

(Photographed  by  Dr.  H.  Morley 

Fletcher.) 


448 


DISEASES   OF  THE   LIVER. 


appear  to  be  more  numerous  than  the  normal  bile-ducts.  They  may 
appear  completely  to  encircle  the  interlobular  vein.  From  the  portal 
space  these  dilated  tubes  can  be  traced  into  the  interlobular  tissue;  they 
are  accompanied  by  fairly  well-formed  fibrous  tissue.  These  epithelial 
extensions  between  the  lobules  are  at  first  somewhat  dilated,  but  as 
they  get  further  away  from  the  portal  space  they  tend  to  become  solid 
cyhnderS;  and  when  cut  obUquely,  may  appear  to  have  more  than  one 
layer  of  cells  lining  them.  There  are  never  any  masses  of  bile  in  these 
tubes  or  cysts. 

The  fibrosis  thus  tends  to  be  unilobular,  with  exaggerations  around 
the  larger  portal  canals ;  there  is  no  intercellular  cirrhosis  and  no  evidence 
of  congenital  syphilis.  In  places  blood  is  seen  to  be  extravasated  into 
the  substance  of  the  hepatic  lobules.     The  hver  cells  are  usually  well 

preserved ;  exceptionallj- 
they  have  been  found  to 
show  a  peculiar  change 
which  at  first  sight  might 
suggest  fatty  metamorpho- 
sis, but,  as  shown  by  the 
absence  of  staining  with 
osmic  acid,  this  is  not  the 
case.  On  the  other  hand, 
this  appearance  may  be 
explained  as  sections  of 
dilated  biliar}^  capillaries 
which,  having  invaginated 
or  indented  the  hver  cells, 
give  the  impression  of 
being  inside  the  cells. 

In  the  adult  form  the 
cysts  are  much  larger,  are 
surrounded  by  weU-formed 
fibrous  tissue,  wliile  there 
may  be   numerous  blood- 
vessels  in  the   immediate 
neighbourhood.      In     the' 
smaller  cysts  the  epithehum  is  colunmar,  in  the  medium-sized  cysts  it 
becomes  cubical  or  polyhedral,  and  in  the  larger  ones  it  is  either  absent 
or  represented  by  a  few  flattened  cells. 

In  exceptional  cases  ciliated  epithelium  has  been  described  in  the  cj^sts.* 

The  bile-ducts  in  the  hver  are  often  dilated  in  parts,  but  this  is  not 
constant.  The  hepatic  cells  are,  generally  speaking,  health}^,  but  may 
show  the  vacuolated  appearance  described  in  congenital  cases. 

Pye  Smitht  regarded  this  change  as  due  to  intracellular  cyst  formation  and  to 
be  a  degenerative  process  beginning  long  after  adult  life. 

*  Lezars:  These  Paris,  1888,  p.  34.     Hanot  et  Gilbert:  Maladies  du  foie,  p.  29.5. 
fPye  Smith:    Trans.  Path.  Soc,  xxxii,  p.  112,  1881. 


Fig.  56. — PHOTOMiCROGRArn  of  Congenital  Cystic  Dis- 
ease OF  THE  Liver. 
Shows  portal  space  with  increased  quantity  of  well- 
formed  fibrous  tissue  and  with  dilated  tubes  lined  bj' 
columnar  epithelium,  which  has  separated  from  the  walls 
in  the  process  of  hardening.  The  hepatic  cells  show 
vacuolation.      (By  Dr.  Harold  Spitta.) 


CYSTIC    DISEASE    OF   THE    LIVER.  449 

A  point  of  interest  is  the  connexion  between  congenital  cystic  disease 
and  the  similar  anatomical  condition  more  often  met  with  in  adults. 
They  are  so  similar  that  it  appears  reasonable  to  regard  the  adult  cases 
as  congenital  in  origin,  and  to  explain  the  survival  by  supposing  that 
the  change  in  the  hver  and  kidneys  is  less  extensive  than  in  those  rare 
cases  where  death  takes  place  in  infancy.  Still  regards  cystic  disease 
of  the  liver  as  a  malformation  which  is  not  progressive,  and  on  this  theory 
it  is  easy  to  understand  that,  if  the  subject  can  survive  the  early  effects, 
life  may  be  prolonged  for  years. 

PATHOLOGY. 

The  causation  of  cystic  disease  of  the  liver  has  given  rise  to  a  great 
deal  of  discussion,  and  various  theories  have  been  put  forward.  It  is  so 
generally  combined  with  similar  change  in  the  kidney  that  it  is  highly 
probable  that  whatever  the  causal  factor  is,  it  is  the  same  for  them  both. 
Pye  Smith,  it  should  be  noted,  considers  the  change  in  the  kidney  and 
in  the  liver  to  be  independent.  The  following  theories  may  be  referred 
to  as  bearing  on  the  causation  of  cystic  disease  of  the  liver. 

Inflammatory  Theory. — The  oldest  view  was  that  there  was  primary 
inflammation  of  the  fibrous  tissue  surrounding  the  bile-ducts,  which 
thus  led  to  dilatation  of  the  bile-ducts.  (Michalovicz,  Juhel,  Renoy, 
Babinsky.)  The  process  might  be  described  as  one  of  pericholangitic 
inflammation  leachng  to  a  bihary  cirrhosis  of  the  liver  with  dilatation 
of  the  bile-ducts.  It  might  perhaps  be  possible  to  explain  the  process 
as  a  fairly  acute  cholangitic  and  pericholangitic  inflammation  during 
fcBtal  life,  which  so  weakens  the  walls  of  the  small  ducts  that  they  then 
dilate  and  never  recover  their  proper  size,  while  the  inflammatory  products 
organise  into  firm  fibrous  tissue.  Further,  the  inflammation  might  be 
followed  by  epithelial  proliferation  and  the  formation  of  new  bile-ducts. 

This  explanation  of  the  change  in  the  liver  is  surrounded  with  diffi- 
culties. If  it  be  regarded  as  bihary  cirrhosis  with  subsequent  dilatation, 
a  form  of  ''epithehal  cirrhosis"  analogous  to  cystic  disease  of  the  breast, 
the  objection  at  once  arises  that  in  bihary  and  indeed  in  the  other  protean 
forms  of  cirrhosis  any  dilatation  of  the  ducts  is  of  extreme  rarity. 

A  further  objection  against  this  view  is  the  absence  of  jaimdice  in 
cystic  disease  of  the  liver  both  in  infants  and  in  adults,  while  in  con- 
genital obliteration  of  the  bile-ducts  where  there  is  an  intra-uterine  in- 
flammation of  the  intra-hepatic  bile-ducts,  practically  identical  with 
that  postulated  by  this  theory,  there  is  persistent  jaundice.  The  absence 
of  jaundice  is  rather  surprising,  whatever  theory  is  held  as  to  the  origin 
of  the  cysts,  for  if  they  are  not  obstructed  ducts  themselves,  but  inde- 
pendent formations,  the  real  ducts  should  be  pressed  upon.  This,  how- 
ever, can  hardly  occur,  for  there  is  no  bile-staining  of  the  liver  itself  or 
accumulations  of  inspissated  bile  in  microscopic  sections  of  the  liver. 
It  is  noteworthy  that  in  the  rare  condition  of  chronic  pericholangitis 
where  the  bile-ducts  must  be  compressed  there  is  no  trace  of  jaundice 
either  locally  in  the  liver  or  elsewhere;  it  is  possible  that  in  both 
29     ' 


450  DISEASES    OF   THE    LIVER. 

instances  this   anomaly  depends  on  the  lymphatics  being  obstructed 
so  that  bile  cannot  be  absorbed. 

Beale*  injected  the  larger  bile-ducts  in  Bristowe's  original  case  -nith  Prussian 
blue  and  found  that  no  injection  passed  into  the  cysts;  from  this  he  concluded  that 
the  formation  of  cysts  did  not  depend  upon  closure  of  a  part  of  the  tube  and  the 
subsequent  accumulation  of  secretion  bej'ond  this  point.  It  is  difficult  to  follow 
this  argument,  for  if  the  cysts  were  due  to  retention,  the  injection  \\-ould  not  be  able 
to  pass  the  obstruction  and  flow  into  the  cysts.  The  fact  that  injection  does  not 
pass  into  the  cysts  does  not,  however,  prove  that  the  cysts  are  unconnected  with 
the  bile-ducts,  for  Barrett, t  in  experiments  on  normal  livers,  found  that  when  the 
common  bile-duct  was  injected,  under  pressures  of  from  45  to  300  mm.  of  mercury 
(the  normal  pressure  under  which  bile  is  secreted  being  20  to  45  mm.  of  mercury), 
with  gelatine,  none  of  the  injection  passed  into  the  bile  canahculi. 

Theory  that  the  Cysts  are  a  New  Formation. — RindfleischJ  be- 
hevecl  the  C3'stic  change  to  be  a  cystic  sarcoma  starting  from  the  bile- 
ducts.  A  number  of  authors  have  regarded  the  changes  in  the  ducts 
as  of  an  adenomatous  nature  (Nauwerck  and  Hufschmidt.§  Workman,  || 
V.  Kahlden).  Malassez**  and  Claude  ff  considered  that  the  disease  was 
a  cystic  fibro-adenoma  homologous  to  an  ovarian  cystadenoma.  Claude 
regarded  the  cysts  as  dilated  new  bile-ducts  and  behoved  that  the  process 
had  a  special  relation  to  arteriosclerosis.  Sabourin,JJ  who  has  paid 
much  attention  to  this  subject,  describes  cj^stic  disease  of  the  liver  as  a 
cavernous  biliary  angioma,  and  regards  it  as  due  to  irritation  which 
leads  to  development  of  new"  bile-ducts  from  various  sources,  such  as 
preexisting  bile  canalicuh,  possibly  from  their  mucous  glands  or  from 
vasa  aberrantia.  The  ducts  thus  formed  unite,  anastomose,  dilate,  and 
lead  to  the  formation  of  larger  ones  by  the  destruction  and  absorjDtion 
of  the  inter\'ening  septa. 

Degenerative  Theories. — Pye  Smith,§§  in  his  case  of  combined  cystic 
disease  in  the  kidneys  and  hver  in  a  man  aged  fifty-three,  described 
vacuolation  of  the  hver  cells.  The  vacuoles  began  in  the  protoplasm, 
one  or  more  occurring  in  the  same  cell;  these  joined,  and  by  fusion  with 
those  formed  by  other  ceUs  led  to  the  formation  of  cysts.  This  change 
he  regarded  as  originating  long  after  adult  hfe  had  been  reached.  This 
appearance  may  be  seen  in  congenital  c^'stic  disease  of  the  liver.  The 
vacuoles  are  probably  sections  of  dilated  bile  capillaries  invaginating  the 
liver  cells.  PillietJUl  regards  cystic  disease  as  a  result  of  atrophy  of  the 
liver  in  which  the  hver  cells  become  changed  into  newly  formed  bile- 
ducts  and  vasa  aberrantia.  These  tubes  by  dilatation  give  rise  to  the 
multiple  cysts. 

Developmental  Theory. — Still  has  put  forward  with  great  ingenuity 

*  Beale,  L.:   Trans.  Path.  Soc,  vol.  vii,  p.  234. 

t  Barrett,  W.:    Jour.  Path,  and  Bact.,  vol.  v,  p.  345. 

+  Rindfleisch:    Lehrb.  d.  path.  Gewebeleh.,  S.  403. 

§  Nauwerck  and  Hufschmidt:    Ziegler's  Beitrage,  Bd.  xii,  S.  1. 

!l  Workman:    Glasgow  Hospital  Reports,  vol.  ii,  p.  363,  1900. 
**Malassez:    Progres  Medical,  April  5,  1876. 
It  Claude:    Bull.  Soc.  Anat.  Paris,  1S96,  p.  117. 

JtSabourin:    Archiv  de  Phvsiol.,  vol.  xiv.  • 

§§  Pve  Smith:    Path.  Trans"!,  vol.  xxxii,  p.  112,  ISSI. 
IlllPilliet:    Tribune  Medical,  1893. 


CYSTIC    DISEASE    OF   THE    LIVER.  451 

a  theor}^  which  is  on  the  same  hnes  as  Shattock's  *  \iew  of  the  nature 
of  cj^stic  kidne3's.  According  to  the  latter  \dew,  the  mesonephros  per- 
sists and  its  dilated  tubules  form  the  cysts,  while  the  metanephros  or 
real  kidney  is  blended  with  and  compressed  by  the  foetal  persistence. 
In  the  case  of  the  liver,  Still  t  supposes  that  some  of  the  columns  of 
hypoblastic  cells  forming  part  of  the  original  duodenal  diverticulum 
develop  irregularty  and  form  the  cystic  tubes,  while  the  bile-ducts  proper 
develop  in  the  ordinar}-  way  and  can  be  seen  in  the  portal  spaces.  The 
excess  of  fibrous  tissue  he  regards  as  a  persistence  of  foetal  mesoblastic 
stroma  and  not  inflammator>^  In  other  words,  the  change  is  a  mal- 
formation, and  is  therefore  not  necessarily  progressive.  Hence  if  death 
does  not  happen  to  occur  in  early  life,  the  cystic  change  may  be  found 
as  a  persistent  condition  in  the  adult  cases.  The  close  association  with 
cystic  kidneys,  also,  according  to  Shattock's  view,  a  malformation,  is 
thus  rendered  intelligible.  It  is  also  significant  that  other  malformations 
may  coexist.  Thus  in  one  case  the  remarkable  association  of  poly- 
dactyhsm,  occipital  meningocele,  and  webbed  toes  was  found;  in  another 
a  misplaced  kidney;  in  another  an  undescended  testis;!  and  in  several 
more  polyclactylism.  These  external  malformations  are  not  met  "udth 
in  adult  cases,  and  are  not  constant  in  the  cases  fatal  at  birth.  It  may 
reasonably  be  supposed  that  the  cases  in  which  the  de^'elopmental  defects 
are  comparatively  slightly  marked  persist  to  adult  life. 

This  theorv^  depends  on  the  demonstration  of  the  normal  bile-ducts 
by  the  side  of  the  cystic  spaces.  If  this  is  not  proved,  and  it  has  not 
appeared  to  me  that  it  is  thoroughly  established,  the  spaces  may  stiU 
be  regarded  as  dilated  bile-ducts,  for  in  any  case  the  spaces  and  the 
bile-ducts  arise  from  a  common  source — the  duodenal  diverticulum.  The 
objections  to  the  hypothesis  that  the  spaces  are  dilated  bile-ducts,  viz., 
the  absence  of  jaundice  and  the  fact  that  injection  driven  into  the  larger 
bile-ducts  does  not  enter  the  cysts,  have  been  already  considered. 

Most  ■v\Titers  accept  Still's  explanation,  but  personally  I  am  not  con- 
vinced that  this  view  is  more  tenable  than  that  cystic  disease  of  the 
liver  is  due  to  some  special  form  of  foetal  cholangitis  and  pericholangitis. 


CLINICAL  PICTURE. 

Cystic  disease  of  the  liver  gives  rise  to  no  characteristic  symptoms 
and  is  usually  only  found  as  a  postmortem  surprise.  Its  presence,  how- 
ever, may  be  suspected  in  a  patient  with  greatly  enlarged  and  probably 
cystic  kidneys  who  has  vague  ursemic  symptoms  and  considerable  enlarge- 
ment of  the  liver.  In  rare  instances  the  cysts  in  the  liver  may  be  so 
large  that  they  imitate  hydatid  or  ovarian  cysts.  In  .Schrocder's  case 
the  abdomen  was  so  widely  occupied  by  the  cystic  liver  that  double 
multilocular  ovarian  cysts  were  diagnosed.  A  single  large  cyst  may 
imitate    a    dilated    gall-bladder.     (Cleaver.)     In    practically    all    cases 

*  Shattock,  S.  G.  :    Trans.  Path.  Soc.  vol.  xxxvii,  p.  2S7. 
t  Still:   Trans.  Path.  Soc,  vol.  xlix,  p.  1.55. 
t  Cases  quoted  by  Still,  ibid.,  p.  164. 


452  DISEASES   OF  THE   LIVER. 

symptoms  pointing  to  the  liver  are  absent,  and  death,  if  not  due  to  some 
intercurrent  affection,  is  from  uraemia.  The  cystic  kidneys  may  be  felt 
in  life  and  sometimes  have  been  regarded  as  hydronephroses,  or  even  as 
pyonephroses. 

A  woman  aged  thirty-five  was  admitted  into  St.  George's  Hospital  on  October 
S,  1902,  with  pain  of  one  week's  duration  on  the  left  side  of  the  abdomen,  where  a 
soft,  obscurely  fluctuating  tumor  could  be  felt  in  the  region  of  the  kidney.  There 
was  pus  in  the  urine,  but  no  fever  or  leucocytosis.  There  had  been  dragging  pain 
in  the  back  from  time  to  time  and  increased  frequency  of  micturition,  especially 
at  night,  for  nine  years.  An  exploratory  operation  by  Mr.  AUingham  showed  that 
both  kidneys  contained  a  large  number  of  cysts  of  considerable  size,  and  that  the 
liver  also  contained  a  large  number  of  cysts.  A  small  piece  of  the  liver  containing 
some  smaU  cysts  was  removed.  I  examined  it  microscopically  and  found  that  the 
cyst  walls  were  composed  of  well-formed  fibrous  tissue  and  that  in  the  immediate 
neighboxirhood  the  liver  tissue  showed  fibrosis  around  the  portal  spaces.  No  epi- 
thelial or  other  lining  could  be  found  in  the  cysts. 

Polydactylism  and  other  external  malformations  are  present  in  a 
majority  of  the  cases  seen  in  the  newly  born,  but  are  not  met  with  in 
adult  cases.  In  the  congenital  case  described  by  Kanthack  and  myself 
the  infant,  aged  one  month,  was  universally  oedematous,  had  a  large 
quantity  of  albumin  in  the  urine,  and  was  extremely  drowsy,  as  if 
ursemic. 

The  treatment,  if  the  condition  be  suspected,  is  that  of  chronic  renal 
disease,  the  object  being  to  prevent  uraemia.  Opening  the  cysts  in  the 
course  of  laparotomy  has  been  done,  but  is  useless,  and  should  be  avoided 
if  the  condition  is  recognised. 


ADENOMA. 

The  subject  of  adenoma  may  be  considered  under  the  two  heads  of 
(I)  single  adenoma,  (II)  the  so-called  multiple  adenomata  which  are 
nearly  always  found  in  association  with  advanced  cirrhosis  of  the  Uver. 

SINGLE  ADENOMA. 

An  innocent  encapsulated  growth  of  epithelial  ceUs  may  occur  in 
the  liver,  but  is  decidedly  rare;  pathologically  they  are  of  great  interest, 
but  clinically  they  seldom  attract  attention. 

True  adenomata  may  theoretically  be  divided  according  to  their 
structure  into :  (I)  those  composed  of  liver  cells,  or  of  cells  derived  from 
the  ordinary  cells  of  the  hepatic  parenchyma ;  (II)  those  derived  from  the 
bile-ducts;   (III)  those  due  to  the  inclusion  of  adrenal  "rests." 

I.  Solitary  Adenomata  Derived  from  the  Liver  Cells. — An  adeno- 
matous tumor  composed  of  liver  cells,  apart  from  the  multiple  growths 
of  this  kind  seen  in  association  with  cirrhosis,  is  rare.  Such  growths  may 
be  spoken  of  as  "acinous  adenomata"  in  contradistinction  to  those  de- 
rived from  the  bile-ducts,  or  as  "solitary  adenomata"  in  order  to  dis- 
tinguish them  from  multiple  adenomata. 

Barbacci,*  who  has  collected  twelve  examples  of  single  adenomata, 
finds  that  they  occur  equally  in  the  two  sexes,  and  that  the  extremes  of 
age  are  two  and  sixty-nine  years. 

Mahomedf  described  a  localised  collection  of  cells  surrounded  by  a  fibrous 
capsule  embedded  in  the  liver,  which  was  "nutmeg";  the  tumor  did  not  share  in 
this  general  change.  I  have  seen  one  similar  specimen.  There  is  a  specimen  (22236) 
of  a  single  necrotic  adenoma  in  St.  Bartholomew's  Hospital  Museum.  Hale  Whitej 
refers  to  an  adenoma,  1\  inches  in  diameter,  projecting  from  the  surface  of  the  liver 
in  the  Guy's  Hospital  Museum.  Specimens  have  also  been  described  by  Engelhardt§ 
and  others. 

Possibly  these  tumors,  which  are  pathological  curiosities,  may  be  due 
to  some  piece  of  liver  substance  which  was  separated  during  foetal  life 
from  the  main  mass  of  the  liver,  becoming  subsequently  embedded  in 
the  organ.  Not  infrequently  small  projections  of  liver  substance,  minia- 
ture lobes,  are  seen  on  the  under  surface  of  the  liver;  if  these  became 
implanted  in  the  substance  of  the  liver,  the  appearance  of  an  encapsulated 
adenoma,  composed  of  liver  cells,  would  be  produced. 

Cristiani  ||  refers  to  the  existence  of  multiple  nodules  of  hepatic  tissue  embedded 
under  Glisson's  capsule,  which  have  been  explained  as  congenital  and  due  to  the 
inclusion  of  tiny  lobes.     Pepere**  supports  the  congenital  origin  of  solitary  adenoma 

*  Barbacci:    La  Clin.  Mod.,  An.  6,  No.  38,  Sept.  19,  1900. 
t  Mahomed:    Trans.  Path.  Soc,  vol.  xxviii,  p.  144. 
t  Hale  White:    Allbutt's  System  of  Med.,  vol.  iv,  p.  210. 
§  Engelhardt:   Dcutsch.  Archiv  f.  klin.  Med.,  Bd.  Lx,  S.  607. 
ii  Cristiani:   Journ.  de  I'Anat.  et  Physiol.,  1891,  p.  271. 
**  Pepere:    Archivio  per  le  Scienze  Mediche,  vol.  xxvi,  p.  117,  1902. 

453 


454  DISEASES    OF  THE   LIVER. 

and  describes  a  case  in  which  there  were,  in  addition  to  one  in  the  liver,  innumerable 
minute  encapsulated  masses  of  liver  tissue  scattered  over  the  peritoneum  and 
omentum. 

A  simple  adenoma  is  nearly  always^solitary ;  it  is  very  rare  that  sev- 
eral are  seen  in  the  same  liver.  Multiple  adenomata  are  nearly  always 
accompanied  by  multilobular  cirrhosis,  and  may  be  regarded  as  secondary 
to  that  condition  and  in  the  Mght  of  compensatory  hyperplasias  of  the 
liver  cells.  A  few  examples  of  multiple  adenoma  without  preexisting 
cirrhosis  are  referred  to  on  page  455. 

In  exceptional  cases  a  solitary  adenoma  is  found  in  a  cirrhotic  liver.  Among 
twenty  cases  of  solitary  adenoma  collected  by  Caminiti,*  four  were  associated  with 
cirrhosis  (Jona,t  Delaunay,|  and  two  of  his  own).  Possibly  in  some  cases  the  as- 
sociation is  a  mere  coincidence,  Delaunay's  case  of  a  columnar-celled  growth  being 
probably  of  this  nature.  But  in  most  cases  it  is  probable  that  a  "solitary  adenoma" 
in  a  cirrhotic  liver  is  only  the  initial  stage  of  the  multiple  adenomata  in  cirrhosis. 
I  have  seen  two  cases  bearing  this  interpretation. 

Morbid  Anatomy. — The  tumor,  often  the  size  of  a  walnut,  projects 
from  the  surface  of  the  liver  and  is  encapsuled.  It  is  a  yellowish  or 
greenish  white  on  section,  and  of  the  same  consistence  as  normal  hver, 
but  does  not  share  in  any  change,  such  as  chronic  venous  engorgement, 
affecting  the  liver  as  a  whole. 

Microscopically  the  tumor  is  composed  of  liver  cells  which  may, 
probably  when  the  tumor  is  of  some  standing,  be  so  modified  as  to  form 
tubules  hned  by  cubical  epithehum,  and  in  this  respect  resemble  the 
structure  of  carcinoma  with  cirrhosis.  The  cubical  character  of  the 
cells  distinguishes  this  form  of  adenoma  from  the  adenomata  derived 
from  the  bile-ducts  or  from  the  mucous  glands  in  their  walls.  In  most 
cases  the  solitary  adenoma  derived  from  the  liver  cells  is  composed  of 
cells  of  various  sizes,  but  showing  a  general  resemblance  to  the  liver 
cells.  There  is  no  definite  arrangement,  but  there  are  capillaries  and 
some  strands  of  fibrous  tissue  running  through  the  tumor. 

There  are  no  clinical  symptoms  referable  to  this  form  of  adenoma. 

II.  Adenomata  Derived  from  the  Bile-ducts. — A  papilloma  spring- 
ing from  the  inside  of  the  extra-hepatic  bile-ducts  would  come  under 
this  heading,  but  is  dealt  vni\\  elsewhere.  {Vide  p.  681.)  In  this  para- 
graph reference  will  be  made  to  tumors  arising  from  the  intra-hepatic 
bile-ducts,  indenting  and  displacing,  but  not  invading,  the  surrounding 
liver  substance;  they  may  be  described  as  tubular  adenomata  hned  by 
columnar  cells.  It  is  possible  that  siixiilar  adenomata  may  be  derived 
from  the  mucous  glands  in  the  wahs  of  the  larger  bile-ducts.  They  may 
be  single  or  multiple. 

A  single  adenoma  derived  from  the  bile-ducts  may  become  cystic; 
Leppmann^  has  coUected  nine  cases  of  this  kind;  under  these  conditions 
the  adenoma  may  reach  such  a  size  that  it  may  imitate  malignant  disease 
or  hydatid  cyst  of  the  liver,  or  a  floating  kidney.     The  nature  of  such 

*  Caminiti:   Archiv  f.  klin.  Chirurg.,  Bd.  Ixix,  S.  630. 

t  Jona:   Gazzetta  d.  Ospidali,  1901,  No.  9. 

X  Delaunay:    Bull.  Soc.  Anat.  Paris,  1876,  p.  241. 

§  Leppmann:    Deutsche  Zeitschrift  f.  Chirurg.,  Bd.  liv,  S.  440,  Fob.,  1900. 


ADENOMA.  455 

tumors   can  only  be  determined  b}'  laparotomy.     Cases  of  this  kind 
have  been  recorded  by  Keen,  Shattuck,  Schmidt. 

Keen*  removed  a  cystic  adenoma,  thought  to  be  derived  from  the  bile-ducts, 
from  a  woman  aged  thirty-one  in  ISOi,  who  was  ahve  in  1899.  Clinically  it  was 
thought  to  be  a  floating  kidney. 

Shattuck's  t  case  is  well  worth  quoting:  A  woman  aged  sixtj^-three  pre- 
sented a  tumor  reaching  from  the  right  costal  arch  to  the  iliac  crest.  It  was 
smooth,  not  tender,  and  presented  a  fluctuating  area  in  the  centre.  At  the 
laparotomy  a  cyst  containing  a  gallon  of  clear  fluid  was  found  and  drained. 
After  some  time  bile  came  away  from  the  sinus.  A  second  operation  was  fol- 
lowed by  death  from  cardiac  failure.  At  the  autopsy  the  cyst  was  found  to 
arise  from  the  liver  near  the  falciform  ligament  and  to  have  displaced  the  liver 
downwards.  Microscopically  the  cyst  Avail  showed  numerous  ducts  and  minute 
cysts,  and  it  was  regarded  as  a  cystadenoma  and  not  as  a  simple  retention  cyst. 

It  is  quite  possible  that  single  adenomata  of  the  bile-ducts  of  large 
size  are  sometimes  regarded  as  cases  of  primary  carcinoma  of  the  hver. 

Peugniez  J  operated  upon  a  woman  aged  fifty-nine  for  a  tumor  diagnosed 
as  a  gall-bladder;  an  encapsuled  tumor  the  size  of  the  fist  was  removed  and 
the  patient  recovered.  The  tumor  was  regarded  as  a  primary  massive  carcinoma 
of  the  liver,  but  the  description  and  figures  given  are  quite  compatible  with  the 
view  that  it  was  a  large  adenoma  of  the  bile-ducts,  like  Keen's  case.     f^aiaSuAl  .>ul 

Multiple  adenomata  derived  from  mucous  membrane  of  the  bile-ducts 
are  occasionally  met  with  (v.  Hippel§).  They  may  undergo  cystic 
change,  as  in  a  remarkable  case  of  Sigmund's  ||  in  a  woman  aged  sixty- 
five.  As  has  been  pointed  out  (vide  p.  450),  multiple  cystic  disease  of 
the  liver  has  been  regarded  by  Malassez,  Claude,  and  others  as  a  fibro- 
adenomatous  growth  of  the  bile-ducts. 

III.  Adenoma  Due  to  Included  Accessory  Adrenal  Bodies. — 
Schmorl**  and  Oberndorfer  ft  have  shown  that  accessory  adrenal  bodies 
are  sometimes  found  embedded  in  the  substance  of  the  liver.  Schmorl 
found  them  in  4  out  of  510  bodies.  A  case  of  an  encapsuled  tumor  of 
the  liver  derived  from  an  included  suj^rarenal  ''rest"  has  been  described 
by  Schmorl,  and  it  is  probable  that  the  development  of  simple  adenomata 
in  accessory  suprarenal  bodies  implanted  in  the  liver  is  not  a  very  rare 
event,  although  only  one  has  been  described.  PeperetJ  has  described  a 
primary  malignant  tumor  of  the  liver  arising  in  an  accessory  suprarenal 
body. 

MULTIPLE  ADENOMATA  OF  THE  LIVER. 

Synonyms:    Nodular  Hyperplasia;    Nodular  Hepatitis. 

Multiple  adenomata  of  the  liver  due  to  multiplication  or  hyj^erplasia 
of  the  liver  cells  are  usually  found  in  association  with  cirrhosis  of  the  liver. 

*  Keen,  W.  W.:  Boston  Medical  and  Surgical  Jour.,  1902,  vol.  i,  p.  804.  Annals 
of  Surgery,   1899,  p.   267. 

t  Shattuck:    Boston  Medical  and  Surgical  Journ.,  April  26,  1900,  p.  427. 

i  Peugniez:     Bull.   Soc.   Anat.  Paris,    1902,   p.   456. 

§  V.  Hippel:    Virchow's  Archiv,  Bd.  cxxiii,  S.  473. 

II  Sigmund:    Virchow's  Archiv,  Bd.  cxv,  S.  155. 
**  Schmorl:    Ziegler's  Beitrage,  Bd.  ix,  S.  523,  1891. 

tt  Oberndorfer:  Centralblatt  f.  allg.  Path.  u.  path.  Anat.,  Bd.  xi,  S.  145,  1900. 
it  Pepere:    Archiv.  de  M6d.  Experimental  et  d'Anat.  path.,  1902,  p.  765. 


456  DISEASES    OF   THE    LIVER. 

This  is  probably  because  cirrhosis  is  the  commonest  disease  which  destroys 
the  Hver  cells  and  renders  a  compensatory  hyperplasia  necessar}^;  but 
considerable  discussion  has  taken  place  as  to  the  relationship  between 
cirrhosis  and  adenomata.  Nodular  Mq^erplasia  may  be  met  T\'ith  in 
the  absence  of  cirrhosis,  as  in  some  cases  of  malarial  infection,  occasionaUy 
in  cases  of  acute  yellow  atrophy  which  nm  a  protracted  course,  and  in 
rare  cases  of  chronic  venous  engorgement  of  the  Hver.  The  terms  "nod- 
ular cirrhosis"  and  "cirrhosis  comphcated  with  adenoma,"  though  de- 
scriptive of  the  vast  majoritj^  of  multiple  adenomata,  from  h}^erplasia 
of  the  liver  cells,  cannot  be  used  as  synonyms  for  multiple  adenomata. 

J.  Bartels  *  draws  a  distinction  betw^een  multiple  adenomata  which 
are  surrounded  by  a  fibrous  capsule,  and  nodular  hyperplasia  where 
there  is  no  capsule. 

Relationship  of  Multiple  Adenomata  and  Cirrhosis. — Kelsch  and 
Eaener, j  and  more  recently  Dieulafoy  and  Engelliardt.J  believe  that  the 
cirrhosis  and  the  adenomata  are  due  to  the  same  poison  and  are  the 
concomitant  results  of  proliferation  of  the  framework  and  of  the  cells 
of  the  liver  respectively.  Dieulafoy  §  regards  the  two  processes  as  not 
only  independent,  but  simultaneous.  In  support,  of  this  it  may  be 
urged  that  in  dogs  tumors  due  to  hyperplasia  of  the  hver  cells,  and  prob- 
ably set  up  by  infection,  are  far  from  rare;  here  the  irritation  attacks 
the  epithehal  instead  of  the  fibrous  parts  of  the  organ.  A  condition 
aUied  to  this  is  seen  in  the  Fuegians  as  the  result  of  eating  mussels,  wliich 
at  certain  periods  of  the  year  contain  a  chemical  poison;  the  Uver  shows 
enlargement  due  to  hyperplasia  of  the  hver  cells  and  subsequently 
becomes  cirrhotic.  (Segers.  ||)  As  the  result  of  injection  of  the  blasto- 
mycetes,  regarded  as  the  j^arasite  of  cancer  by  San  Felice,  Wlaeff**  pro- 
duced adenomatous  tumors  in  the  livers  of  giiinea-pigs.  Areas  of  circum- 
scribed hjT^erplasia  of  the  liver  cells  are  described  in  the  hver  in  some 
cases  of  malaria  and  have  been  seen  in  a  nutmeg  liver.  (Jacobi,tt 
Earl.U) 

A  man  aged  thirty-seven  died  in  St.  George's  Hospital  in  February,  1903, 
wdth  advanced  pulmonary  tuberculosis  and  tuberculous  peritonitis.  The  liver 
was  at  first  thought  to  be  stuffed  with  caseous  tubercles.  Microscopically  these 
white  areas  were  found  to  be  multiple  adenomata;    the  liver  showed  no  cirrhosis. 

Cornil  and  Ranvier  §§  and  Schmieden  ||  ||  regarded  the  adenomata  as  a 
comphcation  of  and  secondarj^  to  cirrhosis  of  the  hver.  Brissaud*** 
described  multiple  adenomata  as  a  hah-way  house  between  cirrhosis 
and  primary  carcinoma,  and  the  term  "hepatoma"  was  suggested  by 

*Wien.  khn.  Wochen.,  1904,  S.  613. 

t  Kelsch  and  Kiener:    Archiv  de  PhvsioL,  1S76.  p.  622. 

t  Engelhardt:    Deutsches  Archiv  f.  klin.  Med.,  Bd.  Ix,  1S9S. 

§  Dieulafov:    Manuel  de  path.   Intern.,  tome  ii,   734,   1901. 

II  Segers:    La  Sem.  Med.,  p.  448,  1891. 
**Wlaeff:    Journ.  de  Med.,  Paris,  Jan.  20,  1901,  p.  27. 
ft  Jacobi,  A.:    Trans.  Assoc.  American  Physicians,  a'oI.  xii,  p.  493. 
JJEarl:    Lancet,   1902,   vol.   ii,   p.   1464. 

§§  Cornil  et  Ranvier:    Manuel  d'histologie  pathologique    tome  ii,  p.  438. 
nil  Schmieden:    Virchow's  Archiv,   Bd.   clix,   S.   290. 
***  Brissaud:    Archiv.  General,  de  Med.    1885,  tome  ii. 


ADENOMA,  457 

Sabourin*  to  describe  the  transitional  stage  between  adenoma  and  car- 
cinoma. Lancereauxf  took  the  extreme  view  that  cirrhosis  was  due  to 
irritation  set  up  by  tlie  presence  of  the  adenomata. 

There  is  some  confusion  in  hterature  between  cirrhosis  with,  multiple 
adenomata  and  primary  carcinoma  with  cirrhosis.  It  appears  that 
Sabourin,  who  uses  the  former  term,  is  sometimes  describing  cases  which 
Hanot  and  Gilbert  would  call  primary  carcinoma  with  cirrhosis.  The 
innocent  condition  of  multiple  adenoma  in  cirrhosis  may  eventually 
pass  into  primary  carcinoma.  When  this  occurs,-  there  will  be  evidence 
of  the  growth  infiltrating  the  walls  of  the  portal  or  hepatic  veins  or  of 
secondary  growths  in  the  lungs  or  elsewhere. 

Nature  of  Multiple  Adenomata. — These  multiple  adenomata  are 
nearly  always,  at  any  rate  in  England,  associated  "with  cirrhosis.  Some 
reservation  is  necessary,  since  nodular  hyperplasia  or  multiple  adenoma- 
tous formations  are  found  in  cases  of  chronic  malarial  infection,  and 
exceptionally  under  other  conditions  already  mentioned.  The  multiple 
adenomata  ordinarily  met  with  are  exaggerations  of  the  hobnails  seen 
in  portal  cirrhosis,  and  represent  a  further  stage  of  nodular  hyperplasia. 
Multiplication  of  the  more  healthy  liver  cells  occurs  in  common  or  portal 
cirrhosis  and  contributes  to  the  size  of  the  hobnails  and  to  the  increased 
weight  of  the  liver  in  latent  cirrhosis.  It  is  when  these  hobnails  undergo 
fatty  degeneration  and  necrosis,  and  appear  white  on  section,  that  thej^ 
are  particularly  liable  to  attract  attention,  for  when  this  change  has 
occurred  they  do  not,  unless  bile-stained,  suggest  cirrhosis,  but  resemble 
multiple  new-growths  or  even  caseous  tubercles.  Fatty  change  and 
necrosis  of  the  hyperplastic  nodules  are  particularly  likely  to  occur 
when  thrombosis  of  the  portal  vein  is  superadded  to  cirrhosis;  hence 
the  frequency  with  which  portal  thrombosis  is  recorded  as  associated 
with  multiple  adenoma,  cancer  with  cirrhosis,  etc.  Thus  in  15  cases 
of  so-called  adenoma  of  the  liver  that  were  analysed  by  Dr.  L.  Powell,  J 
no  less  than  9  had  thrombosis  of  the  portal  vein. 

Those  who  regard  the  condition  as  one  of  primary  carcinoma  of  the 
liver  adduce  the  presence  of  hepatic  cells  in  the  portal  vein  and  throm- 
bosis as  further  proof  of  its  malignant  character.  But  the  presence  of 
some  hepatic  cells  in  the  portal  vein  does  not  absolutely  prove  that  the 
growth  is  malignant,  for  the  hobnails,  being  poorly  nourished  and  having 
by  rapid  proliferation  outgrown  their  blood-supply,  soften  do^wn  and 
may  discharge  into  the  portal  vein  or  hepatic  veins,  and  so  induce  throm- 
bosis. Microscopic  examination  of  the  thrombus  shows  badly  foniied 
blood-clot  with  debris  and  large  fatty  liver  cells. 

Del^pine§  drew  attention  to  this  discharge  of  softened  adenomata  into  the 
portal  and  hepatic  veins,  and  F.  C.  Turner  1|  described  liver  cells  and  frag- 
ments of  liver  tissue  in  the  portal  veins  of  cirrhotic  livers  and  suggested  that  it 

*  Sabourin:    Th^se  Paris,  1881.     Rev.  de  M6d.,  1884,  p.  .321. 

t  Lancereaux:    Gaz.  M6dicale,  1868. 

t  Unpublished  Thesis  for  M.  B.  degree,  Cambridge,  1895. 

§  Delepine,  S.:    Trans.  Path.  Soc,  vol.  xli,  p.  363. 

II  Turner,  F.  C:    Ibid.,  xxxv,  p.  22;    and  vol.  xxxvii,  p.  262 


458  DISEASES   OF  THE   LIVER. 

was  due  to  damage  of  the  vessel  walls  by  the  septic  process  which  was  present 
in  both  his  cases. 

The  proliferation  of  the  liver  cells  may  be  due  to  one  of  two  causes, 
and  very  possibly  to  each  of  the  causes  at  different  stages  of  the  disease : 

(I)  The  multiplication  of  the  hepatic  cells  in  the  hobnails  may  be  set 
up  by  the  same  poison  that  stirs  up  the  connective  tissue  of  the  liver  to 
prohf eration ;  this  would  be  the  case  especially  in  the  early  stages  of 
the  disease.  In  cases  of  poisoning  by  mussels  similar  nodules  are  pro- 
duced, evidently  directly  due  to  the  irritation  exerted  by  the  poison. 

(II)  The  multiplication  of  the  liver  cells  may  be  an  attempt  at  com- 
pensation to  make  good  the  functional  activity  of  the  liver  as  a  whole, 
which  has  been  greatly  reduced  by  the  destruction  of  hepatic  tissue. 

In  favour  of  the  view  that  the  change  is  compensatory  are  the  facts : 

(a)  that  the  adenomatous  formations  are  found  in  portal  cirrhosis,  where 
degeneration  and  destruction  of  the  liver  cells  are  marked  features,  and 

(b)  that  they  are  absent  in  hypertrophic  biliary  cirrhosis,  where  the  liver 
'cells  retain  their  vitahty  for  a  long  time. 

Compensatory  hyperplasia  of  the  Uver  cells  occurs  in  the  most  diverse  con- 
ditions, which  all  have  only  one  factor  in  common,  viz.,  interference  with  the 
functional  activity  or  destruction  of  the  liver  cells,  The  effects  of  removal  of 
portions  of  the  liver  in  animals  ha^-e  been  investigated  by  Tizzoni,  Ponfick,* 
V.  Meister,  Floeck,  Zadoc-Kahn,t  and  others.  Proliferation  begins  and  is  most 
active,  probably  because  nutrition  is  best  there,  in  the  liver  cells  at  the  periphery 
of  the  lobules.  The  compensatory  hyperplasia  in  cirrhosis  is  of  two  kinds: 
(i)  the  earlier  gives  rise  to  the  formation  of  the  so-called  new  bile-ducts;  (ii) 
the  other,  which  occurs  later,  is  that  seen  in  the  so-called  adenomata. 

When  multiple  adenomata  in  cirrhosis  are  seen  at  the  autopsy  of 
fatal  cases  of  cirrhosis,  the  compensatory  mechanism  has  in  most  cases 
broken  down,  and  is  often  explained  by  thrombosis  of  the  portal  vein 
The  compensation  may  also  be  nullified  by  degenerative  processes, 
fatty  change  or  softening  in  the  hyperplastic  hobnails,  or  by  fibrosis 
spreading  into  them.  No  doubt  the  large  size  of  hvers  in  latent  cirrhosis 
is  partly  due  to  this  compensatory  hyperplasia  of  the  liver  cells.  (See 
also  Prognosis  of  Portal  Cirrhosis.)  Nodular  cirrhosis  is  not  very  infre- 
quently seen  in  cases  fatal  from  puhnonary  tuberculosis,  and  may  be 
looked  upon  as  a  compensated  cirrhosis.  In  such  cases,  if  fatty  degenera- 
tion attacks  the  hobnails,  an  appearance  suggesting  caseation  results ;  it 
is  quite  possible  that  a  naked-eye  examination  of  the  liver  might  re- 
sult in  a  diagnosis  of  extensive  tubercle  or  new-growth  of  the  organ. 

Morbid  Anatomy. — The  appearance  of  the  liver  is  verj^  striking  and 
suggests  multiple  secondary  new-growths,  gummata,  or  even  caseous 
tubercle.  The  surface  of  the  fiver  shows  numerous  projecting  nodules, 
which,  however,  are  not  umbificated.  They  are  white  on  section,  usually 
dry  and  friable,  but  may,  especially  when  associated  with  portal  throm- 
bosis, be  softened.  The  surrounding  liver  substance  may  be  deeply  con- 
gested, so  that  the  contrast  between  the  hobnails  and  the  rest  of  the 
liver  still  further  suggests  secondary  malignant  disease.     Adenomata  in 

*  Ponfick:    Virchow's  Archiv,   Bd.   cxviii,   cxix. 
tZadoc-Kahn:    Archiv.  General,  de  Med.,  1897,  p.  165. 


ADENOMA.  459 

children  with  cirrhosis  may  be  extremely  prominent,  and  to  the  naked 
eye  very  closely  resemble  malignant  disease;  probably  this  active  pro- 
liferation is  part  of  a  child's  inherent  power  of  repair  and  growth.  The 
liver  is  usually  enlarged,  and  sometimes  to  a  very  great  extent.  It  is 
only  rarely  that  it  is  actually  smaller  than  natural. 

It  is  impossible  to  draw  a  hard-and-fast  hne  between  a  markedly 
hobnailed  liver,  nodular  cirrhosis,  and  cirrhosis  with  multiple  adenomata; 
the  conditions  pass  into  each  other,  and  what  one  observer  might  speak 
of  as  extreme  cirrhosis  might  by  another  be  called  cirrhosis  -with  adenoma. 
The  portal  vein  is  frequently  thrombosed,  and  microscopic  examination 
of  the  clot  may  show  a  few  liver  cells  due  to  the  discharge  of  one  of 
the  softened  hobnails  into  the  vein.  Sometimes  similar  thrombosis  is 
seen  in  the  hepatic  veins.  The  lymphatic  glands  in  the  portal  fissure 
are  not  enlarged. 

Microscopically  the  hver  shows  marked  cirrhosis;  the  masses  which 
to  the  naked  eye  suggest  new-growth  are  altered  hver  cells  surrounded 
by  a  fibrous  capsule;  the  interstitial  tissue  shows  the  appearance  of 
pseudo-bile  canaliculi,  advancing  cirrhosis,  and  sometimes  extravasated 
blood.  In  a  hyperplastic  nodule  examined  at  an  early  stage  the  liver 
cells  are  larger  than  natural,  in  a  good  state  of  nutrition,  and,  as  shown 
by  karyokinetic  figures,  are  undergoing  active  proliferation.  This  stage 
may  be  spoken  of  as  nodular  cirrhosis.  In  an  early  stage  the  naked-eye 
appearances  are  more  striking  than  the  microscopic.  The  first  impression 
on  looking  at  a  microscopic  section  of  nodular  cirrhosis  is  often  one  of 
disappointment  at  finding  little  more  than  the  changes  of  cirrhosis.  As 
growth  proceeds  the  cells  in  the  centre  of  the  nodule  become  the  bigger, 
while  those  at  the  periphery  become  flattened  from  pressure  and  may 
become  si3indle-shaped.'  The  normal  arrangement  of  the  hepatic  lobule 
is  lost,  and  tortuous  columns  of  cells  are  seen  which  often  tend  to  form 
irregular  circles  around  the  intralobular  vein.  The  cells  forming  this 
anastomosing  network  are  cubical  and  are  larger  than  those  forming 
the  so-called  new  bile-ducts,  but  are  usually  smaller  than  the  liver  cells. 
At  this  later  stage  the  adenoma  has  become  tubular.  Multinuclear 
large  cells  are  occasionally  present  in  the  centre  of  the  adenomatous 
nodule,  and,  according  to  Schmieden,  proliferate  to  form  the  adenomatous 
cells.  Haemorrhage  may  occur  into  the  adenomata  or  around  them,  and 
fatty  change  may  appear  in  the  cells  forming  the  adenomata,  especially 
when  the  portal  vein  is  thrombosed.  Fibrosis  may  extend  into  the  sub- 
stance of  the  adenomata. 

Secondary  Changes  in  Multiple  Adenomata. — The  fatty  metamorphosis 
of  the  cells  already  mentioned  may  lead  to  softening  do^vn  of  the  adeno- 
mata and  the  formation  of  the  C3'stic  spaces.  The  adenomata  may  dis- 
charge into  the  branches  of  the  portal  or  hepatic  veins  and  set  up  throm- 
bosis. From  vigourous  proliferation  of  the  cells  in  the  adenoma  the  process 
may  become  carcinomatous;  this  condition  is  fully  described  in  the 
section  on  "Carcinoma  with  Cirrhosis." 

Clinical  Aspect. — Since  multiple  adenoma  is  usually  a  result  of 
cirrhosis,  its  age  and  sex  incidence,  its  signs  and  symptoms,  treatment, 


460  DISEASES   OF  THE   LIVER. 

etc.,  are  much  the  same  as  in  that  disease.  It  is  found  in  a  high  propor- 
tion of  those  cases  where  at  the  autopsy  cirrhosis  with  thrombosis  of 
the  portal  vein  is  present,  and  is  therefore  very  frequently  associated 
with  ascites  and  hsematemesis.  An  attempt  has  sometimes  been  made 
to  establish  a  difference  between  the  chnical  features  of  ordinary  cirrhosis 
and  multiple  adenomata,  and  the  tendency  has  been  rather  to  lay  stress 
on  the  presence  of  hepatic  pain  and  to  present  a  picture  approaching 
that  of  mahgnant  disease  of  the  liver.  But  no  rehance  can  be  placed 
on  any  such  clinical  differences. 


ANGIOMA. 

Synonyms:  Cavernoma:  Nsevus. 

The  liver  is  more  often  the  seat  of  angiomata  than  any  visciis  in  the 
body,  but  angiomata  are  not  very  common  in  the  hver;  Lancereaux  * 
has  seen  25  cases.  They  are  more  frequently  seen  in  the  livers  of  cats. 
As  to  the  incidence  of  the  ordinary  acquired  nsevi  in  the  two  sexes, 
Hanot  and  Gilbert  f  say  they  are  commoner  in  men,  while  Thoma  } 
states  that  they  are  more  frequent  in  women.  They  may  be  congenital 
and  have  been  seen  in  foetuses,  though  this  is  somewhat  exceptional; 
they  are  then  probably  due  to  some  disturbance  in  the  process  of  devel- 
opment. Usually,  however,  they  are  found  in  the  bodies  of  persons 
advanced  in  years  and  are  then  more  probably  acquired  and  may  be 
due  to  a  combination  of  local  congestion  of  the  hepatic  vessels  and  atrophy 
of  the  liver  ceUs.  Usually  they  are  quite  small.  When  they  form  large 
tumors,  the  patients  are,  as  a  rule,  very  young,  though  very  occasional^ 
large  cavernous  tumors  have  been  seen  in  adults. 

In  Fillipini's  §  case  there  was  a  tumor  as  large  as  an  adult's  head  in  the  left 
lobe  of  the  liver  in  a  woman  aged  twenty-two.  In  Mantle's  case  ||  the  tumor 
which  had  been  growing  for  two  years,  in  a  man  aged  thirty-three  years,  was 
thought  to  contain  8  pints  of  blood. 

They  may  be  multiple,  but  are  more  often  single.  As  many  as  30 
have  been  seen  in  the  same  liver.  In  Schirdeden's  **  32  cases,  18  were 
single,  14  multiple.  Angiomata  may  be  found  at  the  same  time  in  other 
abdominal  viscera. 

In  Payne's  ft  case  there  were  exceptionally  large  cavernous  angiomata  in  the 
liver,  which  weighed  6  pounds,  and  angiomata  in  both  ovaries  and  both  adrenal 
bodies;  while  in  Petroff'sJt  case  there  were  angiomata  in  both  adrenal  bodies. 

Morbid  Anatomy. — ^Their  most  common  situation  is  immediate^ 
under  the  capsule,  and  often  near  the  edge  of  the  liver,  on  the  convexity 
or  in  the  neighbourhood  of  the  falciform  ligament.  After  death  they 
become  partially  empty  and  are  therefore  slightly  depressed  below  the 
level  of  the  surrounding  liver  substance.  In  exceptional  cases  they  be- 
come pedunculated.     Lancereaux  ^  g  figures  a  pedunculated  angioma  at- 

*  Lancereaux:    Traits  ,des  Maladies  du  foie  et  du  pancreas,  p.  528. 
t  Hanot  and  Gilbert:  Etudes  des  Maladies   du  foie,  p.  315. 
X  Thoma:   Pathology,  English  Trans,  by  Bruce,  vol.  i,  p.  5.53. 
§  FiUipini:    II  Policlinico,  April,  1901.      Vide  Epitome,  Brit.  Med.  Journal, 
1901,  ii.  No.  94. 

II  Referred  to  Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  423,  and  described  in  the 
same  journal,  1903,  vol.  i,  p.  365. 

**  Schmieden:    Virchow's  Archiv,  Bd.  clxi,  S.  373. 
tt  Payne,  J.   F.:    Trans.   Path.  Soc,  vol.  xx,  p.   203. 

XX  Petroff:    Bolnichnaya  Gazeta   Botkina,   1899,    No.  30;    abstract  in    Rev. 
de  MM.,  1901,  p.  920. 

55  Lancereaux:   Trait6  des  Maladies  du  loir  v{  du  pancreas,  p.  528,  1899. 

461 


462  DISEASES    OF   THE    LIVER. 

tached  to  a  liver  which  also  contained  other  angioma;  and  Journiac* 
has  also  described  this  condition.  They  are  round  or  wedge-shaped,  with 
the  base  directed  outwards  and  the  apex  inwards  so  as  to  resemble  closely 
that  somewhat  rare  lesion,  a  hsemorrhagic  infarct  in  the  hver.  On  sec- 
tion they  have  a  honeycombed  appearance  when  the  blood  has  been 
removed,  hke  that  of  erectile  tissue  of  the  corpus  cavernosum  penis  or 
of  the  placenta.  They  are  dark  red  in  colour;  occasionally  the  surround- 
ing liver  substance  is  darkened  by  infiltration  with  black  pigment  derived 
from  the  blood.  They  are  sometimes  encapsuled  or  encysted,  and  in 
connexion  with  this  it  is  interesting  to  note  that  Berard  Aine  f  suggested 
they  were  encysted  splenic  ''rests."  When  the  cavernous  tumors  are 
large  there  is  usually  a  fibrous  capsule,  while  in  smaller  specimens  there 
is  often  none,  and  the  cavernous  tissue  is  in  immediate  contact  with  the 
liver  cells.  It  is  possible  that  the  encapsulation  is  a  secondary  process 
and  develops  around  old  naevi,  as  in  the  case  of  other  innocent  tumors. 
In  a  case  recorded  by  Cripps  {  the  capsule  showed  calcification.  Con- 
siderable difference  of  opinion  has  been  expressed  as  to  their  connexions 
with  the  other  vessels  in  the  liver,  and  they  have  been  said  to  be  only 
connected  with  the  veins  or  to  be  in  free  communication  both  with  the 
hepatic  artery  and  with  the  portal  and  hepatic  veins.  There  does  not 
seem  to  be  any  tendency  to  malignant  (endotheliomatous)  change  in 
them. 

Besides  the  pigmented  or  "melanotic"  and  the  encysted  angiomata, 
there  is  another  variety  described — ^the  fibrous  angioma — in  which  the 
trabeculse  increase  markedly  in  thickness  and  thus  tend  to  lead  to  oblitera- 
tion of  the  cavities  or  to  its  cure.  It  is  possible  that  by  degenerative 
changes  these  naevi  may  become  transformed  into  serous  cysts. 

Histologically  there  is  a  communicating  meshwork  of  spaces  containing 
red  blood-corpuscles.  The  walls  of  the  spaces  are  composed  of  fibrous 
tissue  with  a  certain  number  of  young  connective-tissue  cells  and  some 
elastic  fibres.  Smooth  muscle  fibres  are  described  in  some  specimens. 
The  spaces  are  lined  by  flattened  endothelial  cells  covering  the  surface 
of  the  fibrous  trabeculae.  The  structure  is  therefore  that  of  cavernous 
tissue.  I  have  seen  a  specimen  entirely  composed  of  vessels  and  quite 
devoid  of  blood  sinuses.  The  tumor  may  be  separated  from  the  liver 
cells  by  a  layer  of  fibrous  tissue  which  serial  sections  show  to  be  con- 
tinuous with  Glisson's  capsule.  In  many  specimens  there  is  no  limiting 
capsule  and  the  blood-spaces  are  in  direct  contact  with  the  liver  cells, 
which  may  form  columns  running  into  the  cavernous  tissue.  Bile-ducts 
and  liver  cells  may  thus  appear  to  be  embedded  in  the  tumor.  Pigment 
granules  may  be  found  in  the  fibrous  trabeculse  as  well  as  in  the  sur- 
rounding liver  cells ;  Hanot  and  Gilbert  |  give  an  illustration  of  this 
under  the  title  of  ''melanotic  angioma." 

Secondary  Changes. — The  blood  may  clot  in  the  cavernous  spaces  and 

*  Journiac:    Archiv  de  Physiol,  norm,  et  path.,  1S78,  p.  37. 
t  Berard  Aine:    Bull.   Soc.   Anat.   Paris,   1828,  p.  9. 
J  Cripps,  W.  Harrison:  ,  Brit.  Med.  Journ.,  1903,  vol.  ii,  p.  18. 
s   Hanot  and  Gilhert:  Etudes  des  Maladies  du  foie,  p.  341. 


ANGIO.MA. 


463 


the  endothelium  may  then  creep  over  the  remains  of  the  clotted  blood. 
When  the  blood-supply  is  interrupted  Ijy  thrombosis,  the  cavernous 
tissue  may  become  modified  so  as  to  contain  serous  fluid  and  imitate  a 
lymphangioma.  In  other  cases  the  fibrous  framework  of  the  tumor 
may  proliferate  and  compress  and  eventually  obliterate  the  blood-spaces ; 
in  other  instances  hyaline  degeneration  may  occur  in  the  fibrous  stroma. 

Pathogeny. — Different  views  have  been  put  forward  to  explain  the 
formation  of  angiomata  in  the  liver,  and  it  is  probable  that  all  angiomata 
are  not  due  to  the  same  process.  The  congenital  ones  may  with  a  fair 
show  of  reason  be  referred  to  a  different  pathological  process  from  that 
responsible  for  those  observ^ed  late  in  life  (acquired  angiomata).  The 
following  views  may  be  mentioned : 

(I)  That  they  are  a  malformation  due  to  an  excessive  growth  of  the 


Fig.  57.— Drawing    of  Angioma  (Cavernoma)   of  the   Liver,  Showing  Spaces  Containing 
Coagulated  Blood  with  Fibrous  Alveolar  Walls.     It  is  Encapsuled.     X  21, 


vascular  mesoblast.  This  would  account  for  the  congenital  angiomata, 
which  in  rare  instances  reach  a  sufficiently  large  size  to  be  clinically 
recognisable  as  tumors.  Schmieden,*  who  does  not  believe  that  hejjatic 
angiomata  are  the  same  as  those  met  with  elsewhere  in  the  body,  for 
example,  the  cutaneous  angiomata,  refers  their  formation  to  a  malforma- 
tion or  congenital  defect  and  suggests  the  new  term  "caAcrnoma,"  or 
"nsevus  cavernosus  hepatis." 

(II)  That  there  is  a  development  of  now  ])lood- vessels  in  connexion 
with  a  new  formation  of  fibrosis  tissue,  the  vessels  being  derived  from 
preexisting  ones  in  the  neighbourhood.      In  other  words,  there   is  an 

*  Sclnnipclon:    Yircliow's  Archiv,  Bd.  clxi,  S.  373. 


464  DISEASES    OF   THE    LIVER. 

innocent  angiofibroma.  This  explanation  of  Virchow's  *  does  not  ac- 
count for  angiomata  devoid  of  a  fibrous  tissue  capsule.  Again,  if  this 
were  the  true  explanation,  it  would  be  natural  to  expect  to  find  angiomata 
frequently  in  cirrhosis.  Though  new  vessels,  sometimes  in  considerable 
numbers,  are  seen  in  the  newly  formed  fibrous  tissue,  definite  angiomata 
are  rare. 

(III)  The  view  of  Cornil  and  Journiac  is  a  modification  of  the  pre- 
ceding, and  is  to  the  effect  that  there  is  in  the  first  instance  an  embryonic 
proliferation  of  the  perivascular  tissue  of  preexisting  veins  and  capil- 
laries, which  brings  about  dilatation  of  the  vessels,  and  that  eventually 
these  vessels  communicate. 

(IV)  That  stagnation  of  blood  and  congestion  induce  dilatation  of 
the  vessels  vdth  atrophy  of  the  intervening  liver  cells.  Some  increased 
fibrosis  takes  place,  so  that  a  cavernous  nsevus  is  produced.  This  theory, 
supported  by  Chervensky,t  and  by  Hanot  and  Gilbert,^  explains  satis- 
factorily the  acquired  angiomata,  and  especially  those  which  fade  off 
into  the  liver  tissue  without  any  intervening  fibrous  capsule.  The  forma- 
tion of  fibrous  tissue  around  a  hepatic  angioma  may  very  probably  be 
a  secondary  process,  and  the  same  as  the  encapsulation  of  other  innocent 
tumors,  hence  the  presence  of  a  fibrous  capsule  is  not  necessarily  a  strong 
argument  against  the  method  of  formation.  Though  typical  angiomata 
are  not  commoner  in  the  livers  of  chronic  venous  engorgement  than  in 
other  conditions,  microscopically  areas  showing  angiomatous  capillaries 
are  of  course  common  in  nutmeggy  livers.  On  the  other  hand,  this 
method  does  not  explain  congenital  angiomata  or  those  in  early  life. 

Primary  atrophy  of  the  liver  cells  alone  will  not  account  for  the 
formation  of  angiomata,  since  it  is  not  an  infrequent  event  and  is  not 
accompanied  by  angiomata.  As  already  pointed  out,  it  is  unnecessary 
to  refer  all  hepatic  angiomata  to  the  same  method  of  origin.  Some  are 
due  to  congenital  maldevelopment,  while  others  are  due  to  vascular 
engorgement  combined  wdth  atrophy  of  the  liver  tissue. 

Clinical  Aspect. — There  is  no  relation  between  the  amount  of  interest 
that  attaches  to  the  pathology  of  angiomata  of  the  liver  and  their  clinical 
bearing.  In  the  vast  majority  of  cases  no  symptoms  can  be  put  down 
to  the  presence  of  angiomata  in  the  liver.  It  has  been  suggested  that 
murmurs  or  venous  hums  heard  over  the  hepatic  region  are  sometimes 
produced  in  this  way.  In  exceptional  examples  they  have  reached  a 
considerable  size;  thus  Stiffen,§  Chervensky,  ||  Mantle,  Cripps,  and  others 
have  met  with  considerable  hepatic  enlargement  from  this  cause.  ' 

In  Petroff's**  case  of  a  woman  aged  thirty-eight  years  with  symptoms  of  Addi- 
son's disease  jaundice  was  found  to  be  due  to  the  pressure  exerted  by  a  large  an- 
gioma of  the  Hver  on  the  bile-ducts.  There  were  cavernous  angiomata  in  both 
the  suprarenal  bodies.      A  fibrinous  n£evus  compressed  the  right  hepatic  and  the 

*  Virchow:    Virchow's  Archives,  Bd.  v,  S.  525. 
t  Chervensky:    Archiv,de  Physiol.,  1885,  t.  ii,  p.  553. 
X  Hanot  and  Gilbert:    Etudes  sur  les  Maladies  du  foie,  p.  316,  1888. 
§  Stiffen:    Jahrb.   f.   Kinderheilk.,   1883,   S.   348. 
II  Chervensky :    Archiv  de  Phys.,   1885,  ii,  552. 
**  Petroff:  Bohiichnaya  Gazeta  Botkina,  1899,  No.  30.     Abstract  in  Rev.  dc 
Med.,  1901,  p.  920. 


MYXOMA.  465 

cystic  ducts  and  gave  rise  to  jaundice,  colic,  and  distension  of  the  gall-bladder. 
It  was  successfully  removed  by  Tedenat.* 

In  some  cases  the  condition  has  been  diagnosed  as  hydatid  or  merely 
as  a  doubtful  tumor  of  the  liver. 

I  am  indebted  to  Dr.  Seymour  Taylor  for  the  notes  of  a  case  where  a  man 
had  a  tumor  in  connexion  with  the  liver  which  closely  imitated  a  hydatid  cyst; 
it  was  operated  upon,  and  when  exposed,  still  resembled  a  cyst;  on  puncture  it 
bled  profusely  at  every  point  and  the  haemorrhage  was  with  difficulty  arrested. 
The  patient  left  the  hospital  well. 

The  prognosis  is  fairly  good  in  the  cases  which  are  operated  upon, 
which  as  a  matter  of  fact  are  the  only  ones  which  can  be  diagnosed  with 
certainty  during  life. 

Treatment. — As  it  is  only  exceptionally  that  hepatic  angiomata  give 
rise  to  any  signs  or  symptoms,  the  question  of  treatment  rarely  arises. 
As  the  presence  of  a  large  angioma  would  imitate  a  tumor  of  the  liver, 
the  only  method  of  treatment  is  surgical,  but  there  is  considerable  danger 
of  profuse  hemorrhage.  If  the  tumor  was  thought  to  be  an  angioma, 
electrolysis  might  be  tried.  Keen,t  in  a  list  of  75  cases  where  resection 
of  the  hver  has  been  done  for  neoplasms,  refers  to  4  cases  of  angioma 
thus  treated.  A  large  naevoid  growth,  at  first  regarded  as  an  ossifying 
sarcoma,  was  recently  successfully  removed  from  the  liver  by  Cripps.J 
In  1904  Tedenat  could  only  refer  to  six  cases  in  which  excision  had  been 
carried  out. 

LYMPHANGIOMA. 

It  is  possible  that  a  tumor  of  this  nature  may  occur  in  the  liver 
occasionally,  but  I  have  only  been  able  to  find  a  description  of  one  case, 
Maresch's,§  in  which  a  pedunculated  tumor,  diagnosed  as  an  ovarian 
cyst,  was  removed  from  the  right  lobe  of  the  liver  of  a  girl  aged  five 
years.  It  is  quite  conceivable  that  a  tumor  of  this  kind  might  result 
from  degenerative  changes  in  an  angioma  of  the  liver. 


MYXOMA. 

A  very  large  growth  in  the  liver  of  a  patient  who  had  previously  had 
a  tumor  removed  from  the  breast  by  Mr.  Nunnjl  was  described  by  the 
Morbid  Growths  Committee  of  the  Pathological  Society  as  a  myxoma. 
Though  probably  a  myxo-sarcoma,  this  specimen  has  often  been  referred 
to  as  a  myxoma  of  the  liver.  A  few  other  cases  of  myxoma  have  been 
described,  but  it  seems  probable  that  they  are  allied  to  sarcomatous 
rather  than  to  irmocent  tumors.  Cornil  and  Cazalis  **  described  a  primary 
myxoma  in  the  liver  of  a  child  of  nine  months. 

*  Archiv.  gc'n.  de  Med.,  Mar.  8,  1904,  p.  586. 
t  Keen:    Annals  of  Surgery,  Sept.,  1S99,  p.  276. 
t  Cripps:    Brit.  Med.  Jourii.,  190.3,  vol.  ii,  p.  18. 
§  Maresch,  R.:    Zeitschrift  f.  Heilkunde,  Bd.  xxiv,  S.  39,   1903 
II  Nunn,  T.  W.:    Trans.  Path.  Soc,  vol.  xxiv,  p.  120. 
**  Cornil  and  CazaUs:    Gaz.  M6d.  de  Paris,  1872,  p.  539 
30 


466  DISEASES    OF   THE    LIVER. 


FIBROMA. 

A  few  examples  of  fibromata  of  the  liver  have  been  described,  but 
some  caution  must  be  exercised  in  accepting  their  existence.  When  this 
condition  is  met  with  in  infants  it  may  be  a  manifestation  of  congenital 
syphilis  and  belongs  to  the  group  of  cases  described  by  Marchand.* 
Luschka's  f  case  of  fibroma  in  a  child  one  month  old  was  probably  of 
this  nature.  It  is  possible  that  other  cases  would  be  more  correctly 
described  as  fibro-sarcomata ;  while  it  is  conceivable  that  an  angioma 
might  undergo  fibrotic  atrophy  and  eventually  form  a  small  fibrous 
tumor. 

Lancereauxl  described  a  fibroma  infiltrated  with  calcareous  salts,  in  a  woman 
aged  twenty-eight  years.  On  the  under  surface  of  the  right  lobe  of  the  liver  of  a 
woman  aged  fifty-six  Chiari  §  found  a  fibroma  the  size  of  an  egg.  Four  calcified 
fibromata,  varying  in  size  from  a  nut  to  a  grain  of  wheat,  were  found  in  the  liver  of 
a  tuberculous  woman.  (Pisenti.  ||)  In  a  case  of  multiple  neurofibromata  the  sym- 
pathetic nerves  in  the  liver  were  beset  with  fibromata  from  the  size  of  a  bean  to 
that  of  a  millet  seed.     (Ziegler.**) 


LIPOMATA. 

Genuine  fatty  tumors  are  not  met  with  in  the  liver.  But  what  might 
be  spoken  of  as  a  lipoma  may  be  found  indented  on  the  surface  but  out- 
side the  capsule  of  the  liver :  these  small  tumors  are  in  reality  appendices 
epiploicse  which  have  become  detached  from  the  colon  and  have  come  to 
rest  between  the  diaphragm  and  the  convexity  of  the  liver. ff  I  have  now 
seen  several  examples  of  this  condition.  An  encapsulated  mass  of  fat 
of  about  the  size  of  a  nut  is  found  in  a  depression  on  the  convexity  of 
the  liver,  which  it  tightly  fits.  The  capsule  of  the  liver  passes  between 
the  fatty  body  and  the  liver  substance  and  there  is  no  vascular  connexion 
between  the  fatty  tumor  and  the  liver. 

Localised  areas  of  extreme  fatty  change  in  the  liver  cells'  are  some- 
times met  with;  they  probably  depend  on  vascular  obstruction  and 
microbic  activity,  and  ar.e  not  likely  to  be  mistaken  for  real  fatty  tumors. 
The  fat  which  accompanies  the  obliterated  umbilical  vein  in  the  falciform 
ligament  sometimes  increases  in  size  so  as  to  resemble  a  small  fatty  tumor. 
I  have  seen  an  example  of  this  in  a  woman  who  died  from  the  effects  of 
herniotomy. 

*  Marchand:    Centralblatt  f.  allg.  Path.,  Bd.  vn,  S.  273,  1896. 

t  Luschka:    Virchow's  Archives,   Bd.  xv,  S.  168.        . 

X  Lancereaux:    Atlas  d'Anat.  path.,  1871. 

§  Chiari:    Wien.  med.  Wochens.,  1877,  S.  365. 

II  Pisenti:   Quoted  by  Pepere,  I  Tumori  maligni  primarii  del  Fegato,  p.  25,  1902. 
**  Ziegler:    Special  Pathological  Anatomy.     Translated    bv  Macalister,    Part 
ii,  p.  342,  1884. 

ttriolleston:    Trans.  Path.  Soc,  vol.  xhi,  p.  160. 


EMBRYOMATA    AND   TERATOMATA.  467 


EMBRYOMATA  AND  TERATOMATA. 

These  are  extremely  rare  in  the  liver,  and  are  merely  pathological 
curiosities. 

Hanot  and  Gilbert*  refer  to  a  single  instance  of  a  cyst  in  the  liver  containing 
hair,  cartilage,  and  fatty  material.  In  a  baby  aged  six  weeks  Misickf  found  a 
lobular  tumor  the  size  of  a  man's  fist  in  the  right  lobe  of  the  liver;  it  contained 
bone,  cartilage,  and  cysts  derived  from  the  hypoblast,  but  no  epiblastic  elements, 
so  it  should  be  described  as  a  teratoma  rather  than  a  dermoid  cyst.  During  life 
it  was  thought  to  be  a  tumor  of  the  right  kidney. 

Pye  Smith  t  described  a  case  of  a  teratoma  adherent  to  but  not  arising  from 
the  liver  in  an  infant  one  year  old.  During  life  the  tumor  had  been  tapped  several 
times  and  the  disease  was  regarded  as  multilocular  cystic  disease  of  the  liver. 
It  was  an  included  foetus. 

The  secondary  implantation  on  the  surface  of  the  liver  of  fragments 
of  a  ruptured  ovarian  embryoma  is  referred  to  on  page  501.  A  case  of 
this  kind  was  described  by  Hulke.§ 

*  Hanot  and  Gilbert :    Etudes  sur  les  Maladies  du  foie,  p.  295,  1888. 
fMisick:    Jour.   Path,   and  BacterioL,   vol.   v,  p.   128. 
i  Pye  Smith:    Trans.  Path.  Soc,  vol.  xxxvii,  p.  499. 
§  Hulke:    Trans.   Path.   Soc,   vol.   xxiv,   p.    157. 


MALIGNANT  DISEASE  OF  THE  LIVER. 

The  subject  of  malignant  disease  of  the  liver  will  be  considered  in 
the  following  way:  First  the  incidence  and  a  detailed  account  of  the 
morbid  anatomy  of  primary  malignant  disease;  then  the  incidence  and 
a  detailed  description  of  the  morbid  anatomy  of  secondary  malignant 
disease;  thirdly,  the  general  clinical  picture;  and,  lastly,  the  points  of 
distinction  between  the  clinical  manifestations  of  primary  and  secondary 
malignant  disease  of  the  liver. 

PRIMARY  MALIGNANT  DISEASES  OF  THE  LIVER. 

INCIDENCES. 

Primary  malignant  disease  of  the  liver  is  a  rare  disease.  Every  case 
requires  critical  portmortem  investigation  to  make  sure  that  it  is  not 
secondary  to  some  obscure  growth  elsewhere,  and  that  the  growth  did 
not,  in  reality,  start  in  the  gall-bladder  or  larger  bile-ducts. 

In  11,500  autopsies  at  Guy's  Hospital,  Hale  White*  found  11  cases  of  primary 
carcinoma  of  the  liver,  or  0.1  per  cent.  Eggelf  estimates  that  primary  carcinoma 
occurs  once  in  2000  autopsies,  or  0.5  per  cent. 

The  numerical  ratio  between  primary  and  secondary  carcinoma  of 
the  liver  has  been  placed  between  1 :  20  and  1 :  40.     (Vide  p.  485.) 

Primary  sarcoma,  in  which  endothelioma  is  also  included,  of  the  liver 
is  rarer  even  than  carcinoma. 

LeithJ  collected  25  cases  in  1897.  In  1901  Vecchi  and  Guerrini  §  critically 
examined  45  published  cases  of  primary  sarcoma  of  the  liver,  but  only  accepted 
21  cases  as  undoubted  examples  of  this  rare  condition.  I  have  notes  of  64  cases 
of  reputed  primary  sarcoma,  of  which  32  occurred  in  patients  over  ten  years  of 
age  and  32  under  that  age.  These  cases  do  not  include  those  described  as  primary 
melanotic  sarcoma  {vide  p.  483)  or  any  which  appeared  to  be  most  probably  cases 
of  hepatitis  due  to  congenital  syphilis. 

Sex.  — Primary  malignant  disease  of  the  liver  seems  to  be  more  frequent  in 
men  than  in  women,  and  contrasts  with  primary  carcinoma  of  the  gall-bladder, 
which,  like  gall-stones,  is  infinitely  commoner  in  women — gall-stones  and  carcinoma 
of  the  gall-bladder  being  both  about  four  times  more  frequent  in  women  than  in 
men. 

In  74  cases  of  primary  malignant  disease  in  adults  (42  carcinoma,  32  sarcoma) 
which  I  have  collected,  42  were  males  and  32  females.  The  male  sex  was  more 
often  affected  by  carcinoma;  of  the  42  cases,  29  being  males  and  13  females.  In 
Eggel's  collection  of  163  cases  of  primary  carcinoma  63  per  cent,  were  males.  Among 
the  32  cases  of  primary  sarcoma  19  were  females  and  13  males. 

Age. — Primary  carcinoma  of  the  liver  occurs  in  or  after  middle  life 
and  is  rare  before  forty  years  of  age. 

In  42  cases  of  primary  carcinoma  (males  29,  females  13)  the  average  age  was 
47.2  years,  being  42.1  among  the  females  and  49.3  among  the  males. 

*  Hale  White:    Allbutt's  System  of  Medicine,  a^oI.  iv,  p.   197. 
tEggel:    Ziegler's  Beitrage,  Bd.  xxx,  S.  506,  1901. 
I  Leith:    Lancet,   1897,  vol.  i,  p.   170. 

§  Vecchi  and  Guerrini:    Medical  News  (New  York),  Nov.  23,  1901,  p.  816. 

468 


MALIGNANT    DISEASE    OF   THE    LIVER.  469 

The  earlier  observers  described  cases  of  cancer  or  "scirrhus"  in  A^ery 
young  children,  but  most  of  them  were  probably  sarcomatous  or  due  to 
congenital  syphilis. 

Comparatively  recently  Prescott*  recorded  a  congenital  carcinoma  of  the  left 
lobe  of  the  liver  in  an  infant  of  five  months,  but  it  is  highly  probable  that  it  was 
an  endothelioma. 

In  older  children  portal  cirrhosis  \vith  multiple  adenoma  very  closely 
resembles  carcinoma.  H.  Fussell  and  Kelly's  f  case  of  primary  carci- 
noma in  a  girl  aged  sixteen  years  was  regarded  by  Welch  and  Dock  in 
this  light. 

Dr.  Still  has  given  me  sections  of  a  child's  liver  which  looked  exactly  like  malig- 
nant disease  to  the  naked  eye,  but  microscopically  showed  cirrhosis  with  com- 
pensatory hyperplasia  of  the  liver  cells. 

Acland  and  Dudgeon  |  described  an  undoubted  case  of  primary 
carcinoma  of  the  liver  in  a  boy  aged  fifteen  years,  in  which  the  liver 
weighed  nearly  16  pounds,  and  collected  eight  other  cases  of  primary 
carcinoma  of  the  liver  under  twenty  years  of  age. 

Acland  and  Dudgeon's  cases  are  those  of  OUivier,  Deschamps,  Kottman, 
Henschen,  Pye  Smith,  Birch-Hirschfeld,  and  Fussell  and  Kelly.  There  is  con- 
siderable doubt  as  to  OUivier's,  Fussell  and  Kelly's,  and  one  of  Birch-Hirsch- 
feld's  cases  being  genuine  carcinoma.  An  interesting  case  of  primary  carcinoma 
in  a  woman  aged  twenty-two  years  has  been  recorded  by  Gilbert  and  Claude.  § 

Primary  sarcoma  may  occur  at  almost  any  age.  The  oldest  case  of 
which  I  have  a  reference  was  seventy-three  j^ears,  while  congenital  cases 
have  been  recorded.  Primary  sarcoma  of  the  liver  may,  like  sarcoma 
of  the  kidney,  be  divided  into  two  categories :  (a)  those  which  occur  in 
adult  life  and  (h)  those  met  with  very  early  in  life. 

The  average  age  of  32  cases  occurring  in  patients  over  fifteen  years 
of  age  was  47.53  years  (males,  51.6  years;  females,  44.7  years),  or  exactty 
the  same  as  the  average  age  for  primary  carcinoma  of  the  liver.  In 
addition  to  these  32  cases  I  have  tabulated  32  cases  of  primary  sarcoma 
of  the  liver  under  ten  years  of  age. 

In  1883  Picot  ||  made  a  collection  of  424  cases  of  malignant  disease  occurring 
under  seventeen  years  of  age,  which  included  13  of  primary  malignant  disease  of 
the  liver.  R.  Williams**  referred  to  29  cases  of  primary  malignant  disease  of  the 
liver  under  the  age  of  fifteen  years,  the  majority  of  which  were  probably  sarco- 
matous. Noegerrathft  described  a  case  of  primary  malignant  disease  of  the  liver 
in  a  baby  which  interfered  with  delivery;  a  congenital  case  was  also  observed  by 
Jacobi.f  j 

In  connexion  with  sarcoma  occurring  in  early  life  a  caution  must  be 
thrown  out  as  to  the  danger  of  regarding  as  sarcoma  the  lesions  of  con- 
genital syphilis.     Cases   of  pericellular  cirrhosis  in  infants   have  been 

*  Prescott:    Boston  City  Hospital  Reports,  1895. 

t  Howard  Fussell  and  Kelly:    University  Med.  Magazine,  Aug.,  1895. 

X  Acland  and  Dudgeon:    Lancet,  1902,  vol.  ii,  p.  1310. 

§  Gilbert  and  Claude:    Arch,  general,  de  Med.,  t.  clxxv,  1895,  p.  513. 

II  Picot:    Rev.  Med.  de  la  Suisse  Romande,  1883,  p.  660. 
**  R.  Williams:    Lancet,  1897,  vol.  i,  p.  1328. 
tt  Nocgerrath:    Deutsche  Klinik,   Bd.  vi,   S.  496,   1894. 
it  Jacobi:    Therapeutics  of  Infancy  and  Childhood,  p.  371. 


470  DISEASES   OF  THE   LIVER. 

described  as  primary  sarcoma,  lymphosarcoma,  etc.  A  diffuse  peri- 
cellular cirrhosis  in  foetal  life  is,  like  sarcoma,  an  embryonic  connective- 
tissue  growth,  so  that  the  two  processes  have  much  in  common.  Severe 
visceral  S3^hilis  in  early  life  may,  as  shown  by  Morley  Fletcher's  *  case, 
give  rise  to  hEemorrhagic  enlargement  of  the  suprarenal  bodies.  Such 
a  case  might  easily  be  regarded  as  sarcoma  of  the  liver  with  secondary 
growths.  Secondary  growths  in  the  adrenals  may  occur  in  primary 
sarcoma  of  the  liver  (Guy's  Museum,  No.  1571),  or  growths  may  be 
found  in  both  organs  and  it  may  not  be  easj''  to  say  which  of  the  two 
is  the  primary  growth. 

Pepper  f  has  collected  six  cases  of  congenital  sarcoma  of  the  liver  and  adrenal 
glands;  the  question  of  syphilis  as  the  real  change  is  fully  considered  by  him,  but 
not  admitted. 

ETIOLOGY. 

This  is  not  the  place  to  discuss  the  large  and  unsettled  problem  as 
to  the  true  cause  of  malignant  disease  or  to  consider  the  "parasitic"  or 
"habit  of  growth"  theories  on  the  question.  There  is,  however,  one  form 
of  primary  carcinoma  in  the  liver,  viz.,  that  which  develops  in  a  pre- 
viously cirrhotic  liver,  which  favours  the  view  that  carcinoma  is  due  to 
the  acquired  habit  of  proliferation  of  the  liver  cells,  which,  starting  as  a 
comiDensatory  hyperplasia  and  thus  giving  rise  to  multiple  adenoma  in 
cirrhosis,  eventually  becomes  so  excessive  as  to  constitute  carcinoma. 

In  a  few  cases  a  definite  history  of  a  blow  on  the  abdomen  preceding 
the  onset  of  malignant  disease  is  forthcoming  and  may  possibly  have 
played  some  part  in  starting  cellular  proliferation. 

MORBID   ANATOMY. 

Situation  of  the  Growth  in  Primary  Malignant  Disease  of  the 
Liver. — Primary  malignant  disease  of  the  liver  usually  arises  in  the  right 
lobe,  but  occasionally  is  limited  to  the  left  lobe. 

As  a  curiosity,  reference  may  be  made  to  malignant  disease  arising  in  a  tongue- 
like lobe.  In  a  case  of  calculous  cholecystitis  and  pericholecystitis  the  pendulous 
lobe  in  connexion  with  the  gall-bladder  was  found  to  be  the  site  of  primary  car- 
cinoma; at  first  sight  it  was  thought  to  have  started  in  the  gall-bladder,  but  RouxJ 
satisfied  himself  that  this  was  not  the  case. 

On  the  other  hand,  the  growth  may  infiltrate  both  lobes,  so  that  it 
is  impossible  to  make  out  where  it  started,  or  there  may  be  multiple 
primary  growths  in  both  lobes. 

The  morbid  anatomy  will  be  considered  under  the  two  heads  of 
Primary  Carcinoma  and  Primary  Sarcoma. 

VARIETIES   OF  PRIMARY  CARCINOMA. 
There  is  considerable  variety  in  the  forms  of  carcinoma  which  may 
arise  primarily  in  the  liver.     It  will  be  most  convenient  to   consider 
seriatim  the  morbid  anatomy  of  the  different  varieties. 

*  Morley  Fletcher:    Trans.  Path.  Soc,  vol.  1,  p.  138. 

t  Pepper:    American  Journ.  of  Med.  Sciences,  vol.  cxxi,  p.  2S7,  March,  1901. 

i  Roux:  Rev.  Med.  de  la  Suisse  Romande,  Feb.  20,  1897. 


MALIGNANT    DISEASE    OF   THE    LIVER. 


471 


I.  Primary  Massive  Carcinoma  (Synonym :    Cancer  en  Amande) 

(Hanot  and  Gilbeit). — In  this  form  of  primary  carcinoma  there  is  a  large 
white  or  3'ellowish  tumor  which  expands  the  liver,  like  a  shell,  around 
it.  The  surface  of  the  liver  is  usually  smooth;  in  some  cases  the  growth 
may  project  or  there  may  be  irregularities  from  secondary  growths; 
in  the  latter  event  there  may  be  adhesions  between  the  liver  and  adjacent 
structures,  such  as  the  diaphragm,  stomach,  etc.  The  growth  is  more 
or  less  localised,  and  forms  a  mass  as  big  as  a  cocoanut  or  the  foetal  head. 
There  may  be  secondary  growths  elsewhere  in  the  liver.  It  usually 
starts  in  the  right  lobe,  but  in  rare  instances  may  be  found  in  the  left 
lobe.  According  to  Eg- 
gel,  this  form  is  met 
with  in  23  per  cent,  of 
the  cases  of  primary  car- 
cinoma. 

Structurally  it  is  usu- 
ally a  polyhedral  or 
spheroidal-celled  carci- 
noma of  rapid  growth, 
springing  from  the  liver 
cells  themselves,  or  pos- 
sibly from  the  cubical 
epithelium  of  the  smaller 
bile-ducts.  It  has  been 
suggested  that  embry- 
onic relics  derived  from 
the  duodenal  diverticu- 
lum may  be  the  starting- 
point  of  the  growth. 

Exceptionally  the 
growth  is  a  columnar- 
celled  carcinoma  and  has 
then  arisen  in  connexion 

with  the  larger  intra-hepatic  bile-ducts.  Hanot  and  Gilbert  *  figure  a 
giant-celled  form  of  carcinoma  in  which  the  largest  cells  measured  as 
much  as  100  //. 

C.  Powell  White  t  has  described  a  primary  carcinoma  of  the  liver  which  softened 
down  into  a  large  cyst  containing  straw-coloured  fluid;  some  of  the  cells  measured 
30  to  40  //  in  diameter.  A  case  of  massive  carcinoma  with  mucli  filjrosis  resembling 
a  slow-growing  carcinoma  of  the  breast  is  described  in  the  section  on  Diagnosis  {vide 
p.  516).     The  fibrous  tissue  showed  hyaline  change. 

II.  Primary  Infiltrating  or  Diffuse  Carcinoma. — In  this  form  the 
growth  is  diffuse,  and  extends  more  widely  than  in  (he  previous  category. 
The  tumor  may  be  comparatively  slow  growing  and  so  hard  as  to  simulate 
cirrhosis.  The  whole  of  one  lobe  may  become  transformed  into  a  hard 
yellow  growth;  in  such  cases  the  liver  may  not  be  larger  than  natural. 

*  Hanot  and  Gilbert:    Etudes  sur  les  Maladies  dii  foie,  p.  W,  1888. 
t  White,  C.  P.:  lirit.  Med.  Journ.,  1899,  vol.  ii,  p.  1347. 


Fig.  .58. — Photomicrograph  of  Section  of  Diffuse  Car- 
cinoma OF  THE  Liver. 
Shows  a  large  quantity  of  hyaline  fibrous  tissue  and  groups 
of  epithelial  cells.      (By  S.  P.  Mummery,  Esq.)      X  15. 


472  DISEASES    OF   THE    LIVER. 

Hilton  Fagge  *  described  such  a  case  in  which  the  Hver  weighed  36J  ounces 
and  another  weighing  62  ounces,  but  in  his  third  case  it  weighed  186  ounces,  and 
in  Lee  Dickinson's  t  case,  102  ounces. 

It  may,  however,  be  rapidly  growing  and  soft,  and  extend  throughout 
the  whole  of  the  liver,  uniformly  enlarging  it. 

This  was  well  shown  in  the  hver  of  a  man  aged  sixty-four  which  had  a  uniform 
hobnail  appearance  and  on  section  was  universally  altered.  It  weighed  151 
ounces  and  microscopically  was  a  rapidly  growing  spheroidal-celled  carcinoma. | 

Structurally,  the  infiltrating  form  of  carcinoma  of  the  liver  is  nearly 
always  spheroidal-celled,  though  a  few  cases  show  a  transition  from  a 
columnar-celled  to  a  spheroidal-celled  type.  In  the  hard  forms  the  epi- 
thehal  cells  may  be  scanty  and  embedded  in  wide  tracts  of  fibrous  tissue. 
The  fibrous  tissue  may  show  advanced  hyaline  change. 

Numerically,  this  is  the  rarest  form  of  primary  carcinoma  of  the  liver. 
Eggel  estimated  that  it  occurred  in  12  per  cent,  of  the  cases. 

III.  Nodular  or  Multiple  Primary  Carcinoma. — ^The  appearance 
of  the  organ  is  hke  that  seen  when  it  is  occupied  by  secondary  growths, 
the  difference  being  that  there  is  no  primary  growth.  Great  care  must, 
of  course,  be  taken  to  examine  every  possible  situation  in  the  body  for 
a  primary  growth  before  admitting  that  the  condition  is  multiple  primary 
carcinoma  of  the  hver. 

The  vermiform  appendix  should  always  be  most  carefully  scrutinized,  for 
though  it  is  unlikely  that  secondary  growths  would  occur  in  the  liver  while  the 
primary  growth  in  the  appendix  was  so  small  as  to  require  microscopic  examina- 
tion for  its  detection  and  recognition,  it  is  quite  conceivable  that  the  primary 
growth  might  have  been  in  a  vermiform  appendix  removed  for  the  symptoms  of 
perityphlitis.  In  cases  of  primary  carcinoma  of  the  vermiform  appendix  the 
clinical  aspect  is  that  of  perityphlitis,  and  in  one  case  it  was  only  on  microscopic 
examination  that  the  carcinomatous  nature  was  revealed. § 

It  is  quite  possible  that  in  some  instances  multiple  adenomata  with 
cirrhosis  has  been  regarded  as  this  form  of  multiple  primary  carcinoma, 
since  the  naked-eye  resemblance  is  very  close.  In  other  cases  it  is  possible 
that  one  of  the  multiple  nodules  was  primary  and  that  the  others  are 
secondary,  but  have  grown  more  rapidly  and  so  come  to  rival  it  in  size. 
It  is  worth  while  raising  the  hypothesis  that  these  multiple  primar}' 
carcinomata  may  in  some  instances  be  multiple  growths  due  to  prolifer- 
ating cells  derived  from  a  focus  in  the  mucous  membrane  of  the  alimentary 
canal,  which,  though  irritated,  does  not  show  any  carcinomatous  growth. 
As  an  example  of  "secondary  growths  without  any  primary  focus" 
attention  may  be  called  to  the  fact  that  squamous-celled  carcinoma  may 
arise  in  the  inguinal  glands  of  sweeps  whose  scrota,  though  covered  with 
warts  from  the  irritation  of  soot,  do  not  show  any  definite  carcinomatous 
growth.     (ButHn.  ||) 

This  is  the  most  frequent  form  of  primary  carcinoma  of  the  liver. 

*  Hilton  Fagge:    Trans.  Path.  Soc,  vol.  xxviii,  p.  137;   vol.  xxxi,  p.  125. 

t  Dickinson,  L.:    Ibid.,  vol.  xlv,  p.  87. 

t  Rolleston:    Trans.  Path.  Soc,  vol.  xlv,  p.  92. 

§  Rolleston:   Lancet,  1900,  vol.  ii,  p.  11. 

IIButlin,  H.  T.:    Brit.  Med.  Jour.,  1892,  vol.  i,  1341. 


MALIGNANT    DISEASE    OF   THE    LIVER.  473 

In  Eggel's  *  collection  of  163  cases  it  occurred  in  104,  or  64.6  per  cent., 
and  in  about  the  same  proportion  in  Hale  Wliite's  f  H  cases  from  Guy's 
Hospital,  viz.,  in  6.  The  multiple  tumors  groAv  rapidly,  are  prone  to 
degenerate,  to  undergo  necrosis,  and  to  become  infiltrated  with  extra- 
vasated  blood.  Histologically,  the  growth  is  usually  a  spheroidal-  or 
polyhedral-celled  carcinoma.  The  cells  are  often  of  considerable  size, 
ancl  there  is  little  interstitial  connective  tissue.  The  cells  are  probably 
derived  from  proUferation  of  the  hepatic  cells.  In  a  few  cases  the  growths 
are  columnar-celled  and  are  in  aU  probabihty  derived  from  the  larger 
intrahepatic  bile-ducts  or  possibly  from  mucous  glands  in  their  walls. 

IV.  Primary  Carcinoma  Developing  in  a  Cirrhotic  Liver  (Syno- 
nyms: Primary  Carcinoma  with  Cirrhosis;  Cirrhosis  ]\Ialigna;  Cirrhosis 
Carcinomatosa). — ^This  condition  was  described  by  SabourinJ  under  the 
unfortunate,  because  confusing,  title  of  Cirrhosis  ^\dth  Multiple  Adeno- 
mata, and  is  fully  dealt  with  by  Hanot  and  Gilbert  §  under  the  name 
Carcinoma  with  Cirrhosis.  The  latter  writers  state  that  a  third  of  the 
cases  of  primary  carcinoma  of  the  liver  are  of  this  special  variety. 
But  it  is  certainly  much  rarer  than  that  in  England,  and  it  is  highly 
probable  that  more  than  one  condition  has  been  described  under  this 
name. 

Some  of  the  cases  are  probably  that  form  of  cirrhosis  in  which  the 
hobnails  are  extremely  w^ell  marked,  and  in  which  the  hepatic  cells  in 
them  have  undergone  a  compensatory  hyperplasia,  or  cirrhosis  with 
multiple  adenomata.  This  condition  of  nodular  cirrhosis  has  a  great 
resemblance,  naked-eye,  to  multiple  new-growths.  The  contents  of  the 
hobnails  may  undergo  fatty  degeneration,  and  may  discharge  their  con- 
tents into  the  intra-hepatic  branches  of  the  portal,  or  sometimes  the 
hepatic,  veins,  and  give  rise  to  thrombosis;  the  presence  of  liver  cells  in 
the  portal  vein  has  been  regarded  by  some  as  e\ddence  that  the  change 
is  carcinomatous,  but  without  sufficient  reason.  In  other  cases  of  cirrho- 
sis it  seems  probable  that  thrombosis  of  the  portal  vein  is  the  primary 
factor,  and  that  this  leads  to  fatty  degeneration,  necrosis,  and  softening 
of  the  cirrhotic  hobnails,  which  thus  closely  resemble  masses  of  secondary 
new-growth. 

Cirrhosis  with  compensatory  hyperplasia  of  the  hver  cells  forms  a 
connecting  link  between  cirrhosis,  on  the  one  hand,  and  carcinoma,  on 
the  other.  WTiere  the  line  separating  the  proliferation  of  the  hepatic 
cells  from  carcinoma  is  transgressed,  it  may  be  difficult  to  determine, 
but  that  carcinoma  may  thus  result  is  certainly,  though  rarely,  the  case. 
Many  of  the  cases  described  as  multiple  adenocarcinomatous  growths 
associated  with  cirrhosis  are  probal)ly  rather  nodular  cirrhosis  than 
malignant,  and  it  is  noticeable  that  in  this  class  secondary  gro-^i:hs  are 
very  rare.  My  own  impression  is  that  most  of  the  cases  are  the  result 
of  cirrhosis  rather  than  the  beginning  of  carcinoma,  but  it  is  advisable 

*  Eggel:  Ziegler's  Beitrage,  Bd.  xxx,  R.  506,  1901. 
tHale  White:    Allbutt's  System  of  Med.,  vol.  iv,  p.  205. 
iSabourin:    These  de  Paris,  ISSl;    Rev.  de  Med.,   1884,  p.  321. 
§  Hanot  et  Gilbert:    Etudes  sur  les  Maladies  du  foie,  p.  63,  1888. 


474  DISEASES    OF   THE    LIVER. 

to  keep  an  open  mind  on  the  subject,  as  the  demarcation  between  these 
two  conditions  is  difficult  to  draw.  When  secondary  growths  in  the 
hmgs  or  lymphatic  glands  are  present,  as  in  3  cases  of  Hanot  and  Gilbert's 
and  in  cases  recorded  by  Egon  Lindner,*  Travis, f  and  others,  the  cases 
must  be  admitted  to  be  carcinomatous.  Well-marked  invasion  of  the 
veins  by  growth,  when  confirmed  by  the  microscope,  as  has  been  often 
done,  is  also  undeniable  proof  of  carcinoma. 

The  relation  of  the  carcinomatous  growth  to  the  fib ro tic  change  in 
carcinoma  with  cirrhosis  has  been  regarded  in  various  lights.  It  has 
been  thought : 

(a)  That  the  cirrhosis  and  the  carcinoma  both  develop  at  the  same  time  and 
are  due  to  irritation  appUed  respectively  to  the  interstitial  connective  tissue  and  to 
the  cells  of  the  liver.  Hanot  and  Gilbert,  who  hold  this  view,  call  the  condition 
carcinoma  with  cirrhosis. 

(6)  That  the  carcinoma  is  the  primary  change,  and  that  the  cirrhosis  is  second- 
ary to  the  irritation  set  up  by  the  growth  and  is  related  to  it  in  the  same  way  that 
the  interstitial  tissue  of  a  hard  spheroidal-celled  carcinoma  is  to  the  epithelial 
cells.  (Lancereaux.§)  Against  this  is  the  fact  that  secondary  growths  are  com- 
monly present  in  the  liver  with  little  or  at  the  most  only  local  fibrosis  around  them, 
while  in  primary  carcinoma  with  cirrhosis  the  whole  liver,  and  not  merely  the 
parts  affected  by  the  gro-Ri;h,  is  fibrotic. 

(c)  That  cirrhosis  is  the  primary  change  and  that  the  compensatory  hyper- 
plasia of  the  liver  cells  becomes  so  excessive  and  atypical  as  to  pass  into  definite 
carcinoma.  The  history  and  morbid  anatomy  of  the  cases  are  quite  compatible 
with  this  view;  the  duration  of  the  cases  is  much  longer  than  in  other  forms  of 
primary  malignant  disease  of  the  organ;  the  symptoms  are  those  of  cirrhosis,  and 
on  examination  of  the  liver  after  death  the  cirrhosis  is  seen  to  be  old  and  universal, 
while  the  carcinoma  has  the  appearances  of  rapid  growth.  This  view  I  have  long 
held  and  is  definitely  stated  by  Eggel  ||  from  a  comprehensive  study  of  the  subject. 

Since  it  appears  that  cirrhosis  is  the  primary  change,  and  that  car- 
cinoma supervenes  secondarily  in  much  the  same  manner  that  carcinoma 
of  the  mamma  follows  chronic  mastitis,  it  would,  except  for  the  objection 
to  coining  fresh  names,  be  better  not  to  speak  of  Primary  Carcinoma 
with  Cirrhosis,  but  to  alter  the  title  to  Primary  Carcinoma  superv^ening 
in  a  cirrhotic  liver,  or  on  the  analogy  of  Paget's  disease  of  the  nipple. 
Cirrhosis  Mahgna,  or  on  the  analogy  of  carcinoma  supervening  on  a  gastric 
ulcer,  to  call  it  Cirrhosis  Carcinomatosa.** 

Morbid  Anatomy. — The  liver  is  usually  little,  if  at  all,  enlarged;  but 
in  some  instances  it  may  weigh  twice  its  normal  amount.  It  is  universally 
cirrhotic  and  presents  multiple  masses  of  new-growth;  one  tumor  may 
be  so  much  larger  that  it  would  appear  to  be  primary,  while  the  others 
are  secondary.  The  tumors  are  often  soft  or  gelatinous,  and  may  be 
necrotic.  The  nodules  of  growth  are  not  umbilicated;  this  depends  on 
the  fact  that  they  contain  hardly  any  stroma,  and  hence  cicatricial  con- 
traction, which  is  at  any  rate  an  important  factor  in  the  production  of 
umbilication,  does  not  occur.  In  an  early  stage  the  nodules  are  firm  and 
white;    later  they  degenerate  and  soften  down.     They  usually  project 

*Egon  Lindner:    Wien.  klin.  Wochen.,  1899,  S.  1093. 
t  Travis:    Johns  Hopkins  Hosp.  Bull.,  May,   1902. 
§  Lancereaux:    Gaz.  des  Hop.,  186S. 
II  Eggel:    Ziegler's  Beitrage,   Bd.  xxx,  S.   506,   1901. 
**  Rolleston:  Trans.  Path.  Soc,  vol.  Hi,  p.  203. 


MALIGNANT    DISEASE    OF   THE    LIVER. 


475 


on  the  surface  of  the  h^'er,  JDiit  they  may  be  deeply  embedded  in  its  sub- 
stance. The  right  lobe  is  far  the  most  often  affected.  The  growi:h  does 
not  tend  to  spread  by  the  hanphatics  to  the  glands  in  the  portal  fissure. 

The  gro"^1:h  has  an  especial  tendency  to  grow  into  the  portal  and 
hepatic  veins  and  thus  spreads  through  the  liver  and  induces  secondary 
growths.  From  the  portal  vein  the  growth  may  extend  along  pervious 
and  dilated  veins  in  the  falciform  ligament.  The  portal  obstruction  in- 
duces ascites,  which  is  a  constant  feature  of  the  disease.  Extension 
into  the  hepatic  vein  is  not  uncommon. 

Pennato*  describes  three  varieties  of  primary  carcinoma  with  cirrhosis,  but 
it  seems  doubtful  whether  the  distinctions  drawn  are  sufficiently  marked  to  justify 
this. 

The  liver  nearly  always  shows  adhesions  over  the  capsule.  The  spleen 
is  enlarged  in  about  half  the  cases. 

Secondary  growths  are  said  by 
Hanot  and  Gilbert  to  be  as  frequent 
as  in  other  forms  of  primary  carci- 
noma of  the  liver.  After  the  liver, 
they  are  most  frecpiently  seen  in  the 
lungs  or  on  the  pleura,  doubtless 
from  the  fact  that  the  growth  often 
extends  into  the  hepatic  veins. 
Secondary  growths  may  also  occur 
on  the  peritoneum.  There  is  very 
little  tendency  to  lymphatic  infec- 
tion in  this  form  of  primary  carci- 
noma of  the  liver. 

When  primary  carcinoma  super- 
venes on  a  cirrhotic  liver,  the  minute 
structure  is  nearly  always  that 
described  by  Hanot  and  Gilbert 
as  trabecular  carcinoma.  In  some 
instances  other  histological  forms 
have  been  met  with  (Thomson,! 
Travis  J),  but  there  is  evidently  an 
intimate  relationship  between  trabe- 
cular carcinoma  and  cirrhosis,  since 

its  histological  characters  are  not  found  in  other  forms  of  ])rimary 
carcinoma  of  the  liver. 

Hanot  and  Gilbert  §  figure  and  describe  the  groAvth  in  Primary  Car- 
cinoma with  Cirrhosis  as  Epithelioma  trabcculaire.  There  are  tubular 
columns  of  polyhedral  or  subcolumnar  cells  arranged  in  a  single  layer 
around  a  lumen  which  is  usually  obliterated,  but  may  contain  inspissated 
bile.     The  nuclei  of  the  cells  are  situated  externally,  at  the  periphery 

*  Pennato:  Riforma  Medica,  May  6,  1S97;  abstract  in  Brit.  Med.  Journ.,  1S97, 
vol.   ii,   Epitome,   No.   38.  ■ 

t  Campbell  Thomson:    Trans.  Path.  Soc,  vol.  Hi,  p.  207. 

j  Travis,  C.  H.:    Johns,  Hopkins  Ho.sp.  liull..  No.  134,  p.  lOS,  May,  1902. 

§  Hanot  and  Gilbert:   Etudes  sur  les  Maladies  du  foie,  p.  41,  1880^ 


Fig.  .59. — Skction  of  the  Livee  in  Car- 
cinoma WITH  Cirrhosis. 
The  growth  is  seen  invading  the  right 
lobe  and  occupying  the  portal  vein.  (From 
case  described  on  p.  478.  Drawing  by  P.  L. 
Mummery,  Esq.,  F.  R.  C.  S.) 


476 


DISEASES    OF   THE    LIVER. 


Fig.  60. — Shows    Microscopic   Appearances   in   Carcinoma  with   Cirrhosis.     Cirrhosis  to 
THE  Left,  Carcinoma  to  the  Right.     Under  a  Very  Low  Power.* 


Fig.  6L — Microscopic  Structure  of  the  Growth  Under  a  Higher  Power  Shows  Branch- 
ing Columns  of  Subcolumnar  Cells  Separated  by  Capillaries. 

*  For  this  block  I  am  indebted  to  the  Council  of  the  Pathological  Society  of 
I.ondon.     Vide  Transactions,  vol.  lii,  p.  203. 


MALIGNANT    DISEASE    OF   THE    LIVER. 


477 


of  the  tubular  column.  These  columns  branch,  undulate,  and  twist,  and 
are  separated  from  each  other  by  capillaries  which  may  contain  blood. 
Except  for  the  capillary  walls  and  occasionally  well-formed  venules, 
there  is  no  intertubular  stroma.  The  cells  stain  well,  hke  the  pseudo- 
bihary  canahcuh,  and  are  smaller  than  liver  cells,  being  intermediate 
in  size  between  them  and  the  cells  of  the  pseudobile  canaliculi.  Occa- 
sionally multinuclear  cells  are  present.  Both  the  growths  in  the  liver 
and  the  secondary  growths  in  the  lung  have  been  known  to  show  bile- 
stained  contents.* 

The  carcinomatous 
growth  may  be  derived 
from  the  Mver  cells  di- 
rectly or  may  supervene 
on  the  hyperplasia  of  the 
hepatic  cells,  which  occurs 
as  a  compensatory  change 
in  cirrhosis  and  leads — (i) 
to  the  formation  of  multi- 
ple adenomata  in  cirrhosis 
(vide  p.  456)  and  (ii)  to  the 
production  of  the  pseudo- 
bile  canalicuh  in  the  inter- 
lobular connective  tissue. 

Hanot  and  Gilbert  f  and 
Hunter  J  describe  the  direct 
transformation  of  the  hver  cells 
into  carcinoma.  Schmieden  § 
has  traced  the  commencement 
of  carcinoma  in  the  centre  of 
multiple  adenomata  in  a  cir- 
rhotic liver,  and  it  seems 
highly  likely  that  multiple 
adenomata  might  be  an  ante- 
cedent stage  to  carcinoma. 

In  some  cases  the 
trabecular  carcinoma  may 
be  a  further  development 
of  the  pseudobile  canal- 
iculi,   which   were    showai 

years  ago  by  Dreschfeld||  to  be  due  to  rapid  proliferation  of  the  liver 
cells  and  may  be  regarded  in  the  light  of  a  compensatory  hy]Derplasia 
(Hanot**).  The  development  of  carcinoma  might  be  considered  as  an 
outcome  of  the  habit  of  proliferation  which  began  as  a  compensatory 
process,  but,  like  endarteritis,  must  be  considered  as  a  compensatory 
mechanism  which  has  failed. 

*Cloin:    Prag.  med.  Wpchen.,  Bd.  xxvi,  S.  261,  1901. 
t  Hanot  and  Gilbert:    Etudes  sur  les  Maladies  du  foie,  p.  41. 
t  Hunter,  W.:    Brit.  Med.  Journ.,   1901,  vol.  i,  p.  151. 
§  Schmieden:    Virchovv's  Archiv,  Bd.  clix,  8.  290. 

II  Dreschfeld:    Journ.    of  Anat.  and  Physiolog.,  London,  vol.  xiv,  p.  69. 
**  Hanot:    Gaz.  des  Hop.,  Paris,  July  10,  1896. 


iiG.  &2.  —  l^noTO.Mi(H()(.;KAi'H  OF  Cakcinoma  with  Cir- 
rhosis. Showing  I'ubdlar  Columns  of  Cells  En- 
closing Masses  of  Inspissated  Bile. 

In  the  capillaries  separating  the  columns  of  cells  a  few 
leucocytes  are  seen.      (Dr.  H.  Spitta.)     X  220. 


478  DISEASES    OF   THE    LIVER. 

When  the  growth  is  compressed  or  under  pressure,  the  capillary 
walls  may  collapse  and  the  structure  of  the  growth  is  obscured.  Degen- 
eration of  the  cells  may  occur;  the  gro\\i:h  may  become  infiltrated  with 
blood  or  invaded  by  fibrosis. 

The  clinical  aspects  of  carcinoma  with  cirrhosis  are  practically  the 
same  as  those  of  portal  cirrhosis.  It  is  only  when  the  liver  is  large  that 
nodules  can  be  felt;  as  a  rule,  the  liver  is  small.  Ascites  is  constant, 
while  jaundice  and  pain  in  the  hepatic  region  are  said  to  be  more  promi- 
nent than  in  simple  cirrhosis.  Carcinoma  with  cirrhosis  occurs,  as  would 
naturally  be  expected  from  the  greater  incidence  of  cirrhosis  in  men, 
very  much  more  frequently  in  the  male  than  in  the  female  sex.  In  22 
recorded  cases  of  which  I  have  notes  all  were  in  men. 

The  following  case  was  an  example  of  carcinoma  with  cirrhosis* : 

A  Scotchman  aged  forty-four,  who  had  taken  alcohol  and  neat  whisky,  but 
not  in  great  excess,  was  under  my  care  in  St.  George's  Hospital  July-October, 
1900.  For  four  months  before  death  his  abdomen  had  been  swollen;  about  three 
months  before  death  he  had  haematemesis  and  melsena  on  two  occasions.  During 
August  and  September  paracentesis  was  performed  four  times.  A  month  before 
death  he  became  comatose,  but  revived  after  saline  intravenous  transfusion.  There 
was  a  good  deal  of  pain  in  the  hepatic  region.  His  facial  aspect  was  that  of  cirrhosis; 
there  were  distended  abdominal  veins,  but  neither  the  liver  nor  spleen  could  be 
felt.  The  case  was  regarded  as  one  of  cirrhosis,  complicated,  since  paracentesis 
was  required  four  times,  by  chronic  peritonitis.  At  the  necropsy  the  liver  (vide 
Fig.  59)  weighed  .52  ounces  and  was  markedly  cirrhotic  and  hobnailed.  On  the 
convexity  of  the  right  lobe,  close  to  and  involving  the  attachment  of  the  falciform 
ligament,  there  was  a  soft,  whitish  projection  which  invaded  the  liver  for  a  rather 
greater  extent  than  it  projected  above  its  surface,  and  was  about  the  size  of  an 
orange.  On  section,  it  was  gelatinous  and  passed  by  continuity  into  the  bifurca- 
tion of  the  portal  vein  blocking  up  its  trunk  and  its  intra-hepatic  branches,  thus 
giving  rise  to  secondary  growths  in  the  liver.  The  walls  of  the  portal  vein  were 
thickened.  The  falciform  ligament  contained  a  large  vein  the  size  of  a  crow's  quill, 
filled  with  growth. 

Microscopically  the  liver  showed  multilobular  cirrhosis  with  extensive  pseudo- 
bile  canalicular  formation.  In  the  region  showing  new-growi;h  to  the  naked  eye 
there  was  a  formation  composed  of  columns  of  cells  without  any  lumen.  The 
columns  twisted  and  curled  about  and  were  like,  though  larger  than,  pseudobile 
canaliculi.  This  appearance  corresponds  with  trabecular  carcinoma  described  by 
Hanot  and  Gilbert.  The  growth  in  the  portal  vein  was  of  the  same  nature  and 
infiltrated  the  walls  of  the  vein,  which,  in  addition,  showed  endophlebitis  and 
secondary  calcification. 

The  gall-bladder  was  adherent  to  the  pylorus  by  old  adhesions;  it  contained 
small  bilirubin  calculi;    there  was  no  gro-nnth  in  it. 

The  bile-ducts  were  pervious.  The  veins  at  the  lower  end  of  the  oesophagus 
were  dilated,  as  were  those  under  the  peritoneum.  The  stomach  showed  very 
marked  chronic  gastritis.  There  was  no  primary  growth  in  the  pancreas,  intestine, 
or  other  part  of  the  body.  The  spleen  (16  ounces)  was  enlarged,  firm,  and  showed 
perisplenitis  and  the  scar  of  an  old  infarct.  Except  for  slight  thickening  of  the 
capsule  of  the  liver  and  perisplenitis,  there  was  no  chronic  peritonitis.  No  tubercle 
was  found  in  the  body. 

V.  Primary  Melanotic  Carcinoma. — Two  cases  have  been  recorded 
by  competent  observers  in  which  it  appeared  that  there  was  a  primary 
melanotic  carcinoma  of  the  liver.  The  subject  is  one  of  great  pathological 
interest  and  has  given  rise  to  a  good  deal  of  discussion.  In  both  cases 
an  eye  had  been  removed,  in  one  for  glaucoma,  in  the  other  for  a 
sarcoma. 

.*Rolleston:    Trans.  Path.  Soc,  vol.  hi,  p.   203. 


MALIGNANT    DISEASE    OF   THE    LIVER.  479 

Hale  White's*  case  of  primary  melanotic  carcinoma  of  the  liver  was  in  a  man 
aged  sixty-six  whose  eye,  removed  for  glaucoma  one  year  before,  showed  no  sign 
of  malignant  disease.  Fisher  and  Box's  f  case  of  multiple  melanotic  carcinoma 
of  the  liver  (which  weighed  12  pounds  6  ounces),  bones,  lungs,  and  heart  in  a  man 
who  had  had  an  eye  removed  for  melanotic  sarcoma  fourteen  years  before  may 
be  mentioned  in  connexion  with  the  occurrence  of  primary  melanotic  carcinoma 
in  the  liver.  It  is  therefore  open  to  question  Avhether  the  growths  were  really 
primary  in  the  liver;  probabl}^  many  would  regard  the  growths  as  endothelioinata 
rather  than  carcinomata. 

General  Remarks  on  the  Pathology  of  Primary  Carcinoma  of  the  Liver. 

Starting-point  of  Carcinoma. — Primary  carcinoma  may  arise  from  pro- 
liferation of  tiie  liver  cells,  of  the  cubical  epithelium  of  the  small  bile- 
ducts,  or  of  the  columnar  epithehum  of  the  larger  intra-hepatic  bile- 
clucts.  The  liver  cells  are  more  frequently  the  origin  of  carcinoma  than 
are  the  cells  of  the  bile  channels — according  to  Pepere,|  in  the  proportion 
of  7  to  1.  Spheroidal-celled  carcinoma  may  be  derived  from  the  liver 
cells  or  from  the  small  bile-ducts ;  the  larger-celled  growths  are  probably 
derived  from  the  liver  cells.  Hanot  and  Gilbert  §  believed  that  the 
trabecular  form  of  carcinoma,  seen  in  carcinoma  with  cirrhosis,  is  derived 
from  the  liver  cells.  My  own  belief  is  that  it  may  be  directly  derived 
from  the  pseudobile  canaliculi  or  so-called  new  bile-ducts.  The  latter 
are  produced  by  proliferation  of  the  liver  cells  as  an  attempt  at  compen- 
sation. ||  Columnar-celled  growths  are  derived  from  the  larger  intra- 
hepatic bile-ducts  or  possibly  from  mucous  glands  in  their  walls. 

In  addition  to  the  normal  tissues  of  the  liver  it  is,  in  accordance  with 
Cohnheim's  theory,  conceivable  that  carcinoma  might  arise  in  pieces  of 
other  abdominal  organs  which  have  become  included  in  the  liver  as  the 
result  of  some  irregularity  in  the  process  of  development.  It  has  been 
suggested  that  embryonic  relics  of  the  duodenal  diverticulum  might 
persist  and  be  the  starting-point  of  a  carcinoma,  or  that  a  small  piece  of 
pancreas  (Pepere  **)  or  an  accessory  suprarenal  gland  might  be  included 
in  the  liver.  The  question  is  interesting,  but  except  for  the  origin  of 
primary  malignant  tumors  of  the  liver  from  included  accessory  supra- 
renal gland,  there  is  little  but  theory  to  go  on. 

Schmorlft  and  other  writers  have  established  the  fact  that  accessory  suprarenal 
bodies  may  occur  in  the  liver.  The  development  of  a  malignant  disease  in  the 
liver  from  an  included  accessory  suprarenal  body  or  "rest"  is  analogous  to  the 
well-known  malignant  renal  tumors  arising  in  suprarenal  "rests."  Some  doubt 
might  arise  as  to  the  proper  designation  of  such  a  tumor  (hepatic  hypernephroma), 
but  inasmuch  as  they  resemble  carcinoma,  they  may  l)e  tentatively  referred  to 
here,  though  some  writers  might  prefer  to  class  them  with  the  endotheliomata  or 
peritheliomata.  PepereJJ  has  given  an  elaborate  account  of  a  primarj'  malignant 
tumor  of  the  left  lobe  of  the  liver  arising  in  a  suprarenal  "rest,"  which  appears  to 
be  the  first  recorded  case  of  this  kind. 

*Hale  White:    Trans.   Path.  Soc,  vol.  xxxvii,  p.  272. 

t  Fisher  and  Box:    Brit.  Med.  Journ.,  1900,  vol.  i,  p.  639. 

X  Pepere:    I  Tuniori  maligna  primarii  del  Fegato,  p.  171,  1902. 

§  Hanot  et  Gilbert:    Etudes  sur  les  Maladies  du  foie,  p.  41,  ISSS. 

IIRolleston:    Trans.   Path.  Soc,  vol.   Hi,  p.   20.3. 
**  Pepere:    Arch,  per  le  Sc.  Med.,  vol.  xxvi,  p.   US,   1902. 
tt  Schmorl:    Beitriige  z.  path.  Aiiat.  u.  z.  allg.  Path.,  Bd.  ix,  8.  .523. 
%%  Pepere:  Archiv.  de  M.6(\.  expi'riincnl .  et  d'  .\nat.  i)atli.,tome  xiv,  p.  7G.3,  1902. 


480  DISEASES    OF   THE    LIVER. 

Degenerative  Changes  in  the  Tumor. — Necrotic  changes  are  not 
uncommon,  while  the  epithehal  cehs  often  show  fatty  change;  bat, 
probably  owing  to  rapid  gro^i;h,  coUoid  degeneration  is  not  met  with. 
From  extensive  necrosis  the  growth  occasionally  shows  cystic  change 
and  some  haemorrhage  may  take  place.  The  fibrous  tissue  may  undergo 
widespread  hyahne  change. 

The  Incidence  of  Secondary  Growths  in  Primary  Carcinoma  of 
the  Liver. — Secondarj^  groT\i:hs  are  common  in  the  hver,  and,  contrary 
to  what  might  be  expected  and  is  indeed  sometimes  stated,  are  found  in 
other  situations  in  more  than  half  the  cases.  In  Eggel's  *  collection 
metastasis  occurred  outside  the  hver  in  66  per  cent.  Secondary  growths 
are  most  frequent  in  the  immediate  neighbourhood;  thus  infection  may 
spread  by  the  lymphatics  to  the  glands  in  the  hilum,  which  are  often 
enlarged  and  may  exert  pressure  on  the  portal  vein  and  bile-ducts. 
Lymphatic  glands  elsewhere,  in  the  upper  part  of  the  abdomen  and  in 
the  thorax,  may  be  infected.  Metastasis  also  occurs  by  the  blood-stream; 
the  growth  may  extend  directly  into  the  portal  and  hepatic  veins,  and 
thus  give  rise — (i)  to  fresh  gro\si:hs  in  the  substance  of  the  hver  and  (ii) 
by  embohc  masses  of  growth  which  pass  via  the  hepatic  veins  to  set  up  sec- 
ondary nodules  in  the  lungs. 

In  21  cases  of  primary  carcinoma  of  the  liver  Lancereaux  f  found  growths  four 
times  in  the  gall-bladder  and  tmce  each  in  the  peritoneum,  the  lungs,  and  the 
spleen. 

In  cases  of  primary  carcinoma  supervening  in  a  cirrhotic  liver  the  secondary 
growths  in  the  lungs  sometimes  show  bile-pigment.     (Heller, J  Cloin.§) 

Extension  of  the  primary  hepatic  groivth  into  the  portal  or  hepatic  veins 
is  much  commoner  in  the  special  form  of  carcinoma  'uath  cirrhosis  than 
in  the  other  varieties  of  primar}'  carcinoma.  The  growi:h  in  the  vein  may 
lead  to  very  considerable  dilatation  of  its  walls,  so  that  it  is  difficult  to 
make  out  the  exact  limits  of  the  vein  in  the  substance  of  the  hver. 

In  comparing  renal  and  hepatic  new-growths  as  regards  their  mode 
of  extension,  it  may  be  pointed  out  that  one  mode  of  extension,  viz., 
along  the  excretory  duct,  is  extremely  rare  in  mahgnant  disease  of  the 
liver.  Gilbert  and  Claude  ||  have  recorded  a  case,  which  they  beheved 
to  be  unique,  of  extension  of  a  massive  carcinoma  of  the  right  lobe  of 
the  hver  into  the  common  bile-duct  which  set  up  obstinate  jaundice. 

Incidence  of  Gall-stones  in  Primary  Carcinoma  of  the  Liver. — 
Although  gall-stones  occur  in  a  high  percentage — 80-90  per  cent. — of 
cases  of  primarv^  carcinoma  of  the  gall-bladder,  it  is  generally  beheved 
that  there  is  no  special  relationship  between  cholelithiasis  and  primary' 
carcinoma  of  the  liver  itself,  and  that  gall-stones  are  merely  a  coincidence 
in  malignant  disease  of  the  liver.  Confusion  has  existed  in  the  past,  and 
primary  carcinoma  of  the  gall-bladder  has  sometimes  been  described  as 
primary  carcinoma  of  the  liver,  so  any  statistics,  like  some  of  my  own, 

*  Eggel:    Ziegler's  Beitriige,  Bd.  xxx,   1901. 

t  Lancereaux:   Traite  des  Maladies  du  foie  et  du  Pancreas,  p.  472,  1S99. 

t  Heller:    Centralbl.  f.  allg.  Path.,  Oct.  15,  1S96. 

H^oin:    Prag.  med.  Wochen.,  Bd.  xxvi,  S.   261,   1901. 

il  Gilbert  and  Claude:    Archiv.  gen.  de  Med.,  t.  clxxv,  1895,  p.  513. 


MALIGNANT    DISEASE    OF   THE    LIVER.  4S1 

in  which  there  is  a  high  percentage  of  gaU-stones  in  primary  carcinoma, 
mtist  be  carefull}'  criticised  from  this  point  of  -view. 

Voelcker,  at  a  meeting  of  the  Pathological  Society  of  London,  on  Nov.  15, 
1S98,  said  that  he  had  examined  9  cases  of  primary  carcinoma  of  the  liver,  in  none 
of  which  were  any  gall-stones  present.  In  twenty-one  and  a  half  years,  at  St. 
George's  Hospital,  there  were  IS  cases  regarded  as  primary  carcinoma  of  the  liver, 
about  two-thirds  of  which  I  saw  or  examined  myself;  four  of  these,  or  22.2  per 
cent.,  contained  calculi  in  the  gall-bladder. 

Varieties  of  Primary  Sarcoma. 

I.  Primary  Massive  Sarcoma. — Tliere  is  a  large  tumor,  usuaUy  in 
the  right  lobe,  which  is  analogous  to  the  massive  form  of  primary  carci- 
noma (p.  471).  There  may  be  secondary  tumors  in  other  parts  of  the 
hver,  but  from  their  relative  size  there  is  no  doubt  as  to  which  is  the 
primary  gro^'th.  In  some  instances  the  gro'^'th  may  project  from  the 
under  surface  of  the  liver  so  as  to  become  pedunculated.  A  fair  propor- 
tion, probably  about  one-third,  of  the  cases  of  primary  sarcoma  belong 
to  this  group. 

In  44  cases  tabulated  by  Pepere  *  14  were  in  this  category. 

The  cells  may  be  small,  round,  spindle,  or  of  various  shapes  and  sizes; 
sometimes,  especially  when  growi:h  is  rapid,  multinuclear  giant-cells  are 
present.  Haemorrhage  freciuently  takes  place  into  the  growth  and  gives 
rise  to  a  mottled  or  red  appearance.  The  groT\i:hs  frequently  have  a 
spongy  aspect  on  section.  Large  sarcomatous  tumors  may  be  very 
hsemorrhagic  and  break  clown  into  cystic  cavities  and  e\en  imitate 
abscesses. 

A  case  recorded  1d}-  Bramwell  and  Leithf  simulated  an  abscess;  aspiration  was 
performed  three  times,  -ndth   removal  of  123  ounces  of  anchovy  coloured  fluid. 

In  a  woman  aged  sixty-four  under  the  care  of  my  colleague,  Dr.  Penrose,  there 
was  a  large  cystic  tumor  continuous  with  the  right  lobe  of  the  liver  and  reaching 
down  to  the  iliac  crest.  It  was  explored  by  Mr.  Turner,  and  a  large  quantity  of 
blood-stained  fluid  and  a  little  gro-^-th  removed;  it  was  thought  possilsle  that  it 
was  a  pancreatic  c^-st,  but  the  fluid  contained  nothing  l:)ut  altered  blood  and  had 
none  of  the  characters  of  the  fluid  in  a  pancreatic  cyst.  Microscopically  the  growth 
was  a  mixed-celled  sarcoma.  Subsequently  the  patient  died  of  bronchitis.  At 
the  necropsv  there  was  an  enormous  cystic  tumor,  still  containing  brown,  blood- 
stained fluid,  projecting  from  the  portal  fissure  and  carrying  the  cystic  and  common 
bile-ducts  and  portal  vein  in  front  of  it.  There  was,  however,  no  jaundice  or  ascites. 
There  were  secondary  growths  in  the  retroperitoneal  glands  and  in  the  lungs. 

II.  Nodular,  or  Multiple,  Primary  Sarcoma. — There  are  a  number 
of  discrete  nodules  scattered  in  the  substance  of  the  liver  which  are  so 
much  of  the  same  size  that  no  individual  nodule  can  be  regarded  as 
primary  and  antecedent  to  the  others.  This  ap]3ears  to  be  the  most 
frequent  anatomical  form  of  primary  sarcoma.  It  was  present  in  IS 
out  of  44  cases  of  primary  sarcoma  tabulated  l)y  Pepere.  "Where  the 
nodules  are  small  and  very  numerous,  they  tend  to  become  confluent  and 
to  produce  either  a  massive  growth,  like  the  form  just  described,  or  a 

*  Pepere:    I  Tumori  maligiii  prinuirii  del  Fegato,  p.  IIS,  Xapoli,  1902. 
t  Bramwell  and  Leitli:    Lancet,   1897,  vol.  i,  p.   170. 
31 


482 


DISEASES    OF   TPIE    LIVER. 


more  diffuse  infiltration,  in  which  the  cut  surface  has  an  apjDearance  not 
unlike  granite. 

Structurally,  the  cells  of  the  growth  may  be  of  very  A^arious  types — 
spindle,  round,  irregular,  or  giant-cells. 

There  is  a  good  example  of  a  multiple  primary  spindle-celled  sarcoma  of  the 
liver  in  the  museum  of  the  Royal  Free  Hospital.  The  late  Miss  Mabel  Webb,  jSI.B., 
curator  of  the  Museum,  kindlv  gave  me  a  slide  from  this  case  which  is  reproduced 
below  (Fig.  63). 

III.  Diffuse  or  Infiltrating  Primary  Sarcoma. — Sarcoma  may  uni- 
formly infiltrate  both  lobes  of  the  liver.     This  form  is  not  infrequently 


Fig.  63. —Drawing  of  a  Small,  Spindle-celled  Sarcoma. 
The  liver  tissue  which  is  being  invaded  is  very  lightly  stained. 


seen  in  very  early  life,  and  must  be  carefully  distinguished  from  the 
changes  due  to  congenital  syphilis.  Some  of  the  hard  infiltrating 
grow-ths,  formerly  spoken  of  as  "scirrhus"  of  the  liver,  belong  to  this 
category,  since  they  show  a  structure  like  that  of  an  endothelioma. 
There  are  large  endothelial  cells  and  large  quantities  of  hyaline  fibrous 
tissue. 

IV.  Sarcoma  Arising  in  a  Cirrhotic  Liver. — This  development  of 
primary  sarcoma  in  a  cirrhotic  liver  corresponds  to  carcinoma  with 
cirrhosis;  in  the  former  the  hyperplasia  of  the  connective  tissues  has 
gone  on  to  em])ryonic  connective-tissue  (sarcoma)  formation,  while  in 
the  latter  the  compensatory  proliferation  of  the  liver  cells  has  become 
at3^ical  and  carcinomatous.     Primary  sarcoma  has  as  j^et  onlj^  been 


.MALIGNANT    DISEASE    OF   THE    LIVER. 


483 


described  as  arising  in  a  cirrhotic  liver  in  two  cases,  viz.,  by  Ford,*  and 
by  Vecchi  and  Guerrini.f 

W.  W.  Ford  described  a  remarkable  case  of  primary  sarcoma,  forming  a  tumor 
5  by  8  cm.,  developing  in  a  highty  cirrhotic  liver.  This  growi;h,  which  was  friable, 
was  composed  of  spindle-  and  round-cells  and  had  produced  secondarj'^  gro^n^ths 
on  the  peritoneum.  There  was  ascites.  The  patient,  an  alcoholic  male  aged 
fifty-nine,  died  from  cerebral  hajmorrhage. 

V.  Primary  Melanotic  Sarcoma  of  the  Liver. — I  have  references  to 
8  published  cases, |  but  it  is  doubtful  whether  they  are  genuine  and  not 
secondary  to  a  small  growth  in  the  uveal  tract  or  in  a  cutaneous  mole 
which  has  been  overlooked.     As  shown  by  Dr.  Pitt's  case  (vide  p.  498), 


^:. 


Fig.  64. — Photomicrograpfi  Shows  the  Edge  op  a  Small  Round-cell  Sarco.ma  Infiltrat- 
ing THE  Liver  Diffusely  in  an  Infant. 
The  giowth  was  primary  in  the  liver.     (By  S.  G.  Penny,  Esq.)     X  200. 

a  very  minute  growth  in  the  uveal  tract,  which  escapes  ophthalmoscopic 
examination  and  gives  rise  to  no  symptoms  during  life,  may  produce 
great  enlargement  of  the  liver.  Thus  no  case  can  be  accepted  unless  it 
is  clear  that  the  eyes  were  specially  examined  after  death,  and  this  does 
not  appear  to  have  been  clone.  In  the  recorded  cases  the  most  that  can 
be  found  about  the  eyes  is  that  there  were  no  symptoms  during  life. 

*  Ford,  W.  W. :  American  Journal  of  the  Medical  Sciences,  vol.  cxx,  p.  43, 
Oct.,   1900.  t  Vecchi  and  Guerrini:    La  Riforma  Med.,  tome  xvii,  1901. 

X  Frerichs:  Di.seases  of  the  Liver,  vol.  ii,  p.  326.  Transl.  New  Svdenham  Soc. 
Block,  O.  C:  Archiv  der  Heilkunde,  Bd.  xvi,  S.  412,  1875.  Legg,"W.:  St.  Bar- 
tholomew's Hosp.  Reports,  vol.  xiii,  p.  160,  1S77.  Delepine,  S.:  Trans.  Path. 
Soc,  vol.  xlii,  p.  161.  Penrose,  F.  G.:  Trans.  Path.  Soc,  vol.  xlii,  p.  172.  Mid- 
dlesex Hospital  Reports,  1891,  p.  278.  Holsti:  Brit.  Med.  Journ.,  1895,  vol.  ii, 
epitome  No.  395.     Belin:  France  Medicale,  1887. 


484  DISEASES    OF   THE    LIVER. 


STARTING-PLACE  OF  SARCOMA. 


Sarcoma  may  arise  primarily  from  the  general  comiective  tissue  of  the 
liver  in  the  portal  spaces,  from  the  perivascular  connective  tissue,  from 
Kupffer's  star-like  cells  around  the  capillaries,  and  from  the  endotheMum 
of  the  blood-vessels  and  lymphatics.  The  growths  arising  from  the 
tissues  of  the  vessels,  angiosarcomata,  may  be  further  divided  into — (i) 
those  arising  from  the  lining  endothelium  of  the  blood  or  lymphatic 
vessels,  the  enclotheliomata,  and  (ii)  those  arising  from  the  perivascular 
sheaths  formed  of  endothelium  covering  the  vessels  externally,  the  peri- 
theliomata.  Probably  a  large  proportion  of  the  primary  growths  usually 
classed  as  sarcoma  of  the  liver  belong  to  the  angiosarcomata. 

Among  44  cases  of  primary  sarcoma  of  the  liver  tabulated  by  Pepere  *  22  were 
regarded  as  derived  from  the  vessels,  and  of  these,  11  were  endotheliomata  and  8 
peritheliomata. 

As  already  mentioned,  sarcoma  has  been  found  to  arise  in  the  pro- 
liferation of  the  interstitial  tissue  of  a  cirrhotic  liver.  ( W.  W.  Ford  f ; 
Vecchi  and  Guerrini.J) 

Microscopically  there  is  a  general  tendency  for  sarcoma  in  the  liver 
to  assume  an  alveolar  arrangement  and  so  to  imitate  carcinoma;  it 
is,  indeed,  not  unlikely  that  some  cases  of  large  or  medium-sized  round- 
celled  sarcomata  of  the  liver  have  been  described  as  carcinomata,  as 
there  is  often  considerable  difficulty  in  coming  to  a  satisfactory  decision 
as  to  the  nature  of  the  growth  in  such  cases.  One  reason  why  a  sarcoma 
is  often  alveolar  is  that  the  growth  is  an  endothelioma,  derived  from  the 
endothelium  lining  the  small  blood-vessels  or  lymphatics. 

The  forms  of  sarcoma  met  with  are  very  various — small  round-celled, 
large  round-cell,  spindle-celled,  irregular-celled  sarcoma  with  giant-cells, 
lymphosarcoma,  angiosarcoma,  including  under  this  head  the  endo- 
theliomata, and  melanotic  sarcoma,  have  all  been  described. 

Condition  of  the  Remainder  of  the  Liver  in  Primary  Malignant  Disease. 

There  may,  of  course,  be  secondary  growths  in  parts  of  the  liver 
remote  from  the  main  tumor.  In  some  cases  compensatory  hyperplasia 
of  the  liver  cells  may  form  nodules  which  are  with  difficulty  distinguished 
from  secondary  growths.  Local  venous  engorgement  from  pressure  on 
the  trunks  of  the  intra-hepatic  veins  or  local  bile-staining  from  compres- 
sion of  the  bile-ducts  may  also  be  met  with.  The  occurrence  of  cirrhosis 
has  already  been  dealt  with.  As  a  curiosity,  the  association  of  primary 
malignant  disease  of  the  liver  with  calcified  hydatid  cysts  in  the  organ 
may  be  mentioned. § 

Growths  in  the  liver  may  become  invaded  by  micro-organisms;  this  may  occur 
during  life  and  give  rise  to  suppuration.     It  is  not  uncommon  for  micro-organisms 

*  Pepere:    I  Tumori  maligni  primarii  del  Fegato,  p.  118,  1902. 

t  Ford,  W.  W.:    American  Journ.  Med.  Sciences,  vol.  cxx,  p.  43,  Oct.,  1900. 

I  Vecchi  and  Guerrini:    La  Riforma  Med.,  tome  xvii,  1901. 

§  St.  Thomas'  Hospital  Reports,  vol.  xxix,  p.  141. 


MALIGNANT    DISEASE    OF   THE    LIVER.  485 

to  gain  access  to  the  gro-ni^h  at  or  after  death;  they  are  then  of  no  importance. 
Hebb  *  found  long  bacilU  in  a  case  of  primary  carcinoma  and  Delepine  t  staphylo- 
cocci in  primary  melanotic  sarcoma  of  the  liver. 

Secondary  Malignant  Disease  of  the  Liver. 
INCIDENCE. 

Numerical  Ratio  Between  the  Incidence  of  Secondary  and  Pri- 
mary Malignant  Disease  of  the  Liver. — Secondary  malignant  growths 
in  the  hver  are  very  common,  while  primary  growths  of  the  liver  substance 
are  rare.  The  numerical  relationship  between  primary  and  secondary 
malignant  disease  of  the  liver  is  often  stated  to  be  about  1  to  20.  Even 
this  is  rather  overstating  the  frequency  of  primary  malignant  disease  of 
the  liver.  Possibly  cases  of  malignant  disease  of  the  gall-bladder  or 
larger  bile-ducts  have  been  regarded  as  primary  in  the  liver  by  some 
observers  and  so  have  tended  to  vitiate  statistics. 

Hale  White  J  puts  the  proportion  of  undoubted  primary  to  secondary  carci- 
noma as  1  to  25.  He  found  that  primary  malignant  disease  was  the  cause  of 
death  in  0.1  per  cent.,  and  that  secondary  growths  were  present  in  3  per  cent,  of 
patients  examined  after  death  at  Guy's  Hospital. 

Hansemann,§  in  twenty  years, — 1870-1889, — found  that  258  autopsies  show- 
ing malignant  disease  in  the  liver  had  been  performed  in  the  Pathological  Institute 
at  Berlin.  Of  these,  25  were  primary  in  the  gall-bladder,  2  in  the  larger  ducts, 
and  either  6  or  4  primary  in  the  liver.  This  shows  a  ratio  of  primary  to  secondary 
growths  of  nearly  1  to  40. 

Incidence  of  Secondary  Carcinoma  and  Sarcoma  in  the  Liver. — 

Secondary  carcinoma  is  far  more  often  met  with  than  secondary  sarcoma. 

In  100  cases  of  secondary  malignant  disease  of  the  liver  abstracted  from  the 
postmortem  records  of  St.  George's  Hospital,  77  were  carcinoma  and  23  sarcoma. 
The  cases  of  sarcoma  include  endotheliomata,  such  as  the  malignant  tumors  of  the 
suprarenal  body,  of  which  there  were  5.  There  were  3  cases  of  melanotic  sarcoma. 
In  Hale  White's  ||  figures  the  percentage  was  92.65  carcinomatous,  and  7.35  sarco- 
matous, secondary  growths.  In  his  136  cases  of  secondary  growths  in  the  liver  at 
least  126  were  carcinomatous. 

The  smaller  incidence  of  secondary  sarcoma  in  the  hver  is  readily 
explained  not  only  by  the  fact  that  carcinoma  is  a  commoner  growth 
than  sarcoma,  but  also  by  the  infrequency  of  primary  sarcoma  in  the 
alimentary  canal,  or,  in  other  words,  within  the  territory  of  the  portal 
vein.  Sarcoma,  like  pyaemia,  travels  by  the  veins  to  and  through  the 
lungs,  which  tend  to  filter  out  the  micro-organisms  or  infecting  cells  and 
thus  at  their  own  expense  protect  the  rest  of  the  body. 

Sex. — Secondary  malignant  disease  of  the  liver  is  rather  more  fre- 
quent in  women  than  in  men. 

During  the  four  years — 1897-1900 — there  were,  according  to  the  registrar- 
general's  returns  for  England  and  Wales,  8654  female  and  5532  male  deaths  from 
mahgnant  disease  of.  the  liver;  though  these  figures  include  malignant  disease  of 
the  gall-bladder,  which  is  much  commoner  in  women,  it  is  probable  that  they  rep- 

*  Hebb,  R.  G.:   Westminster  Hospital  Reports,  vol.  iii,  p.  180. 

t  Del(^pine,  S.:   Trans.  Path.  Soc,  vol.  xlii,  p.  161. 

t  Hale  White:    AUbutt's  System,  vol.  iv,  p.  204. 

§Hansemann:  Berlin,  klin.  Wochen.,  1890,  S.  353. 

P  Hale  \Mute:    Allhutt's  Sy.stem  of  Med.,  vol.  iv,  p.  194. 


486  DISEASES    OF   THE    LIVER. 

resent  very  fairly  the  incidence  of  secondary  malignant  disease  and  correspond 
with  Hale  White's*  estimate  of  4  to  3. 

The  greater  frequency  of  secondary  malignant  disease  of  the  hver 
in  women  depends  not  only  on  the  greater  incidence  of  malignant  disease 
in  that  sex,  but  also  on  the  special  predominance  of  malignant  disease 
of  the  mamma  and  female  genital  organs.  Secondary  growths  in  the 
liver  often  follow  cancer  of  the  mamma  and  genital  organs,  but  rarely 
occur  in  malignant  disease  of  lip,  mouth,  and  tongue,  which  are  much 
commoner  in  the  male  than  in  the  female  sex. 

Payne's  statistics  t  show  that  the  incidence  of  cancer  generally,  and 
especially  of  the  alimentary  canal,  is  absolutely  and  steadily  increasing. 
According  to  the  registrar-general's  statistics,  although  at  the  present 
time  women  suffer  more  severely  from  mahgnant  disease  than  men  in 
the  aggregate,  the  incidence  of  malignant  disease  has  increased  more 
rapidly  among  men  than  in  the  other  sex.  It  is,  therefore,  highly  proba- 
ble that  secondary  malignant  disease  of  the  liver  is  becoming  more 
frequent  in  males  than  formerly. 

In  100  cases  of  secondary  malignant  disease  of  the  liver  examined  at  St. 
George's  Hospital  and  taken  in  continuity  from  the  postmortem  records,  1892- 
1902,  I  was  surprised  to  find  that  the  number  of  males  (66)  were  nearly  double 
that  (34)  of  the  females. 

Age. — Secondary  malignant  disease  of  the  liver  occurs  most  fre- 
quently after  forty  years  of  age. 

The  average  age  of  100  cases  of  secondary  malignant  disease  of  the  liver  examined 
at  St.  George's  Hospital  was  49.8  years.  The  average  ages  of  the  66  males  was 
51.3  years,  and  of  the  34  females,  47  years. 

The  average  age  is,  as  might  be  expected,  higher  in  the  cases  of 
secondary  carcinoma  than  in  those  of  secondaiy  sarcoma. 

Among  100  cases  of  secondary  mahgnant  disease  of  the  liver  the  average  age 
of  77  cases  of  carcinoma  was  51.9  years  (50  males  cases,  average  age,  53.1  years; 
27  female  cases,  average  age,  48.5) ;  while  the  average  age  of  23  cases  of  secondary 
sarcoma  was  43  years  (16  males,  43.8  years;    7  females,  41.1). 

Probabty  the  earliest  recorded  case  of  secondary  carcinoma  of  the  hver  is 
Zuppinger's,J:  in  a  girl  aged  twelve  years.  The  primary  growth  was  a  columnar- 
celled  carcinoma  of  the  sigmoid  flexure. 

MORBID  ANATOMY    AND   HISTOLOGY. 

The  liver  is  sometimes  of  the  normal  size,  with  a  few  secondary  growths 
scattered  over  its  surface.  Often,  however,  the  secondary  gro'uiihs  in  the 
liver  increase  very  rapidly,  and  if  the  primary  gro^^'th  in  the  alimentary 
canal  is  comparatively  stationary,  the  liver  may  reach  a  ver}^  large  size. 
In  cases,  such  as  carcinoma  of  the  breast  or  melanotic  sarcoma  of  the 
uveal  tract,  where  the  primary  growth  may  have  been  removed  after 
infection  of  the  liver  has  actually  taken  place,  the  liver  may  subsecjuently 
become  greatly  enlarged.     The  largest  livers  known  occur  in  secondary 

*  Hale  White:    Allbutt's  System,  vol.  iv,  p.   197 

t  Payne,  J.  F.:    Lancet,  1899,  voL  ii,  p.  765. 

J  Zuppinger:  Wien.  klin.  AVochen.,  April  26,  1900,  S.  389. 


MALIGNANT    DISEASE    OF   THE    LIVER.  487 

malignant  disease.  Hilton  Fagge  *  mentions  a  liver  weighing  28  pounds, 
and  Litten  described  a  case  of  secondary  melanotic  sarcoma  in  which 
the  liver  weighed  27  pounds. 

Secondary  invasion  of  the  liver  is  hardly  ever  Umited  to  a  single 
nodule  of  growth.  The  Uver  may  show  a  number  of  multiple  and  dis- 
crete growths,  or  may  be  widely  and  diffusely  infiltrated  for  a  greater 
or  less  extent.  The  latter  condition  is  sometimes  well  seen  in  carcinoma 
of  the  breast  or  in  melanotic  sarcoma.  When  widety  infiltrated,  the 
liver  is  enlarged,  but  preserves  its  general  shape  and  anatomical  outlines 
very  fairly. 

"Farre's  tubercles"  was  formerly  a  well-known  synonym  for  secondary  growths 
in  the  liver.  This  -vmter  described  "Tubera  circmnscripta "  and  "Tubera  diffusa," 
corresponding  to  the  two  forms  mentioned  above. f 

In  some  instances  nodules  originally  separate  may  unite  and  form 
a  large  irregular  mass.  The  growths  are  scattered  throughout  the  liver, 
but  are  especially  frequent  near  the  surface  of  the  organ,  and  are  rarely 
seen  on  section  when  entirely  absent  from  the  surface.  They  grow 
rapidly  and  receive  their  blood-supply  from  the  hepatic  artery,  which 
is  sometimes  considerably  enlarged. 

In  this  connexion  it  is  interesting  to  refer  to  a  plate  of  Bright's  J  showing  a 
large  artery  supplying  a  mass  of  secondary  new-growth. 

Whether  carcinomatous  or  sarcomatous,  the  naked-eye  appearances 
of  the  nodules  have  much  in  common.  They  are  usually  white  in  colour, 
and  are  not  infrequently  bile-stained  and  may  be  speckled  with  blood 
or  extremely  hgemorrhagic.  In  secondary  melanotic  sarcoma  there  may 
be  isolated  pigmented  nodules,  areas  of  diffuse  melanotic  infiltration,  or 
both  combined.  In  some  cases  the  secondarj^  melanotic  growi:hs  are 
almost  or  quite  devoid  of  pigment,  at  any  rate  to  the  naked  eye.  Sar- 
comatous gro^vths  are  more  likely  to  be  hsemorrhagic  and  to  form  soft- 
ened pseudo-cysts;  as  a  nde,  they  are  not  depressed  in  the  centre  or 
umbiHcated,  a  change  often  seen  in  secondary  carcinomatous  growths 
on  the  surface  of  the  liver.  It  has  been  said  that  secondary  sarcomatous 
nodules  are  never  umbilicated,  and  may  thus  be  distinguished  from 
secondary  carcinomatous  growths  in  the  liver.  This  is  too  dogmatic  a 
statement  and  must  admit  of  some  exceptions. 

In  St.  Bartholomew's  Hospital  Museum  there  is  the  liver  of  a  boy  aged  ten 
years  enormously  enlarged  and  studded  with  umbilicated  nodules  secondary  to 
sarcoma  of  the  kidney  (No.  2215  c). 

The  dead-white  colour  of  some  secondary  carcinomatous  nodules, 
especially  columnar-celled  growths,  may  give  rise  to  an  appearance  ver}' 
like  a  gumma,  so  that  considerable  difficulty  may  arise  in  distinguishing 
between  the  two  conditions,  especially  when  only  a  limited  examination 
can  be  made,  as  at  exploratory  laparotomies. 

*  Fagge:  Principles  and  Practice  of  Medicine,  vol.  ii,  p.  296,  1886. 
t  J.  R.  Farre:  Morbid  Anatomy  of  the  Liver,  1815. 
t  Bright:  Guy's  Hospital  Reports,  vol.  i,  p.  638,  1836. 


488 


DISEASES    OF   THE    LIVER. 


I  Have  several  times  examined  fragments  removed  during  life  which  have 
turned  out  to  be  columnar-ceUed  growths  secondary  to  a  latent  carcinoma  in  the 
stomach  or  colon  and  which  it  was  natural^  hoped  might  be  gummata.  Gouget  * 
described  a  columnar-celled  carcinoma  of  the  liver  which  was  at  first  regarded 
as  a  gumma. 

The  consistency  of  the  growths  varies  considerably.     Diffuse  areas 
of  infiltration  may  be  hard,  but  as  a  general  rule  the  larger  the  size  of 
a  secondary  groT\i:h,  the  softer  it  is,  since  degeneration  and  necrotic 
changes  are  more  prone  to  supen^ene  than  in  smaller  nodules.     Small 
discrete  nodules  cut  with  the  same  kind  of  resistance  as  a  cream  cheese. 
Degenerative   Changes. — The  central  parts  of  the  larger  nodules 
readily  undergo  fatty  degeneration  or  necrosis  and  may  have  a  caseous 
or  softened  appearance.     I  have  seen  a  rapidly  grovdng  mass  of  car- 
cinoma    i^resent     the     honey- 
combed  and   softened    appear- 
ance of  actinomycosis.  Extreme 
softening  may  in  some  instances 
be  due  to  suppuration  from  in- 
fection.    The  necrosed  portions 
may  be  yellow  or   green  from 
bile-staining,    or    may    become 
infiltrated    with     blood.      This 
hgemorrhagic   condition  is  more 
often  seen  in  sarcoma,  but  it 
may  also  be  met  with  in  secon- 
dary    carcinomatous     grovi:hs. 
Sometimes  the  haemorrhage  into 
the   degenerated  growth  is    so 
profuse    as  to   lead  to   serious 
syncope,  but  when  this  occurs, 
the  growth  has  usually  ruptured 
and  allowed  blood  to  pass  into 
the  peritoneal  cavity.     In  other 
instances  a  sanguineous  ascitic  effusion  is  clue  to  comparativeh^  insig- 
nificant leakage  from  a  small  nodule. 

Colloid  degeneration  rarely  occurs  in  a  secondaiy  growth  in  the  liver. 

There  is  a  good  specimen  of  a  mass  of  coUoid  carcinoma,  the  size  of  a  man's 
fist,  in  St.  Bartholomew's  Hospital  Museum,  secondarv  to  a  gro-«-th  in  the  rectum. 
(No.  2216  H.) 

According  to  Schueppel,t  diffuse  coUoid  cancer  of  the  peritoneum 
may  spread  by  the  lymphatics  of  the  capsule  of  the  Uver  and  pass  into 
its  substance  like  strings.  Eventually  a  whole  lol^e  of  the  li\-er  may 
become  transformed  into  a  colloid  mass. 

M^Tcomatous  and  hyaline  degeneration  may  attack  the  fil^rous  tissue 
of  a  slow-growing  secondary  nodule  of  carcinoma,  or  occur  in  secondar\- 
endotheliomatous  nodules  even  though  growing  rapidly. 

*  Gouget:  Bull.  Soc.  Anat.  Paris,  1S90,  p.  605. 

t  Schueppel:  v.  Ziemssen's  Cyclopaedia  of  Practical  Medicine,  \o\.  ix,  p.  33S. 
English  trans. 


Fig.  65. — Drawing  of  Cyst  Due  to  Softening  of 
A  Secondary  Carcinomatous  Growth  in  the 
Liver  from  a  Specimen  in  St.  George's 
Hospital  Museum.  (Series  ix,  184  L.) 
(Drawn  by  L.  Jones,  Esq.,  il.B.,  F.R.C.S.) 


MALIGNANT    DISEASE    OF    THE    LIVER.  489 

Formation  of  Pseudo-cysts. — Degeneration  and  softening  of  sec- 
ondary malignant  growths  may  lead  to  the  formation  of  definite  cysts. 
This  may  occur  in  any  form  of  carcinoma,  even  in  the  squamous-celled 
variety,  and  in  sarcomata.     It  is,  however,  a  rather  rare  condition. 

In  a  case  of  carcinoma  of  the  stomach  recorded  by  Hawthorne  *  there  were 
numerous  cysts  in  the  right  lobe  of  the  liver,  due  to  softened  new-gro-ni:h;  the 
largest  had  a  diameter  of  4i  inches.  Aspiration  during  life  resulted  in  the  ^^^th- 
drawal  of  58  ounces  of  blood-stained  fluid.     The  case  imitated  an  abscess. 

In  a  case  of  carcinoma  of  the  pylorus  recorded  by  Nicaise  f  the  liA'er,  which 
weighed  75  ounces  and  contained  numerous  secondary  growths,  had  a  tongue- 
shaped  lobe  with  a  htemorrhagic  cyst  due  to  destruction  6i  the  groAvth. 

In  a  case  of  carcinoma  of  the  liver  probably  secondary  to  the  pancreas  in  a 
man  aged  fifty-one  under  Dr.  Sainsburj'^'s  care  there  were  numerous  cystic  spaces 
with  caseous  contents.  Microscoijically  the  growi:h  was  a  carcinoma,  showing  a 
transition  from  a  columnar  to  a  spheroidal  type,  with  a  considerable  amount  of 
fibrous  tissue  and  extensive  necrotic  and  cystic  changes.  The  liver  is  in  the  Museum 
of  the  Royal  Free  Hospital,  and  by  the  courtesy  of  the  late  Miss  M.  Webb,  M.B., 
Curator,  I  was  enabled  to  cut  sections  of  the  growths. 

Voelcker  J  described  secondary  squamous-celled  carcinomatous  nodules  with 
cystic  change,  a  smooth  thin  layer  of  new-gro-n^h  alone  being  left  as  the  wall  of 
the  cyst.  Thomson  §  met  -Rath  a  similar  case  where  the  cyst-wall  could  easily  be 
peeled  out  of  the  liver;  it  closely  resembled  an  hydatid  cyst  and  contained  clear 
yeUow  fluid.  There  is  a  somewhat  similar  specimen  with  cysts  the  size  of  a  mandarin 
orange  in  St.  Bartholomew's  Hospital  Museum  secondary  to  a  growth  in  the  oesoph- 
agus. In  a  case  described  by  Sharkey  ||  the  liver  was  studded  with  cysts  lined 
by  squamous  epithelium. 

In  St.  Bartholomew's  Hospital  Museum  there  is  a  specimen  (2215e)  of  sec- 
ondary sarcomatous  growths  in  the  liver  which  have  broken  down  so  extensively 
that  the  appearance  is  not  unlike  that  of  cystic  disease  of  the  organ  in  the  adult; 
the  primary  growth  was  in  the  skin  of  the  back.  I  have  seen  the  same  thing  in 
a  secondary  endothelioma  of  the  liver  which  weighed  18  pounds,  the  primary  gro-ni;h 
being  in  the  left  kidney.     {Vide  p.  517.) 

Umbilication. — Not  uncommonly  nodules  of  secondary  growth  on 
the  surface  of  the  liver  show  a  central  depression  or  cupping  which  is 
spoken  of  as  umbilication.  It  occurs  in  comparatively  slow-growing 
carcinomatous  nodules  and  is  very  rare  in  secondary  sarcoma.  (Vide 
p.  487.) 

This  umbilication  is  due  to  the  cells  in  the  central  part  of  the  nodule 
undergoing  degeneration  and  becoming  compressed  by  the  surrounding 
fibrous  tissue,  which,  from  the  greater  age  of  the  growth  in  the  centre, 
is  better  developed  than  in  the  more  recent  peripheral  parts  of  the  nodule. 
Another  factor  is  the  more  exuberant  cellular  proliferation  at  the  edge 
of  the  nodule,  which  leads  to  a  heaping-up  of  growth.  The  depression 
of  the  oldest  part  of  an  oyster's  shell,  viz.,  that  near  the  hinge,  illustrates 
the  production  of  umbilication.  (Wilks.**)  Umbilication  is  often  absent 
in  rapidly  growing  nodules  of  small  size. 

Growths  in  the  liver  frequently  press  on  the  branches  of  the  portal 
vein  and  may  thus  help  to  cause  ascites;  pressure  on  the  hepatic  veins 
is  often  seen,  and  gives  rise  to  local  chronic  venous  engorgement.     In  a 

*  Hawthorne,  C.  O.:  Clinical  Journal,  vol.  viii,  p.  .361. 
t  Nicaise,  V.:  Bull.  Soc.  Anat.,  1900,  p.  146. 
t  Voelcker,  A.  F.:  Trans.  Path.  Soc,  vol.  xlvii,  p.  43. 
§  Thomson,  H.  C:  Practitioner,  Oct.,  1899,  p.  411. 
II  Sharkey,  S.  J.:   Trans.  Path.  Soc,  vol.  xxxv,  p.  374. 
**  Wilks:  Pathological  Anatomy,  p.  474. 


490  DISEASES    OF   THE    LIVEE. 

certain  number  of  instances  the  secondary  growths  project  into  the 
veins  and  set  up  thrombosis;  detachment  of  small  pieces  of  growth  pro- 
jecting into  the  lumen  of  the  hepatic  veins  leads  to  secondary  growths 
in  the  lungs.  Occasionally  a  secondary  growth  may  form  a  polypoid 
mass  in  the  hepatic  or  portal  veins. 

Pressure  on  the  intra-hepatic  bile-ducts  is  common  and  results  in 
local  bile-staining  of  the  liver  tissue. 

In  rare  instances  malignant  disease  in  the  liver,  after  eating  its  way 
into  the  larger  bile-ducts,  may  grow  along  the  lumen  of  the  duct  without 
infiltrating  the  wall  of  the  tube.  This  process  is  like  the  downward  pro- 
jection of  a  renal  growth  into  the  ureter.  Cases  of  prolongation  of 
malignant  disease  of  the  liver  along  the  lumen  of  the  bile-ducts  have 
been  described  by  Fauvel,  Durand-Fardel,*  Gilbert  and  Claude. f 

Effects  of  Secondary  Growths. — Secondary  growths  on  the  surface 
of  the  liver  frequently  set  up  attacks  of  perihepatitis  and  so  give  rise 
to  a  good  deal  of  pain.  It  is  verj^  rare  for  a  secondary  growth  on  the 
surface  of  the  liver  to  grow  directly  into  the  abdominal  wall;  this  is 
probably  prevented  by  the  respiratory  movements.  It  does,  however, 
sometimes  occur,  and  the  diaphragm  or  anterior  abdominal  wall  may  be 
so  firmly  united  by  the  gro^\i:h  to  the  liver  that  after  death  they  can 
be  separated  only  by  the  knife.  A  growth  on  the  anterior  surface  of  the 
liver  may  infect  the  opposed  surface  of  peritoneum  on  the  abdominal 
wall  without  any  adhesions  between  the  two,  the  growth  being  implanted 
by  contact. 

Histology. 

Structurally  the  secondary  nodules  resemble  the  primary ;  but,  being 
more  rapid  in  their  growi^h,  are  softer  and  more  liable  to  break  down. 
When  secondary  to  carcinoma  of  the  stomach,  the  hepatic  groAvths  may 
be  either  columnar-celled  or  spheroidal-celled;  when  the  colon  is  affected, 
the  hepatic  growths  are  columnar-celled;  in  both  these  instances,  how- 
ever, the  secondary  tumors  may  differ  somewhat  from  the  primary,  the 
cells  showing  a  transition  from  the  columnar  to  the  spheroidal  type. 
When  secondary  to  carcinoma  of  the  breast,  the  gro\\i;h  is  spheroidal- 
celled;  and  when  a  primary  growth  in  the  lower  part,  of  the  a?sophagus 
infects  the  liver,  the  structure  of  the  secondary  nodules  is  that  of  a 
squamous-celled  carcinoma.  But  here  again  from  more  rapid  groAAi:h 
the  cells  may  be  spheroidal  rather  than  squamous. 

Secondary  sarcoma  is  very  often  alveolar  in  its  arrangement;  this 
depends  on  the  growth  starting  from  emboli  inside  the  small  vessels  of 
the  liver. 

In  some  cases  of  secondary  carcinoma  the  cells  of  the  liver,  which 
are  atrophied  and  compressed  by  the  columns  of  invading  cells,  show 
very  considerable  pigmentation.  This  may  be  due  to  retained  bile- 
pigment.     In  cases  where  the  liver  is   independently  pigmented,  as   in 

*  Fauvel,  Durand-Fardel:  Quoted  by  Devic  et  Gallavardin,  Rev.  de  Med., 
July,  1901,  p.  570. 

t  Gilbert  and  Claude:  Archiv.  general,  de  Med.,  t.  cLxxv,  1S95,  p.  513. 


MALIGNANT    DISEASE    OF   THE    LIVER. 


491 


malaria  or  in  hsemochromatosis,  a  secondary  growth  in  the  li\'er  is  not 
pigmented. 

A  man  aged  forty-six  died  under  my  care  with  a  primary  endotheliomatous 
growiih  in  the  spine.  The  Hver  was  of  a  deep  brick-red  colour  and  had  a  number 
of  minute  Avhite  nodules  in  it,  which  are  shown  in  the  accompanying  photomicro- 
graph to  be  quite  free  from  gro-Ri;h. 

In  some  instances  of  secondary  carcinoma  there  is  prohferation  of 
the  liver  cells  in  parts  remote  from  the  growth,  which  may  be  regarded 
as  an  attempt  to  replace  the  destroyed  liver  substance — a  comjjensatory 
hypei-plasia. 

In  a  case  of  secondary  sarcoma  Cornil*  observed  proliferation  of  the  hepatic 
cells  and  the  formation  of  pseudobile  canaliculi  at  a  short  distance  from  the  growth. 

Braultf  has  noticed  that  in  some  instances  where  the  cells  of  the  secondary 
growths  contain  glycogen  the  hepatic  cells  contain  none. 


Fig.  66. — Photomicrograph  of  a  Secondary  Villous  Carcinoma  of  the  Liver.     The  Prim- 
ary Growth  was  in  the  Kidney.      (Vide  case  on  p.  .52L     Photographed  by  Dr.  H.  Spitta.) 


A  certain  amount  of  local  fibrosis  is  often  seen  around  carcinomatous 
nodules  in  the  liver,  which  may  be  regarded  as  an  attempt  on  the  part 
of  the  organ  to  liinit  the  extension  of  the  growth.  When  this  change  is 
more  general  and  there  is  obstinate  jaundice,  the  fibrosis  has  been  thought 
to  be  due  to  biliary  obstruction  set  up  l)y  the  tiunor.J 

Condition  of  the  Remainder  of  the  Liver. — From  ])rcssurc  on  the 
bile-ducts  the  whole  or  parts  of  the  liver  may  be  bile-stained.  The 
occurrence  of  local  areas  of  chronic  venous  engorgement  from  pressure 

.     *  Cornil:  Bull.  Soc.  Anat.  Paris,  1902,  p.  195. 

fBrault:  Archiv.  de  M6d.  Expc^'riment.  et  d'Anat.  path.,  t.  xiv,  p.  467,  1902. 
j  Gilbert  and  Claude:  Arcliiv.  general,  de  Medecine,  1895,  t.  clxxv,  p.  513. 


492 


DISEASES    OF   THE    LIVER. 


on  branches  of  the  hepatic  veins  has  just  been  referred  to.  In  some 
instances  the  engorgement  is  so  extreme  that  extravasation  occurs  in 
the  immediate  neighbourhood  of  nodules  of  growth  and  produces  an 
appearance  of  a  hsemorrhagic  infarct.  Infarctions,  both  hsemorrhagic 
and  anaemic,  have  been  met  with  in  the  Hver,  as  a  result  of  venous  ob- 
struction due  to  pressure,  exerted  by  nodules  of  growths,  on  the  portal 
or  hepatic  veins.     (Vide  p.  105.) 

Secondary  malignant  growths  are  very  rare  in  cirrhotic  livers;  they 
occur,  of  course,  in  the  special  form  of  primary  carcinoma  with  cirrhosis. 

Hale  White*  mentions  a  case  of  a  man  with  sarcoma  of  many  bones  with  a 
growth  in  the  Hver  which  was  hard  and  cirrhosed.  Poulain  f  met  with  a  secondary 
nodule  of  growth  in  a  cirrhotic  hver;    the  primary  growth  was  a  columnar-celled 

carcinoma  of  the  stomach. 
Achard  and  Laubry  |  described 
secondary  gro'ni^hs  in  a  large 
cirrhotic  liver,  the  primary 
growth  being  in  the  colon. 

It  is  not  very  common 
to  find  cirrhosis  of  the  liver 
in  patients  with  intra-ab- 
dominal malignant  disease; 
this  is,  of  course,  the  main 
reason  for  the  rarity  of  sec- 
ondary growths  in  cirrhotic 
livers.  It  is  conceivable 
that  portal  obstruction  in- 
terferes with  the  passage 
of  emboli  of  infecting  cells 
from  the  colon  and  stomach, 
and  that  the  cirrhotic  hver 
is  not  a  good  soil  for  their 
development. 

When,  as  not  uncom- 
monly happens,  secondary 
growths  occur  in  tight-laced 
livers,  the  constriction  lobe  attached  to  the  right  lobe  may  be  quite 
free  from  growth,  suggesting  that  its  somewhat  isolated  position  has 
prevented  the  advent  of  emboli  of  infecting  cells  by  the  blood-stream. 
On  the  other  hand,  secondary  growth  may  be  almost  confined  to  the 
constriction  lobe,  as  if  its  diminished  resistance  was  specially  favourable 
to  the  development  of  any  embolic  masses  of  new-groT\i;h  which  gain 
access  to  it.  Examples  of  these  two  different  events  are  given  in  the 
section  on  the  tight-laced  hver  (p.  9). 

As  a  coincidence  secondary  nodules  of  new-growth  may  develop  in 
a  liver  which  is  already  affected  by  hydatid  disease.  I  have  met  with 
one  such   case  (vide  p.  395),  and  Dr.  R.  N.  Salaman  has  shown   me 

*  Hale  White:  Allbutt's  System,  vol.  iv,  p.  208. 

t  Poulain:  Bull.  Soc.  Anat.  Paris,  Dec,  1899,  p.  1089. 

t  Achard  et  Laubry:  Soc.  M^d.  des  Hop.,  April  25,  1902,  p.  335. 


Fig.  67. — Photomicrograph  of  Liver  with  Secondary 
Endotheliomatous  Growths. 
The  liver  was  deeply  pigmented  from  haemochroma- 
tosis;  the  small  nodules  of  growth  were  entirely  free  from 
pigment.     (S.  G.  Penny,  Esq.) 


MALIGNANT    DISEASE    OF   THE    LIVER. 


493 


two  specimens  in  which  secondary  nodules  of  carcinoma  happened  to  be 
in  actual  contact  with  old  hydatid  cysts. 

Secondary  growths  may  arise  in  a  syphilitic  liver,  and  even  in  one 
containing  gunnnata,  but  it  is  a  rare  coincidence. 

A  man  aged  forty  who  died  with  carcinoma  of  the  colon  had  gummata  in  one 
testis  and  much  scarring  of  the  liver,  which  contained  numerous  gummata  and 
nodules  of  new-growth.  The  man  was  under  Dr.  Cavafy  in  St.  George's  Hospital 
in  1891.  I  did  the  postmortem  and  microscopically  determined  that  there  were 
both  gummata  and  new-growths  in  the  hver. 

Tubercles  and  secondary  growths  may  exist  in  the  same  liver.  There 
is  no  antagonism  between  the  two  processes,  as  was  formerly  thought. 


Fig.  68. — Drawing  of  a  Liver  showing  the  Constriction  Lobe  Divided  and  its  Halves 
Separated  so  as  to  Display  Large  Secondary  Carcinomatous  Growths  in  its  Sub- 
stance. 

There  were  in  addition  only  two  small  white  nodules  in  the  right  lobe  of  the  liver.  The  pri- 
mary growth  was  carcinoma  of  the  breast.      (Drawn  by  L.  Jones,  Esq.,  M.B.,  F.R.C.S.) 


Dalton*  briefly  records  a  case  of  secondary  columnar-celled  carcinoma  in  the 
liver  with  miliary  tubercles  in  the  immediate  neighbourhood.  The  primary  growth 
was  in  the  sigmoid  flexure. 

The  existence  of  two  different  kinds  of  secondary  growths  in  the  same 
liver  must  be  almost  a  unique  experience. 

Simon t  records  the  case  of  a  woman  who  died,  two  years  after  removal  of  her 
right  eye,  with  widespread  melanotic  sarcoma.  The  liver  was  greatly  enlarged 
with  melanotic  sarcoma  and  contained  a  white  nodule  which  microscopically  had 
the  structure  of  columnar-celled  carcinoma.  Unfortunately  the  stoinach  and 
intestines  were  not  examined  at  the  autopsy,  so  the  site  of  the  primary  growth  was 
not  discovered. 

Methods  of  Metastasis. — The  dissemination  of  secondary  growths  is 
due  to  embolism  of  the  intra-hepatic  l)ln()(l-A'essels.     In  most  cases,  since 

*  Dalton:  Trans.  Path.  Soc,  vol.  xxxvi,  p.  235. 
t  Simon:  Bull.  Soc.  Anat.  Paris,  1900,  p.  213. 


494 


DISEASES    OF   THE    LIVER. 


the  primary  growth  is  within  the  territory  drained  by  the  portal  vein, 
the  emboh  of  carcinomatous  cells  travel  up  that  vessel.  Wlien  the  pri- 
mary growth  is  elsewhere,  as  in  the  eye  or  mamma,  the  emboli  are  dis- 
tributed by  the  hepatic  artery.  The  dissemination  of  secondary  growths 
in  the  liver,  contrary  to  what  is  the  rule  in  the  spread  of  carcinoma  else- 
where, is  not  dependent  on  the  lymphatic  vessels. 

This  depends  on  two  factors :  (i)  That  the  liver  does  not  receive  the 
lymphatics  of  the  other  abdominal  viscera,  but  sends  its  own  out  at 
the  portal  fissure ;  hence  carcinoma  w^ould  have  to  spread  in  against  the 
direction  of  the  flow  of  lymph.  This  does  occasionally  occur,  it  is  true, 
but  it  is  quite  exceptional.  In  carcinoma  of  the  stomach  growth  can 
sometimes  be  seen  tracking  into  the'portal  fissure.     Colloid  cancer  of  the 


Fig.  69. — Shows  Minute  Emboli  in  the  Intra-hepatic  Branches  of  the  Portal  Vein  (a). 

A  small  bile-duct  is  represented  at   b.     From  a  case  of  secondary  carcinoma  of  the  liver.     The 

primary  growth  was  in  the  stomach.      X  50. 


peritoneum  may  pass  into  the  subserous  lymphatics  of  the  capsule  and 
invade  the  liver,  (ii)  That  the  primary  carcinomatous  gro^A.'ths  in  the 
alimentary  canal  frequently  invade  the  radicles  of  the  portal  vein.  When 
this  has  occurred,  emboli  readily  pass  up  to  the  liver,  inasmuch  as  there 
are  no  valves  in  the  portal  vein. 

Secondary  Growths  due  to  Retrograde  Embolism. — In  rare  instances  a 
carcinomatous  or  sarcomatous  embolus,  when  in  the  right  auricle  or 
inferior  vena  cava  close  to  the  diaphragm,  is  driven,  by  some  expiratory 
effort,  into  the  hepatic  veins  against  the  stream  of  blood.  Thus  Welch* 
refers  to  Heller's  cases  of  malignant  disease  of  the  ciecum  in  which  a 
loose  plug  of  growth  was  found  in  one  hepatic  vein,  and  to  Bonome's 

*  Welch:  AUbutt's  System  of  Medicine,  vol.  vi,  p.  232. 


MALIGNANT    DISEASE    OF   THE    LIVER.  495 

case  of  cancer  of  the  thyroid  gland  with  metastatic  growths  in  the  hver 
developing  from  plugs  in  the  hepatic  veins.  M}^  friend  Professor  Adami, 
of  Montreal,  has  told  me  of  a  primary  growth  of  an  accessory  adrenal 
which  extended  into  the  inferior  vena  cava  and  right  auricle,  where  it 
ended  in  a  ball-like  termination  and  gave  rise  to  secondary  gro^^i:-hs,  evi- 
clentty  by  retrograde  embolism,  in  the  liver. 

Direct  Invasion  of  the  Liver  by  a  Growth. — It  is  not  ver}^  uncommon 
for  a  growth  starting  in  the  gall-bladder  to  infiltrate  the  liver  by  direct 
continuity,  and  in  some  instances  the  appearances  have  led  to  an 
erroneous  diagnosis  of  primary  malignant  disease  of  the  liver.  Primary 
carcinoma  of  the  extrahepatic  bile-clucts  may  extend  up  into  the  liver. 

^lalignant  disease  of  the  stomach,  especially  at  the  cardiac  end,  may 
spread  directly  into  the  substance  of  the  liver.  In  Fenwick's*  131  cases 
of  gastric  carcinoma  this  occurred  in  13.7  per  cent.  In  such  cases  the 
growth  in  the  liver  may  undergo  necrosis  or  become  infected  and  give 
rise  to  a  gangrenous  abscess  cavity  and  to  a  certain  amount  of  fever. 
In  rare  instances  carcinoma  of  the  lower  end  of  the  oesophagus  may  extend 
directly  into  the  liver.  I  have  seen  direct  invasion  of  the  liver  occur  in 
cases  of  primary  endothelioma  of  the  right  suprarenal  body. 

SITUATION  OF  THE    PRIMARY  GROWTH  IN  SECONDARY  MALIGNANT  DISEASE 

OF  THE  LIVER. 

The  iTiost  frequent  sites  of  the  primary  carcinomatous  gro'^1:-hs  are  in 
the  alimentary  canal,  viz.,  stomach,  colon,  oesophagus,  pancreas,  from 
which  small  emboli  of  infecting  cells  pass  along  the  portal  vein  and  form 
carcinomatous  emboli  in  the  capillaries  of  the  liver;  thus  secondary 
growi;hs  start,  and  are  for  a  time  inside  the  hepatic  capillaries,  while 
primar}'  carcinoma  is  outside  the  vessels,  or  extra-vascular. 

In  100  consecutive  cases  of  secondary  malignant  disease  of  liver  abstracted 
from  the  postmortem  books  of  St.  George's  Hospital  from  1892-1902  the  following 
were  the  situations  of  the  primary  growths: 

Carcinoma.  Sarcoma. 

Stomach 24  Suprarenal  bodies 5 

Colon    12  Mediastinum 4 

(Esophagus    10  Melanotic 3 

Pancreas 8  Generalized 3 

Gall-bladder 5  Bone 2 

Uterus    4  Lung 2 

Mamma    3  Stomach    1 

Kidneys 3  Liver    1 

Bile-ducts 3  Thyroid  1 

Biliary  papilla 1  Uterus 1 

Vermiform  appendix ...    1  — 

Bladder    1  23 

Ovary 1 

Generalized    1 

77 

The  stomach  is  the  most  frequent  site  of  the  primary  growth  in 
secondary  malignant  disease  of  the  liver.     According  to  Hale  White,! 

*  Fen  wick:  Cancer  and  other  Tumors  of  the  Stomach,  p.  55. 
t  Hale  White:  AUl)utt's  System  of  Medicine,  vol.  iv,  p.  197. 


496  DISEASES    OF   THE    LIVER. 

25  per  cent,  of  the  cases  of  secondary  malignant  disease  of  the  hver  are 
secondary  to  mahgnant  disease  of  the  stomach;  this  is  practically  the 
same  as  my  o.wn  estimate. 

In  malignant  disease  of  the  stomach  there  are  secondary  growths  in 
the  liver  in  about  35  per  cent,  of  the  cases  (Fenwick*).  Welch  gives 
30  per  cent.,  Perry  and  Shaw,  f  40  per  cent.,  and  Lebert,  40.9  per  cent. 
In  47  fatal  cases  of  gastric  carcinoma  tabulated  by  Osier  and  McCrae  J 
the  liver  w^as  affected  in  23.  According  to  Fenwick,  the  right  lobe  is 
involved  in  carcinoma  of  the  pylorus  and  middle  of  the  stomach,  and 
the  left  lobe  when  the  cardiac  end  is  the  site  of  carcinoma. 

Carcinoma  of  the  colon  is  probably,  after  malignant  disease  of  the 
stomach,  the  most  frequent  cause  of  secondary  growths  in  the  liver. 

In  100  cases  of  secondary  malignant  disease  of  the  liver  the  colon  or  rectum 
was  the  site  of  the  primary  growth  in  12.  In  100  fatal  cases  of  primary  carcinoma 
of  the  colon  examined  after  death  I  found  that  secondary  growths  occurred  in 
the  liver  in  34.  But  in  many  of  these  the  secondary  nodules  were  quite  small  and 
could  not  have  given  rise  to  any  clinical  manifestations.  Of  these  100  cases,  52 
were  males  (19  secondary  growths)  and  48  females  (15  secondary  growths). 

It  is  a  remarkable  fact  that  secondary  growths  in  the  liver  are  more 
frequent  and  often  more  extensive  when  the  primary  gro"v\i}h  in  the 
colon  is  small  than  when  it  is  large.  A  patient  may  be  quite  unconscious 
of  a  growth  in  the  rectum  when  the  liver  is  greatly  enlarged.  Hence  the 
rectum  should  always  be  examined  in  suspected  cases  of  malignant 
disease  of  the  liver  when  the  site  of  the  primary  growth  is  not  at  once 
clear. 

The  following  is  a  typical  example  of  extensive  malignant  disease 
of  the  liver  following  carcinoma  of  the  sigmoid  flexure : 

Primary  Carcinoma  of  the  Sigmoid  Flexure,  Secondary  Growths  in  the  Liver, 
Asthenia,  Slight  Jaundice,  and  Ascites;  Death  in  Coma. — A  man  aged  fifty-six  was 
admitted  into  St.  George's  Hospital  on  July  6,  1900,  with  abdominal  pain,  rapid 
emaciation,  and  increasing  weakness.  He  was  slightly  jaundiced,  had  a  large, 
knobby  liver,  which  was  hard  and  tender.  The  patient  had  had  pain  on  def£ecation 
and  had  passed  blood  by  the  bowel.  He  complained  of  constant  perspiration. 
There  was  some  oedema  of  the  feet.  His  condition  was  very  bad,  and  on  July  13th 
he  became  comatose  and  died  in  twenty-four  hours.  At  the  autopsy  there  was  a 
primary  columnar-celled  carcinoma  in  the  lower  part  of  the  sigmoid  flexure.  The 
liver  weighed  11  pounds  and  was  stuffed  with  white,  almost  caseous,  gro-wths; 
there  were  no  growths  anywhere  else.     There  was  some  ascites. 

Metastatic  growths  in  the  liver  are  found  in  about  half  the  cases  of 
primary  carcinoma  of  the  gall-bladder. 

In  Musser's§  100  cases  the  liver  contained  secondarj^  nodules  in  52  and  was 
directly  invaded  by  the  growth  in  2  more. 

Secondary  growths  are  frequently  found  in  the  liver  in  fatal  cases 
of  carcinoma  of  the  breast.  Thus  in  423  postmortem  examinations  of 
mammary  carcinoma  tabulated  by  Gross,  1|  the  liver  was  affected  in  206, 

*  Fenwick :  Cancer  and  Other  Tumors  of  the  Stomach,  p.  182. 

t  Guy's  Hosp.  Reps.,  vol.  Iviii,  p.  155. 

X  Osier  and  McCrae:  Cancer  of  the  Stomach,  p.  141. 

§  Musser:  Boston  Medical  and  Surgical  Journ.,  a^oI.  cxxi,  1889. 

II  Gross:  American  Journ.  Med.  Sciences,  vol.  xc,  p.  235,  18SS. 


MALIGNANT    DISEASE    OF   THE   LIVER.  497 

or  48.6  per  cent.;  in  735  cases  investigated  by  S.  Paget*  the  liver  was 
involved  in  241,  or  34  per  cent.  This  is  much  lower  than  Gross's  estimate, 
and  is  much  the  same  as  Beadles'f  observation  that  in  100  cases  of 
malignant  disease  of  various  parts  of  the  body  secondary  growths  in  the 
liver  were  found  in  36. 

Carcinoma  of  the  oesophagus  is  more  likely  to  lead  to  secondary 
growths  in  the  hver  when  the  lower  third  of  the  gullet  is  the  site  of  the 
growth. 

In  55  cases  of  oesophageal  carcinoma  there  were  secondary  nodules  in  the  liver 
in  10  instances.  J 

Secondary  Sarcoma. — As  has  already  been  pointed  out,  secondary- 
sarcoma  is  much  less  frequent  in  the  liver  than  secondary  carcinoma. 
{Vide  p.  485.)  Hale  White  found  7.35  per  cent,  of  secondary  sarcoma. 
My  figures,  which  give  a  much  higher  percentage  of  secondary  sarcoma, 
viz.,  23,  include  cases  of  endothelioma,  for  example,  malignant  growths 
primary  in  the  suprarenal  glands. 

Melanotic  Sarcoma. — The  occurrence  of  secondary  melanotic 
growths  in  the  liver  is  well  known,  and  is  such  a  striking  morbid  lesion 
that  once  seen — and  all  museums  have  specimens  illustrating  it- — it  is 
never  forgotten.  Since  this  is  a  condition  every  one  is  familiar  with 
and  is  a  matter,  so  to  speak,  of  common  knowledge,  it  might  be  thought 
that  it  is  frequently  met  with  in  ordinary  hospital  work.  This,  however, 
is  not  the  case. 

In  twelve  years — 1890-1901 — there  were  3806  postmortem  examinations  per- 
formed at  St.  George's  Hospital,  and  in  3  cases  there  were  secondary  melanotic 
growths  in  the  liver,  or  in  0.08  per  cent. 

The  primary  sites  of  malignant  melanotic  growths  are  chiefly  those 
where  the  pigment  melanin  is  normally  present,  viz.,  in  the  uveal  tract 
and  in  the  skin,  especially  in  pigmented  moles.  It  may  be  mentioned 
that  melanotic  cutaneous  growths,  though  from  custom  usually  spoken 
of  as  sarcomata,  are  now  generally  regarded  as  pigmented  endothelioma- 
tous  growths.  In  rare  instances  a  primary  melanoma  has  been  seen  in 
the  rectum  or  at  the  margin  of  the  anus,  but  secondary  growths  in  the 
liver  are  very  rare  in  these  cases. 

De  Buck  and  Vanderlinden  §  describe  a  case  with  secondary  gro-ni^hs  in  the 
liver.  In  neither  Heaton's  ||  case  nor  one  examined  by  myself  were  there  hepatic 
metastases. 

Recurrence  in  the  liver  usually  occurs  within  three  years  of  the 
appearance  of  the  primary  growth,  and  the  prognosis  is  ver}'  bad.  Occa- 
sionally long  periods  of  immunity  are  met  with.  In  one  of  the  first  pub- 
lished cases  of  secondary  melanotic  sarcoma  there  was  an  interval  of 

*  Paget,  S.:  Lancet,  1889,  vol.  i,  p.  571. 
t  Beadles,  C.  F. :  Trans.  Path.  Soc,  vol.  xlvii,  p.  77. 
j  Allbutt's  System  of  Medicine,  vol.  iii,  p.  374. 
§  De  Buck  and  Vanderlinden:  Belgique  Mi'd.,  Nov.  9,  1899. 
II  Heaton:  Trans.  Path.  Soc,  vol.  xlv,  p.  85. 
32 


DISEASES    OF   THE    LIVER. 

eight  or  nine  years  between  the  removal  of  the  eye  and  the  occurrence 
of  symptoms  indicating  hepatic  growth.* 

Fisher  and  Boxf  reported  to  the  Ophthalmo logical  Society  a  case  of  primary 
pigmented  tumor  of  the  eye  removed  fourteen  years  before  death  from  generalised 
pigmented  carcinoma  affecting  the  liver  (which  weighed  21  pounds  6  ounces),  lungs, 
bones  of  the  skull,  and  heart.  The  pigmented  tumor  in  the  eye  appears  to  have 
been  a  sarcoma;  so  the  patient  was  the  subject  of  two  independent  outbreaks  of 
malignant  disease.  This  case  is  referred  to  elsewhere  (p.  479)  as  a  possible  example 
of  primary  melanotic  carcinoma  of  the  liver. 

Lawbaugh  J  has  briefly  recorded  a  case  where  seventeen  years  elapsed  between 
enucleation  of  the  eye  for  a  melanotic  sarcoma  and  death  frcm  the  same  growth  in 
the  liver.  The  most  extraordinary  case  is  one  in  which  there  were  thirty-two  years 
between  the  removal  of  the  eye  for  melanotic  sarcoma  and  death  frcm  the  same 
disease  in  the  liver.  Wilder, §  who  mentions  this  case,  saw  the  liver  in  Kundrat's 
laboratory  at  Vienna. 

Very  occasionally  the  liver  may  be  widely  infiltrated  with  secondary 
melanotic  sarcoma,  while  the  primary  growth  is  very  small  and  may 
escape  notice. 

In  the  London  Hospital  Museum  ||  there  is  a  liver  infiltrated  with  melanotic 
sarcoma  and  weighing  16  pounds;  the  primary  growth  in  the  eye  was  only  discov- 
ered at  the  autopsy. 

Dr.  Newton  Pitt  has  kindly  given  me  notes  of  a  similar  case.  A  man  aged 
twenty-nine  had  cutaneous  tumors,  one  of  which  was  excised  and  found  to  be 
an  alveolar  melanotic  sarcoma,  and  enlargement  of  the  liver.  Ophthalmoscopic 
examination  of  the  eyes  was  negatiA^e.  There  was  no  melanin  in  the  urine.  At 
the  postmortem  there  was  extremely  widespread  generalisation  of  the  growth;  the 
liver  weighed  16  pounds.  There  was  a  small  growth  in  the  outer  edge  of  the  uveal 
tract  in  the  right  eye. 

Lawford  and  Collins  and  C.  D.  Marshall  have  collected  statistics  as 
to  the  results  of  melanotic  sarcoma  of  the  uveal  tract.  The  former  ob- 
servers found  that  in  26  cases  that  were  known  to  have  died  there  was 
evidence  that  the  liver  was  affected  in  16. 

In  age-incidence  malignant  melanotic  growths  resemble  carcinoma 
and  rarely  occur  in  early  life. 

In  103  cases  of  sarcoma  of  the  uveal  tract,  all  of  which,  except  one,  where 
no  note  was  made,  being  more  or  less  melanotic,  collected  by  Lawford  and  Collins,** 
the  average  age  was  48.4  years,  the  extremes  of  age  being  15  years  and  84  years. 
In  35  cases  of  secondary  melanotic  growths  in  the  liver  which  I  have  collected, 
the  average  age  almost  exactly  corresponds  to  this,  being  48.7  years,  or  46.7  years 
for  the  males  and  53.3  for  the  females,  the  estremes  being  27  years  and  75  years. 

Of  Lawford's  and  Collins'  103  cases,  59  were  males  and  44  were  females ; 
in  my  35  collected  cases  where  the  sex  was  stated  25  were  males  and  10 
were  females ;  this  shows  a  much  more  marked  preference  for  males  than 
in  the  series  of  primary  growths  of  the  uveal  tract.  The  right  eye  was 
affected  41  times  and  the  left  60  times  in  Lawford's  and  Collins'  cases, 
while  in  the  cases  I  have  collected  of  hepatic  growths  the  riglit  eve  Avas 

*  Murchison:  Trans.  Path.  Soc,  vol.  xxiv,  p.  123. 
t  Fisher  and  Box:  Brit.  Med.  Journ.,  1900,  vol.  i,  p.  639. 
X  Lawbaugh:  Journ.  of  the  American  Med.  Assoc,  Nov.  24,  1900,  p.  1363. 
§  Wilder:  Ibid. 

I!  Vide  London  Hospital  Gaz.,  Chnical  Supplement,  June,  1900. 
**  Royal  London  Ophthalmic  Hospital  Reports,  vol.  xiii,  p.  104. 


MALIGNANT    DISEASE    OF  THE   LIVER.  499 

rather  more  frequently  the  primary  seat  of  gro^i^h,  but  the  numbers  are 
small. 

Metastatic  melanotic  tumors  of  the  hver  are  more  often  secondary  to 
a  primary  growth  in  the  uveal  tract  than  in  the  skin.  Thus,  in  37  cases 
of  melanotic  sarcoma  in  the  liver  the  primary  gro'svth  was  24  times  in 
the  eye  and  13  times  in  the  skin.  This  is  partly  due  to  melanotic  sar- 
coma being  commoner  in  the  uveal  tract  than  in  the  skin.  Examination 
of  the  recorded  cases  shows  that  the  growths  in  the  liver  following  cuta- 
neous melanosis  are  not  so  big  or  so  striking  as  those  following  melanotic 
sarcoma  of  the  uveal  tract.  Primary  cutaneous  melanotic  growths  may, 
indeed,  give  rise-  to  very  widespread  secondary  growths  in  the  viscera, 
the  liver  being  one  of  the  few  organs  not  affected.  In  most  of  the  cases 
I  have  collected  where  the  liver  contained  secondary  growths  following 
cutaneous  melanosis,  the  organ  was  little  above  the  ordinary  size,  though 
in  two  cases  it  weighed  over  7  pounds,  while,  on  the  other  hand,  some 
of  the  largest  hvers  recorded  have  been  due  to  melanotic  sarcoma  origin- 
ating in  the  eye.  Thus  Litten  *  has  described  a  case  where  the  liver 
weighed  27  pounds,  Sayref  one  of  23  pounds,  and  Hamburger  J  one  of 
22  pounds.  In  two  cases  that  I  have  examined  mj^self  the  weight  was 
in  both  within  a  few  ounces  of  16  pounds.  The  average  weight  of  the 
liver  in  22  cases  of  melanotic  growth  secondary  to  a  growth  in  the  uveal 
tract  was  13  pounds  3  ounces. 

In  a  case  §  where  the  growth  began  in  the  left  toe  there  were  numerous  growths 
in  the  skin  elsewhere,  the  lungs,  kidneys,  and  brain,  but  the  liver  and  spleen  were 
quite  free. 

The  two  following  cases  illustrate  the  difference  in  the  tendency  to 
metastasis  in  the  hver  exliibited  by  melanotic  sarcoma  starting  in  the 
skin,  on  the  one  hand,  and  when  it  is  primary  in  the  eye,  on  the  other 
hand. 

Primary  Growth  in  the  Skin  of  the  Big  Toe;  Widespread  Metastasis. — A  man 
aged  sixty-four  years  had  had  his  foot  removed  for  a  melanotic  sarcoma  starting 
in  the  big  toe  after  an  injury.  The  gro-niih  recurred  in  the  stump,  and  at  the  autcpsy, 
which  I  performed,  there  were  metastases  in  the  lungs,  brain,  left  kidney,  pancreas, 
abdominal  glands,  and  liver.  The  liver  contained  numerous  isolated  gro^^i:hs,  but 
weighed  only  52  ounces.     The  growiih  was  a  spindle-celled  sarcoma. 

Primary  Growth  in  the  Eye,  Excision,  Recurrence  in  the  Liver. — A  man  aged 
fifty-nine  years  was  admitted  under  my  care  with  the  history  that  his  right  eye 
had  been  removed  two  years  previously  for  a  melanotic  sarcoma.  The  liver  was 
enormously  enlarged  and  knobby,  but  there  was  no  ascites.  He  had  melanuria. 
The  legs  were  oedematous.  At  the  autopsy  there  were  a  few  small  secondary 
growths  on  the  diaphragm,  in  the  mucous  membrane  of  the  intestine,  and  in  one 
adrenal  body.  The  liver  was  enormously  enlarged,  weighing  1.5  pounds  12  ounces, 
and  was  extensively  occupied  by  growths  of  a  spindle-celled  melanotic  sarcoma. 

The  liver  is  a  very  favourite  site  for  secondary  infiltration  in  melanotic 
sarcoma  of  the  uveal  tract.  In  a  few  cases  it  is  found  to  co-exist  with 
an  intra-ocular  growth,  but  it  usually  occurs  within  three  years  after 
removal  of  the  eye  and  generally  without  there  being  any  local  recurrence 

*  Deutsche  med.  Wochen.,  Bd.  xv,  S.  41,  l.S,S9. 

t  Transactions  of  the  New  York  Pathological  Society,  1S79,  vol.  iii,  p.  42. 

t  Johns  Hopkins  Hospital  Bull.,  March,  1898. 

§  Levi:  Bull.  Soc.  Anat.  Paris,  1899,  p.  709. 


500  DISEASES    OF   THE    LIVER. 

in  the  optic  nerve  or  orbit.  It  would  thus  appear  that  the  infective  cells 
of  the  growth  must  remain  latent  in  the  liver  for  some  time.  The  Hver 
may,  indeed,  be  the  only  organ  in  the  body  affected,  while  in  other 
instances  almost  every  viscus  and  tissue  shows  metastases.  It  is  re- 
markable that  the  cells  of  melanotic  sarcoma  being,  as  they  usually  are, 
larger  than  the  cells  of  the  other  sarcomata  which  are  stopped  by  the 
lungs,  manage  to  pass  through  the  pulmonary  capillaries  and  to  infect 
the  hver. 

The  liver  evidently  offers  the  most  favourable  situation  for  the  growth 
of  melanotic  sarcoma.  But  though  it  may  be  the  only  organ  affected, 
as  a  rule  secondary  growths  are  very  widely  disseminated  throughout 
the  body.  The  growths  in  the  liver  almost  always  progress  very  rapidly, 
but  in  Litten's  *  case  there  was  evidence  of  a  tumor  of  some  kind  in  the 

liver  for  the   exceptionally 
-  -"nso  •^'- .-,  ^o^S  period  of  four  years. 

■'^'1^^&^^-X^<i^  The  liver  may  be  either 

nodular,  from  the  presence 
of  discrete  growths,  or  there 
may  be  diffuse  infiltration, 
so  that  the  organ,  though 
enlarged,  is  not  altered  in 
shape.  When  infiltrated 
with  melanotic  growth,  the 
liver  substance  presents  a 
variegated  appearance  like 
that  of  granite.  In  excep- 
tional cases  the  liver  is  so 
extensively  infiltrated  that 
it  looks  as  if  it  had  been 
'•tciX:'i''J^^*S^i'-  soaked  in  tar.     Not  uncom- 

monly the  liver  shows  nod- 

FiG.  70. — Secondary  Infiltration  of  the  Liver  with  .  , 

A  Melanotic  Sarcoma.  ules      m     SOmO      partS      and 

The  cells  are  chiefly  round-cells,  and  vary  very  con-  rliffnao  infil+rn+inn  in  n+Viprcj 

siderably  in  the  amount  of  melanin  they  contain.     The  ClinUSe  mmirdtlOn  HI  OXneib. 

arrangement  is  more  or  less  alveolar.  The  primary  growth  ^g  ^  rare  eveut  a  peduUCU- 
was  in  the  uveal  tract.     (Photomicrograph     by   S.    G.  T        (■ 

Penny,  Esq.)  lated  growth  may  be  found 

attached  to  the  hver.  I 
have  seen  this  once.  Sometimes  parts  of  the  gro^vt-hs  are  free  from 
pigment  and  appear  white;  in  other  cases  the  pigment  is  sparse  and 
the  tumors,  to  the  naked  eye,  appear  of  a  mottled  grey  or  greenish 
colour. 

Histologically,  secondary  melanotic  growths  in  the  liver  may  be 
sarcomatous  or  endotheliomatous ;  when  sarcomatous,  they  may  be 
spindle-celled,  oval  or  oat-shaped,  or  round-celled.  The  cells  start  as 
emboli  inside  the  hepatic  capillaries,  and  hence  the  gro-v\i:h  frequently 
has  a  more  or  less  alveolar  appearance. 

Malignant  Disease  Primary  in  the  Suprarenal  Glands. — In  26  cases  of 
primary  malignant  disease  (carcinoma,  endothelioma,  or  sarcoma)  of  the 
*  Litten:  Deutsch.  med.  Woch.,  1889,  S.  4L 


■     »-;i 


MALIGNANT    DISEASE    OF   THE    LIVER.  501 

adrenal  bodies  collected  by  Marks  and  myself*  the  liver  was  the  organ 
most  frequently  affected  by  secondary  growths,  viz.,  in  14,  and  was, 
in  addition,  invaded  by  direct  continuity  in  3.  In  46  cases  of  sarcoma 
of  the  suprarenal  glands  collected  by  Pepper f  there  were  metastases  in 
the  Hver  in  14.  A  suprarenal  growth  may  extend  into  the  inferior  vena 
cava  and  give  rise  to  retrograde  embolism  in  the  hepatic  veins  and  so 
to  secondar}'  growihs,  as  in  Adami's  case  (p.  495). 

In  generahsed  sarcoma  the  liver  often  shows  discrete  nodules  of 
growth.  The  portal  spaces  may  be  infiltrated  with  green  growth  in  the 
interesting  though  very  rare  disease,  chloroma,  which  has  been  re- 
garded in  the  past  as  a  form  of  round-celled  sarcoma,  but  is  probably 
lymphatic  leukaemia.  TrevithickJ  has  recently  reported  a  case  of  this 
kind. 

An  exceptional  origin  for  secondary  gro-^i^hs  in  the  liver  is  so  interest- 
ing that  a  brief  reference  may  be  made  to  it.  Embryomata  andterato- 
mata  in  the  abdoininal  cavity  may  take  on  malignant  growth  and  infect 
the  liver. 

Out  of  10  cases  of  malignant  teratomata  collected  by  Montgomery, §  four  led 
to  secondary  growths  in  the  liver.  Hulke  ||  described  a  secondary  dermoid  growth 
on  the  surface  of  the  liver  following  rupture  of  an  ovarian  embryoma  (dermoid). 
The  same  kind  of  generalisation,  or  rather  implantation,  took  place  in  a  case  briefly 
described  by  Latham.**  Abdominal  dermoids  (embryomata)  are  practically  tera- 
tomata, as  they  are  not  composed  of  skin  alone,  but  of  tissues  derived  frcm  all 
three  layers  of  the  embryo,  and  are  really,  as  Wilms  ff  showed,  complex  tumors. 


CLINICAL  FEATURES  OF  MALIGNANT  DISEASE  OF  THE  LIVER. 

It  will  be  most  convenient  to  describe  the  signs  and  symptoms  of 
both  primary  and  secondary  malignant  disease  of  the  Uver  together, 
since  the  two  conditions  are  so  frequently  indistinguishable,  and  to  note 
the  points  of  difference  between  them  in  a  special  section  (vide  p.  520). 

The  latency  of  malignant  disease  of  the  liver  is  dealt  with  on  page 
514,  under  the  heading  of  Diagnosis. 

PHYSICAL  SIGNS. 

The  facial  aspect  of  a  patient  wdth  advanced  malignant  disease  of 
the  liver  is  that  of  a  grave  and  wasting  illness.  The  e^^es  are  usually 
sunken,  and  the  skin  dirty,  sallow,  or  showing  varying  degrees  of  jaundice. 
But  in  the  earlier  stages,  even  when  nodular  enlargement  of  the  hver 
can  be  felt,  there  may  be  little  to  note  in  the  patient's  aspect  except 
some  anaemia,  and  it  cannot  be  maintained  that  the  facial  aspect  is 
characteristic  at  this  early  stage.  Steady  loss  of  flesh  and  weight  is 
very  commonly  met  with  in  malignant  disease  of  the  liver.     The  sub- 

*  RoUeston  and  Marks:  American  Journ.  Med.  Sciences,  vol.  cxvi,  p.  390. 

t  Pepper:  Ibid.,  vol.  cxxi,  p.  287. 

t  Trevithick:  Lancet,  1903,  vol.  ii,  p.  158. 

§  Montgomery:  Journ.  Experiment.  Med.,  May,  1898. 

II  Hulke:  Trans.  Path.  Soc,  vol.  xxiv,  p.  1.57. 
**  Latham,  A.:  Trans.  Path.  Soc,  vol.  1,  p.  232. 
tt  Wilms:  Deutsch.  Arch.  f.  klin.  Med.,  Bd.  Iv,  S.  289. 


502  DISEASES    OF   THE    LIVER. 

cutaneous  fat  is  absorbed,  and  as  a  result  the  cheeks  and  temples  fall 
in  and  give  rise  to  a  hollow  and  haggard  appearance  to  the  patient. 
AbsorjDtion  of  fat  helps  to  render  the  skin  inelastic. 

It  has  been  noticed  that  during  the  emaciation  an  associated  fatty  tumor  has 
greatly  diminished  in  size  from  absorption  of  its  fat.     (Bell.*) 

In  very  rare  instances  the  patients  actually  gain  in  weight  as  the 
liver  increases  in  size. 

In  a  case  recorded  by  Delepine  t  a  man  with  primary  melanotic  sarcoma  gained 
3  pounds  in  weight  during  the  last  three  months  of  life.  A  boy,  aged  fifteen  years, 
who  died  with  primary  carcinoma  of  the  liver,  gained  19f  pounds  before  his  death; 
this  was  due  to  the  enormous  size  of  the  liver,  which  weighed  nearly  16  pounds, 
or  two-fifteenths  of  the  total  body  weight,  and  also  to  the  presence  of  ascites. 
(Acland  and  Dudgeon. |) 

The  gain  in  weight  of  the  individual  as  a  whole  depends  on  the  increase 
from  the  tumor  gro%vth  more  than  counterbalancing  the  loss  due  to  general 
emaciation.  The  same  phenomenon  is  sometimes  seen  in  rapidly  growing 
renal  sarcomata  in  infants.  Some  increase  in  weight  and  improvement 
in  general  nutrition  may  follow  on  careful  feeding,  especially  in  the  early 
stages  of  malignant  disease  of  the  liver. 

Progressive  emaciation  is  more  marked  in  cases  of  secondary  malignant 
disease  of  the  liver,  for  here  there  is  in  addition  the  effect  of  the  primar}^ 
growth,  often  in  the  stomach  or  colon,  which  has  already,  and  perhaps 
for  some  considerable  time,  interfered  with  digestion  and  assimilation 
of  food.  In  such  cases  nutrition  may  be  so  impaired  that  bed-sores 
develop;  their  occurrence  is  probably  favoured  by  the  fact  that  the 
patient  generally  lies  in  one  position — on  the  back. 

Exceptionally,  however,  death  may  occur  from  secondary  malignant 
disease  of  the  Hver  when  the  patient  is  well  nourished  or  even  fat. 

A  man  aged  sixty-three  years,  a  patient  in  St.  George's  Hospital,  had  enlarge- 
ment of  the  liver  and  ascites.  He  had  never  had  any  hsematemesis  and  was  not 
jaundiced.  He  was  thought  to  have  cirrhosis.  At  the  autopsy,  the  abdominal 
walls,  mesentery,  etc.,  contained  much  fat.  There  was  a  primary  carcinoma  of 
the  hepatic  flexure,  and  the  liver,  which  weighed  10^  pounds,  was  full  of  secondary 
growths. 

In  primary  malignant  disease  the  progress  of  the  disease  is  so  rapid, 
death  often  following  even  within  three  months  of  the  first  symptoms, 
that  there  may  not  be  time  for  emaciation  and  there  may  be  plenty  of 
subcutaneous  fat. 

In  a  very  rapid  case  which  I  examined  postmortem  some  years  ago  the  man 
— -who  was,  by  the  way,  sent  into  the  hospital  for  intestinal  obstruction — was 
very  fat.  An  enormously  fat  woman  aged  forty,  weighing  over  20  stone,  died  wdth 
multiple  gro-svths  in  the  liver,  which  weighed  10  pounds  11  ounces.  Except  for  a  few 
minute  nodules  in  the  spleen,  no  other  growth  could  be  found  elsewhere  in  the  body. 
It  was  apparently  a  case  of  inultiple  primary  carcinoma  of  the  li^'er.  Microscopically 
the  growth  was  a  rapidly  growing  carcinoma  composed  of  cells  showing  transitional 
forms  from  columnar  to  spheroidal  type. 

*  Bell:  Brit.  Med.  Journ.,  1902,  vol.  i,  p.  15S8. 
t  Delepine,  S.:  Trans.  Path.  Soc,  vol.  xlii,  p.  170. 
j  Acland  and  Dudgeon:  Lancet,  1902,  vol.  ii,  p.  1310. 


MALIGNANT    DISEASE    OF   THE    LIVER.  503 

Cachexia  is  important  in  differentiating  malignant  from  other  enlarge- 
ments of  the  liver,  such  as  deeply  seated  hydatid  cysts,  hypertrophic 
bihary  cirrhosis,  and  from  some  cases  of  nutmeg  liver.  The  progressive 
character  of  the  cachexia  is  of  especial  importance.  The  causation 
of  cachexia  is  probably  to  be  found  in  an  auto-intoxication  emanating 
from  the  rapidly  prohferating  epithehal  gro^^i:lls.  As  is  well  known,  the 
cells  of  many  normal  glands,  such  as  the  pancreas,  thyroid,  suprarenal, 
provide  an  internal  secretion  which  passes  directly  into  the  lymphatics 
or  veins,  and  helps  to  keep  up  the  condition  of  equihbrium  we  know  as 
health.  Allien  epithehal  cells  run  riot  and  form  atypical  growths,  or 
what  might  be  called  abnormal  glands,  it  is  not  unreasonable  to  beUeve 
that  they  may  produce  a  morbid  internal  secretion  which,  when  absorbed, 
poisons  the  body  generally,  and  gives  rise  to  the  cachexia  of  malignant 
disease.  In  support  of  this  view  it  is  noticeable  that  innocent  tumors 
composed  of  normal  tissues  do  not,  however  large  they  may  be,  give  rise 
to  cachexia,  unless  they  mechanically  interfere  with  absorption  and 
nutrition.  There  are  other  w^ays  in  which  poisonous  substances  can  be 
supphed  by  mahgnant  gro-^ths.  As  the  result  of  necrosis  and  disinte- 
gration of  growths,  toxic  bodies  are  probably  produced  which,  when 
absorbed,  will  tend  to  produce  toxaemia  and  cachexia. 

Fever. — It  is  generally  beheved  that  mahgnant  disease  of  the  liver  is 
not  accompanied  by  fever  or  only  by  transient  elevations  of  temperature 
due  to  independent  causes.  This,  however,  is  very  far  from  being  a  hard- 
and-fast  rule.  Eggel  *  estimated  that  fever  was  present  in  14  per  cent,  of 
the  147  cases  of  primary  carcinoma  of  the  liver  which  he  collected.  It  is 
important  to  recognise  that  fever  may  be  present  in  mahgnant  disease 
of  the  liver,  whether  primary  or  secondary,  and  that  the  existence  of  a 
raised  temperature  does  not  necessarily  exclude  new-growth  in  favour 
of  some  form  of  hepatic  suppuration.  In  mahgnant  disease  the  tempera- 
ture, if  raised,  is  usually  irregular  and  not  \erj  high,  but  if  comphcated 
by  suppuration,  it  may  closely  imitate  hepatic  abscess. 

The  raised  temperature  may  be  due  to  the  rapid  growth  and  multi- 
phcation  of  cells  inside  the  hver;  cases  occur  in  which  no  other  cause  is 
forthcoming ;  this  may  be  seen  in  primary  malignant  disease  of  the  liver. 
The  liver  forms  a  very  suitable  soil  for  rapid  tumor  groAvth  and  hence 
fever  is  more  often  seen  in  malignant  disease  of  the  liver  than  of  other 
organs. 

Fever  is,  moreover,  not  very  rare  in  malignant  disease  elsewhere  in 
the  body;  as  pointed  out  by  Butlin  and  Colby,  fever  is  not  very  uncom- 
mon in  cases  of  sarcoma  of  the  femur  and  tibia. 

In  secondary  malignant  disease  of  the  liver  fever  may  be  independent 
of  the  rapid  cellular  proliferation  and  destruction  in  that  organ,  and  may 
be  due  to  toxic  or  septic  absorption  from  the  ulcerated  surface  of  the 
primary  growth  in  the  stomach,  colon,  or  elsewhere.  Again,  the  necrotic 
growths  may  become  infected  with  micro-organisms  either  from  the 
alimentary  canal  or  from  the  blood-stream,  and  from  these  secondary 
infections  fever  and  rigors  may  result.  Suppuration  is  occasionally  found 
*  Eggel:  Ziegler's  Beitrage   Bd.  xxx,  1901. 


504  DISEASES    OF   THE    LIVER. 

in  association  with  secondary  growths  in  the  liver.  In  some  instances  a 
primary  growth  in  the  stomach  may  directly  invade  the  liver  and  carry 
infection  into  that  organ. 

A  woman  aged  fifty-four  had  a  primary  spheroidal-celled  carcinoma  of  the 
cardiac  end  of  the  stomach  which  perforated  directly  into  the  under  surface  of  the 
liver  and  produced  a  large  abscess  in  close  contact  with  numerous  secondary  nodules 
in  the  liver.  The  hepatic  abscess  leaked  into  the  peritoneal  cavity  and  set  up 
fatal  peritonitis. 

Suppurative  cholangitis  may  develop  in  the  course  of  mahgnant  dis- 
ease of  the  liver  when  the  ducts  are  dilated  from  obstn;ction. ;  this  is 
more  likely  to  occur  in  secondary  malignant  disease  of  the  liver,  since 
obstruction  to  the  ducts  is  comparatively  infrequent  in  primary  growths 
of  the  hver  substance. 

Osier  *  refers  to  a  case  of  cancer  of  the  liver  where  intermittent  fever  and  rigors 
were  so  marked  that  the  question  of  abscess  was  raised  during  life.  After  death, 
in  addition  to  secondary  growths,  there  were  several  abscesses  caused  by  the  growths 
compressing  the  bile-ducts. 

A  good  example  was  seen  in  a  woman  aged  forty-four  who  had  jaundice  due 
to  growths  in  the  portal  fissure,  secondary  to  carcinoma  of  the  splenic  flexure  of 
the  colon,  compressing  the  hepatic  ducts.  The  intra-hepatic  bile-ducts  showed 
suppuration.  There  was  high  fever  in  this  case,  which  was  under  the  care  of  my 
colleague.  Sir  Isambard  Owen. 

Primary  carcinoma  of  the  second  part  of  the  duodenum  involving  the 
bihary  papilla  (perivaterian  duodenal  carcinoma)  is  especially  prone  to 
set  up  suppurative  cholangitis;  usually  it  kills  the  patient  in  this  way 
before  there  has  been  time  for  secondary  growths  to  occur  in  the  Hver, 
but  secondary  growths  may  be  found  in  association  with  suppurative 
cholangitis. 

A  man  aged  fifty-two  was  under  the  care  of  my  colleague.  Sir  Isambard  Owen, 
with  jaundice,  rigors,  and  a  lump  in  the  prostate.  At  the  necropsy  there  was  a 
primary  columnar-ceUed  carcinoma  of  the  bihary  papilla,  secondary  growths  in 
the  liver,  suppurative  cholangitis,  and  empyema  of  the  gaU-bladder,  and  pysemic 
abscesses  in  the  prostate  and  kidneys. 

A  resemblance  between  mahgnant  disease  and  cirrhosis  of  the  hver 
may  be  noted  in  the  fact  that  fever  may  occur  in  both,  from  secondary 
infections  or  from  auto-intoxication.  Cases  of  malignant  disease  of  the 
liver  with  fever  may  thus  simulate  pylephlebitis,  hepatic  abscess,  or 
possibly  even  typhoid  fever. 

The  liver  is  enlarged,  and  the  enlargement  is  progressive.  When  the 
surface  of  the  organ  is  irregular,  the  growth  is  in  the  great  majority  of 
cases  secondary;  the  nodules  may  be  felt  to  be  umbilicated  or  depressed 
in  the  centre,  and  thus  can  be  distinguished  from  the  hobnails  of  a  cirrhotic 
hver,  from  which  the  progressive  character  of  the  enlargement  further 
separates  it. 

It  does,  however,  sometimes  happen  that  the  depression  between 
hobnails  on  a  cirrhotic  hver  conveys  the  impression  of  umbilication,  while 
umbilication  cannot  always  be  felt  OA^er  secondary  hepatic  gro"^i:hs.  In 
cirrhosis  the  enlargement  is  more  uniform  than  in  malignant  disease 
which  chiefly  affects  the  right  lobe. 

*  Osier:  Johns  Hopkins  Hospital  Reports,  vol.  ii.  No.  1. 


MALIGNANT    DISEASE    OF   THE    LIVER.  505 

In  primary  malignant  disease  of  the  liver  there  is  usually  a  uniform, 
firm,  and  hard  tumor  in  the  position  of  the  right  lobe  of  the  liver.  Occa- 
sionally there  are,  in  addition,  nodules  of  secondary  groT\i;h  elsewhere 
on  the  surface  of  the  liver.  This  condition  cannot  be  distinguished  from 
secondary  mahgnant  disease  in  which  the  primary  growth  is  latent. 
Occasionally  the  growth  is  so  soft  that  it  fluctuates  and  imitates  an  ab- 
scess. (Vide  p.  517.)  In  rare  cases  it  may  pulsate,  either  because  the 
growth  is  a  hsemorrhagic  sarcoma  or  from  transmitted  pulsation. 

Sir  T.  Lauder  Brunton  *  met  with  a  case  of  malignant  disease  of  the  left  lobe 
of  the  liver  -wath  pulsation  and  a  bruit  over  the  tumor  which  imitated  an  abdominal 
aneurysm. 

A  mass  of  new-growth  may  be  found  at  the  umbilicus  in  association 
with  secondary  mahgnant  disease  of  the  liver.  Small  outlying  secondary 
growths  may  also  form  in  the  falciform  ligament  of  the  liver,  and  be  felt 
during  life  near  the  hnea  alba ;  their  presence  greatly  assists  in  forming 
a  diagnosis  of  mahgnant  disease.  They  may,  however,  be  closely  simu- 
lated by  small  islands  of  fat  left  intact  when  emaciation  is  proceeding 
rapidly. 

In  a  case  of  secondary  malignant  disease  of  the  liver  in  which  small  masses 
were  felt  during  life  in  the  line  of  the  falciform  ligament  I  could  not  find  postmortem 
the  growths  which  I  thought  I  had  felt  during  life,  and  which  had  assisted  in  the 
diagnosis. 

Nodules  of  new-growth  on  the  surface  of  the  liver  may,  of  course,  be 
closely  simulated  by  perihepatitic  adhesions  or  by  irregularities  due  to 
gummata  and  syphihtic  cicatrices. 

A  venous  hum  or  murmur  is  occasionally  heard  over  the  liver.  It 
may  be  due  to  pressure,  exerted  by  nodules  of  growth  or  enlarged  glands, 
on  the  portal  vein,  or  possibly  to  constriction  of  the  inferior  vena  cava 
where  it  is  in  contact  with  the  liver.  Friction  from  perihepatitis,  set  up 
by  growths  involving  the  capsule,  may  be  detected  in  some  instances  and 
is  usually  accompanied  by  pain  and  tenderness  on  pressure.  It  is  com- 
moner in  secondary  than  in  primary  growths  of  the  liver,  not  only  because 
secondary  growths  are  met  with  in  such  an  overwhelming  proportion, 
but  because  they  are  more  likely  to  involve  the  capsule  than  primary 
growths. 

Haemorrhages  into  the  skin,  mucous  membranes,  and  other  parts  of 
the  body  may  occur  in  association  with  jaundice  and  cholsmia.  They 
may  also  be  met  with  when  there  is  little  or  no  jaundice,  though 
the  liver  is  extensively  infiltrated  by  growth  or  when  rapidly  destructive 
changes  in  the  liver  cells,  allied  to  those  of  icterus  gravis,  are  in  progress. 
As  the  result  of  failure  in  the  protective  or  antitoxic  function  of  the  liver 
cells,  poisons  absorbed  from  the  intestinal  tract  pass  into  the  general 
circulation  and  give  rise  to  the  manifestations  of  cholaemia.  The  presence 
of  bile  in  the  circulation  is  quite  subordinate  in  importance  to  these  toxic 
substances. 

Jaundice  and  ascites  are  not  essential,  but  rather  accidental,  symp- 

*  T.  Lauder  Brunton:  Trans.  Med.  Soc.  London,  vol.  xix,  1896. 


506  DISEASES    OF   THE    LIVER. 

toms  of  malignant  disease  of  the  liver.  Their  occurrence  may  be  due  to 
a  piece  of  the  growth  pressing  on  the  portal  vein  and  bile-duct,  or  on 
their  main  branches;  a  secondary  growth  in  the  glands  in  the  portal 
fissure  may  thus  give  rise  to  both. 

One  or  both  of  them  may  appear  almost  at  any  period  of  the  disease. 
They  are  not  evidences  of  the  extent  or  severity  of  the  disease,  but  only 
of  its  situation.     They  both  occur  in  about  50  per  cent,  of  the  cases. 

Jaundice,  if  marked,  is  a  severe  complication,  and  by  giving  rise  to 
cholsemia  may  accelerate  the  necessarily  fatal  issue  of  the  case.  In  a 
collection  of  cases  of  primary  malignant  disease  of  the  liver  Hale  White  * 
found  that  jaundice  when  present  was  comparatively  slight  and  not  of 
the  marked  character  and  prolonged  duration  sometimes  met  with  in 
secondary  malignant  disease  of  the  organ.  Jaundice  is  sometimes  de- 
pendent on  the  associated  catarrh  of  the  bile-ducts  and  not  necessarily 
on  mechanical  pressure,  and  may  then  be  relieved  by  treatment.  (Mayo 
Robson.f)  During  life,  however,  jaundice  in  malignant  disease  is  gener- 
ally explained  by  mechanical  pressure;  though  if  it  disappeared,  catarrhal 
swelling  of  the  duct  might  suggest  itself.  The  onset  of  jaundice  in 
malignant  disease  may  be  sudden  and  accompanied  by  sickness  and 
vomiting,  so  as  to  simulate  catarrhal  jaundice  very  closely,  but  instead 
of  disappearing,  it  persists  and  becomes  deeper. 

In  secondary  malignant  disease  of  the  liver  jaundice  is  rather  more 
likely  to  supervene  and  to  occur  early  when  the  primary  growth  is  situated 
near  the  bile-ducts,  as,  for  example,  at  the  pylorus  or  in  the  gall-bladder. 
Primary  growth  in  these  positions  is  prone  to  spread  directly  to  the  portal 
fissure  and  to  produce  obstructive  jaundice,  while  multiple  embolic 
nodules  of  growth  scattered  broadcast  over  the  periphery  of  the  liver 
have  much  less  tendency  to  induce  biliary  obstruction.  The  following 
case  illustrates  this  point : 

'  A  man  aged  thirty-four  years  became  jaundiced  a  few  weeks  before  his  death 
from  primary  spheroidal-celled  carcinoma  near  the  pylorus.  The  lesser  omentum 
was  I  inch  thick,  being  infiltrated  with  growth  which  surrounded  and  compressed 
the  common  bile-duct.  Microscopically  the  bile-duct  was  much  infiltrated  with 
growth,  the  infiltration  extending  up  to  the  neck  of  the  gall-bladder  and  into  the 
portal  fissure.  The  gall-bladder  and  intra-hepatic  bile-ducts  were  distended,  but 
the  extra-hepatic  ducts  were  all  compressed.  The  liver  weighed  66  ounces  and 
had  a  green,  nutmeggy  appearance;  there  were  small  masses  of  growth  in  the  intra- 
hepatic branches  of  the  portal  vein.  This  patient  was  under  the  care  of  Dr.  Pen- 
rose in  St.  George's  Hospital. 

Obstruction  to  one  of  the  intra-hepatic  bile-ducts,  provided  it  be  fairly 
large,  may  give  rise  to  jaundice;  in  such  a  case  the  other  bile-ducts  convey 
bile  into  the  intestine  and  the  fseces  are  not  clay-coloured.  At  the  autopsy 
of  such  cases  pressure  on  the  gall-bladder  will  cause  bile  to  flow  into  the 
duodenum.     This  was  shown  in  the  following  case: 

A  man  aged  fifty-five  years,  a  barman,  was  admitted  to  St.  George's  Hospital 
under  my  colleague.  Dr.  Penrose,  with  a  large  liver  and  distinctly  palpable  glands 
above  the  right  clavicle.  The  liver  was  manifestly  knobby,  but  no  umbilication 
could  be  made  out.     The  urine  contained  much  urobilin;     the  faeces  contained 

*  Hale  White:  Guy's  Hospital  Reports,  1890,  p.  59. 
t  Mayo  Robson:  Brit.  Med.  Journ.,  1897,  vol.  i,  p.  641. 


MALIGNANT    DISEASE    OF   THE    LIVER.  507 

bile,  and  jaundice  of  no  great  intensity  finally  developed.  Except  for  some  diffi- 
culty in  swallowing,  there  was  nothing  to  suggest  the  site  of  the  primary  growth. 
At  the  autopsy  the  liver  weighed  14  pounds,  and  contained  numerous  secondary 
growths,  some  of  which  were  umbilicated.  Pressure  on  the  gall-bladder  brought 
bile  out  of  the  duodenal  papilla.  There  were  nvmierous  growths  in  the  liver  near 
the  portal  fissure,  which  compressed  some  of  the  bile-ducts.  No  calculi;  no  cirrhosis 
of  the  liver,  which  was  somewhat  nutmeggy.  Spleen  showed  venous  engorgement. 
There  was  a  primary  spheroidal-celled  carciix^ma  in  the  middle  third  of  the  oesoph- 
agus, and  a  secondary  growth,  probably  due  to  implantation,  much  resembling 
to  the  naked  eye  another  primary  neoplasm,  at  the  cardiac  end  of  the  oesophagus. 
There  were  a  few  ounces  only  of  ascitic  fluid. 

On  the  other  hand,  it  should  be  noted  that  experimental  ligature  of  the  left 
hepatic  duct  in  cats  performed  by  V.  Harley  and  Barratt  *  did  not  give  rise  to 
jaundice.  Possibly  this  was  due  to  some  collateral  biliary  anastomoses  between 
the  right  and  left  lobes  of  the  liver. 

An  interesting  but  extremely  rare,  cause  for  jaundice  is  extension  of 
malignant  disease  along  the  lumen  of  the  bile-ducts  in  an  analogous 
manner -to  the  prolongation  of  a  renal  growth  down  the  ureter. 

Gilbert  and  Claude  f  have  recorded  primary  carcinoma  of  the  liver  in  a  girl 
aged  twenty-two,  in  whom  attacks  of  biliary  colic  and  obstinate  jaundice  were 
due  to  a  process  of  the  growth  extending  along  and  blocking  up  the  common  bile- 
duct.  The  growth  did  not  infiltrate  the  walls,  but  grew  in  a  polypoid  form  along 
the  lumen  of  the  duct. 

When  jaundice  is  absent,  the  skin  is  usually  anaemic,  sallow,  and 
sometimes  dirty-looking;  slight  pigmentation,  as  in  other  forms  of  ab- 
dominal disease,  is  sometimes  seen. 

Legg  J  figures  marked  pigmentation  suggesting  argyria  in  a  man  with  melanotic 
growths  in  a  liver  weighing  5700  grammes  (178  ounces)  who  also  had  melanuria. 
Williamson  §  lays  stress  on  small  black  patches  appearing  on  the  skin  as  diagnostic 
of  internal  melanotic  growth;  he  also  mentions  piginented  nodules  which  would 
naturally  suggest  melanotic  sarcoma. 

Ascites. — When  the  liver  is  extensively  infiltrated  with  new-growth 
its  capillaries  become  obstructed  over  a  correspondingly  wide  area,  either 
by  pressure  from  without,  as  in  primary  carcinoma,  or  from  the  presence 
of  growth  inside  their  lumen,  as  in  secondary  growth,  and  especially  in 
one  form  of  primary  angiosarcoma  (endothelioma). 

Hektoen  and  Herrick  ||  have  drawn  special  attention  to  embolic  blocking  of 
the  capillaries  in  secondary  melanotic  sarcoma  of  the  liver. 

The  obstructed  portal  circulation  thus  resembles  that  in  portal  cirrho- 
sis, and  an  attempt  at  compensation  by  dilatation  of  the  veins  at  the 
lower  end  of  the  oesophagus  may  be  found  in  some  cases. 

In  a  case  under  my  care  of  secondary  melanotic  sarcoma  of  the  liver,  which 
weighed  16  pounds,  there  were  markedly  varicose  veins  at  the  lower  end  of^the 
oesophagus.     Frerichs  **  records  a  similar  case. 

*  Brit.  Med.  Journal,  1S98,  vol.  ii,  p.  1743. 

t  Gilbert  and  Claude:  Archiv.  gen.  de  Med(^'cine,  1895,  t.  clxxv,  p.  513. 

I  Legg:  Trans.  Path.  Soc.  London,  vol.  xxxv,  p.  367. 

§  Wiliiamson,  K.  T.:  Lancet,  Dec.  29,  1900,  vol.  ii,  p.  1874. 

II  Hektoen  and  Herrick:  American  Journal  of  the  Medical  Sciences,  vol.  cx\\, 
p.  255,  1898. 

**  Frerichs:  Diseases  of  Liver,  vol.  ii,  p.  239,  New  Sydenham  Soc. 


508  DISEASES    OF   THE    LIVER. 

Portal  thrombosis  due  to  an  extension  of  the  growth  from  the  intra- 
hepatic branches  into  the  trunk  of  the  portal  vein  may  also  account  for 
ascites  in  malignant  disease  of  the  liver,  but  it  is  usually  due  to  con- 
comitant malignant  disease  of  the  peritoneum  or  to  local  inflammation 
of  the  capsule  of  the  liver  set  up  by  an  underlying  growth. 

The  ascitic  fluid  is  usually  serous  and  clear,  hke  that  in  cirrhosis  or 
in  simple  chronic  peritonitis,  but  is  bile-stained  when  there  is  jaundice. 
The  effusion  may  be  blood-stained  from  extravasation  of  blood  into  the 
growths,  especially  when  they  are  necrotic  and  have  ruptured  into  the 
general  peritoneal  cavity.  In  some  cases,  especially  in  sarcoma,  the  loss 
of  blood,  due  to  extravasation  into  the  growths,  may  be  so  excessive  as 
to  give  rise  to  faintness  and  collapse,  while  at  the  same  time  there  is 
marked  increase  in  the  size  of  the  hepatic  tumor,  which  may  even  fluc- 
tuate and  iiTiitate  very  closely  hepatic  abscess. 

Cases  of  this  kind  have  been  recorded  by  Byrom  Bramwell,*  Hawthorne, f 
and  others. 

It  has  been  stated  that  ascites  is  rare  or  even  that  it  does  not  occur 
in  melanotic  sarcoma  of  the  liver,  but  this  is  not  borne  out  by  the  cases 
I  have  collected,  for  it  was  stated  to  be  present  in  10  of  the  37  collected 
cases  of  secondary  melanotic  disease  of  the  liver;  and  in  at  least  three 
of  the  reputed  primary  melanotic  growths  of  the  liver  there  was  ascites; 
in  a  case  examined  by  Dr.  Penrose  in  St.  George's  Hospital  in  1888  there 
was  as  much  as  three  gallons  of  fluid.  Occasionally  in  these  cases  the 
ascitic  fluid  is  of  a  dark  colour,  from  the  presence  of  melanin ;  more  often 
it  is  like  ordinary  ascitic  fluid. 

In  a  woman  aged  thirty-three  who  died  with  melanotic  sarcoma  of  the  liver 
there  were  100  ounces  of  dark  fluid  in  the  peritoneal  cavity  and  a  pint  of  brown 
fluid  in  each  pleura.  (Middlesex  Hosp.  Reports,  1890-91,  p.  278.)  In  this  case 
the  colour  was  presumably  due  to  the  escape  of  melanin  from  the  melanotic  sarcoma. 
Wickham  Legg  %  and  Senator  §  have  also  recorded  cases  of  melanotic  sarcoma  of 
the  liver  with  brown  ascitic  fluid. 

In  cases  of  melanotic  sarcoma  of  the  lii^er  the  ascitic  fluid  may  be 
clear  and  yet  contain  cells  with  pigment-granules  inside  them  (Hektoen 
and  Herrick||).  In  a  case  under  my  care  the  ascitic  fluid,  though  of  the 
ordinary  straw  colour,  really  had  melanogen  in  it,  as  shown  by  adding  a 
watery  solution  of  ferric  chloride  and  getting  a  dark  ring.  On  the  other 
hand.  Dr.  Garrod  tells  me  that  in  two  similar  cases  with  melanuria  the 
ascitic  fluid  did  not  give  the  reaction. 

In  rare  instances  the  ascitic  effusion  may  be  chylous  as  a  result  of 
transudation  of  chyle  or  even  riipture  of  a  lymphatic  tnmk,  due  to  the 
pressure  and  obstruction  exerted  by  a  secondary  growth  in  the  course  of 
the  chyliferous  trunks.  A  chyliform  or  fatty  ascitic  effusion,  not  due  to 
the  escape  of  chyle,  but  the  result  of  fatty  degeneration  and  disintegration 

*  Bramwell,  B. :  Lancet,  1897,  vol.  i,  p.  170. 
t  Hawthorne,  C.  O.:  Clinical  Jour.,  vol.  viii,  p.  361. 
j  Legg:  Trans.  Path.  Soc.  London,  vol.  xxix,  p.  225. 
§  Senator:  Charite  Annalen,  1890,  Bd.  xv,  S.  261. 

II  Hektoen  and  Herrick:  American  Journal  of  the  Medical  Sciences,  vol.  cxvi, 
p.  255,  Sept.,  1898. 


MALIGNANT   DISEASE   OF  THE   LIVER.  509 

of  cells  suspended  in  the  peritoneal  effusion,  is  not  so  rare.  The  fluid 
resembles  chjdous  ascites  to  the  naked  eye,  but  differs  from  it  micro- 
scopically in  the  size  of  the  fat-globules,  which  are  large  and  not  in  the 
fine  emulsion  characteristic  of  true  chylous  ascites.  The  oil-globules  may 
be  formed  either  in  the  cells  of  the  growths  and  discharged  into  the  peri- 
toneal cavity,  or  in  leucocytes.  Corselli  and  Frisco  *  suggest  that  when 
malignant  gro^^'ths  involve  the  peritoneum,  toxic  bodies  are  formed 
which  induce  degenerative  changes  in  the  cells  suspended  in  the  ascitic 
fluid  and  so  lead  to  fatty  ascites. 

In  a  case  under  the  care  of  Dr.  Whipham  in  St.  George's  Hospital  a  fatty  effusion 
of  a  milky  appearance  was  drawn  off  during  life  and  was  found  at  the  autcpsj^  to 
be  associated  with  numerous  secondary  growths  in  the  liver,  which  weighed  15 
pounds;  there  was  also  a  large  growth  involving  the  receptaculum  chyli,  but  no 
rupture  of  lymphatic  vessels  was  forthcoming.  The  primary  growth  was  in  the 
gall-bladder. 

In  other  cases  there  is  milky  ascites  in  which  the  opalescence  is  due 
to  the  presence  of  nucleo-albumins  and  not  to  fat. 

In  a  case  of  secondary  carcinoma  in  a  cirrhotic  liver  recorded  by  Achard  and 
Laubry  f  the  amount  of  fat — 0.6  per  cent. — was  too  slight  to  account  for  the  milki- 
ness  of  the  ascites. 

The  number  of  leucocytes  in  the  ascitic  fluid  may  be  so  great  as  to 
suggest  a  purulent  ascitic  effusion  without  there  being  any  sign  of  peri- 
tonitis. 

This  was  evidently  the  nature  of  a  case  described  as  "Cancer  nodulaire  du  Foie 
avec  Ascite  purulent"  by  Gentes,J  for  it  is  especially  stated  that  there  was  no 
lymph  or  adhesions  on  the  peritoneum. 

As  the  result  of  perforation  of  a  viscus  or  secondary  infection,  how- 
ever brought  about,  an  ascitic  effusion  in  hepatic  carcinoma  may  be 
genuinely  pundent. 

The  blood  shows  diminution  in  the  red  cells,  with  a  more  marked 
diminution  in  the  amount  of  haemoglobin — a  secondary  anaemia.  Leuco- 
cytosis  may  be  present,  but  is  not  constantly  found,  and  may  be  inter- 
mittent.    It  is  usually  moderate  in  degree. 

In  14  cases  examined  by  Cabot  §  leucocytosis  was  present  in  8.  In  discussing 
leucocytosis  in  carcinoma  of  various  organs  Da  Costa  ||  states  that  in  his  experience 
leucocytosis  is  more  marked  in  hepatic  carcinoma  than  in  carcinoma  of  other  organs. 

The  urine  is  usually  diminished  in  amount,  and  occasionally  shortly 
before  death  there  may  practically  be  suppression.  It  is  high  coloured, 
as  a  rule,  and  often  lithatic,  and  may  be  of  a  rather  high  specific  gravity. 
When  there  is  jaundice,  bile-pigment  is  usually  found  in  the  urine,  but 
when  the  jaundice  is  very  slight,  it  may  be  difficult  or  impossible  to 
demonstrate  its  presence  in  the  urine.     When  jaundice  is  marked,  casts 

*  Corselli  and  Frisco:  Riforma  Med.,  Roma,  1897,  p.  278. 

t  Achard  et  Laubry:  Bull,  et  Mem.  Soc.  Med.  des  Hop.,  April  2.5,  1902,  p.  335. 

t  Gentes:  Journ.  de  Med.  de  Bordeaux,  April  2,  1899. 

§  Cabot:  Clinical  Examination  of  the  Blood,  p.  301. 

Jl  Da  Costa:  Clinical  Hematology,  p.  388. 


510  DISEASES    OF   THE    LIVER. 

are  found  on  centrifugalising  the  urine.  Urobilin  is  found,  and  some- 
times in  increased  quantities,  unless  the  entrance  of  bile  into  the  duode- 
num is  entirely  prevented.     Indican  is  sometimes  present. 

Albuminuria  is  very  rare  in  malignant  disease  of  the  liver,  and  its 
presence  in  a  doubtful  case  is  in  favour  of  some  other  condition,  such  as 
lardaceous  disease,  renal  tumor,  cystic  disease,  or  hydronephrosis.  It 
may,  however,  be  induced  when  the  liver  is  so  extensively  infiltrated  with 
growth  that  it  is  unable  to  stop  poisons  absorbed  from  the  alimentary 
canal.  The  action  of  these  poisons  on  the  kidneys  may  result  in  albu- 
minuria. In  biliary  obstruction  with  absence  of  bile  from  the  intestines 
excessive  fermentation  may  give  rise  to  auto-intoxication  and  so  to 
albuiTiinuria.  Teissier  *  has  described  this  "hepatogenous  albuminuria." 
As  already  pointed  out,  albuminuria  is  very  rare  in  malignant  disease  of 
the  liver,  while  these  disposing  conditions — hepatic  insufhciency  and 
jaundice — are  fairly  common;  it  would,  therefore,  appear  that  some 
other  factor  is  necessary  to  produce  albuminuria;  the  requisite  factor 
is  probably  some  primary  feebleness  or  want  of  tone  in  the  kidneys 
themselves. 

Hydronephrosis  may  in  rare  instances  be  due  to  the  pressure  of  the 
greatly  enlarged  liver  on  the  right  kidney.  (Litten.t)  When  the  hver 
is  extensively  infiltrated  with  growth,  the  amount  of  urea  may  be  dimin- 
ished, and  leucin  and  tyrosin  have  been  found  in  the  urine,  probably  from 
cell  destruction. { 

In  melanotic  sarcoma  the  pigment  melanin  may  appear  in  the  urine 
(melanuria).  It  has  been  said  to  be  absent  even  when  the  liver  is  very 
extensively  infiltrated  with  melanotic  growih,  but  it  is  possible  that  it 
may  be  sometimes  overlooked. 

The  urine,  when  passed,  is  generally  of  the  ordinary  colour  and  gradu- 
ally darkens  on  standing  and  exposure  to  the  air.  This  darkening  may 
be  brought  about  rapidly  by  the  addition  of  an  oxidising  agent,  such  as 
bichromate  of  potash  or  nitric  acid.  A  delicate  test  for  melanin  in  the 
urine  is  the  addition  of  a  solution  of  ferric  chloride,  which  even  in  dilute 
solutions  produces  a  black  colour ;  this  reaction  was  discovered  by  -von 
Jaksch§  and  Pollaklj  in  1889.  In  some  instances  the  urine  is  said  to  be 
black  or  dark  brown  when  passed  from  the  bladder;  the  colour  is  due 
to  melanin.  When  the  urine  darkens  after  being  passed  the  pigment  is, 
we  may  suppose,  at  first  in  the  form  of  a  colourless  chromogen — ^melano- 
gen — which  by  oxidation  yields  melanin.  The  melanin  from  the  growth 
passes  into  the  circulation,  and  may  either  be  excreted  as  such,  blackening 
the  urine,  or  it  may  be  changed  by  the  tissues  into  melanogen  and  not 
proddce  any  very  manifest  alteration  in  freshly  passed  urine.  Mela- 
nuria may  thus  escape  notice  unless  the  urine  is  kept  for  a  time  or  acted 
upon  by  oxidising  agents.  Nepven  and  Chausel  described  pigment- 
granules  in  the  blood  and  in  the  urine  of  patients  with  melanotic  sarcoma. 

*  Teissier:  La  Semaine  M^dicale,  Aug.  23,  1899. 
t  Litten:  Quoted  in  La  Semaine  Mcdicale,  1892,  p.  80. 
t  Compare  Ulricli:  Nordiskt.  Med.  Arkiv.,  1896,  No.  11. 
§  V.  Jalvsch:  Zeitschr.  f.  physiolog.  Chem.,  Bd.  xiii,  S.  385. 
II  Pollak:  Wien.  med.  Wochenschr.,  1889,  39,  40,  41. 


MALIGNANT    DISEASE    OF   THE    LIVER.  511 

In  a  man,  aged  fifty-nine  years,  under  my  care  in  St.  George's  Hospital,  there 
were  extensive  melanotic  sarcomatous  groM'ths  in  the  liver,  which  weighed  16 
pounds.  The  primary  growth  was  a  melanotic  sarcoma  of  the  eye  removed  twenty 
months  before  at  Moorfields ;  the  urine  was  clear  when  first  passed,  but  darkened 
on  standing  and  on  the  addition  of  nitric  acid  and  ferric  chloride. 

Melanuria  very  seldom  or  never  occurs  without  secondary  growths 
being  found  in  the  Hver.  The  reasons  for  this  probably  are:  (i)  That 
there  must  be  a  considerable  area  of  growth  to  provide  a  sufficiency  of 
the  pigment,  and  (ii)  that  the  liver  is  involved  more  or  less  in  most  cases 
of  generalised  melanosis. 

In  one  of  the  earliest  cases  described  in  this  country  as  melanuria  there  was 
no  hepatic  growth  (Hilton  Fagge*),  but  it  is  possible  that  the  pigment  was  not 
melanin,  but  metha3moglobin. 

The  occurrence  of  melanuria  does  not  depend  in  any  way  on  the 
presence  of  secondary  growi:hs  in  the  kidneys  and  urinary  tract ;  neither 
does  it  necessarily  depend  on  the  kidneys  being  healthy,  for  it  has 
been  observed  when  the  kidneys  showed  the  changes  of  arteriosclerosis. 
Cases  have  been  observed  in  which  melanuria  has  been  said  to  be 
intermittent. 

The  presence  of  melanin  or-  of  melanogen  in  the  urine  may  be  of  great 
use  in  arriving  at  an  accurate  diagnosis  of  a  case  of  enlarged  hver.  Thus 
in  cases  where  the  primary  growth  in  the  eye  remains  latent,  melanuria 
would  show  that  the  enlargement  was  due  to  a  melanotic  growth.  It  has 
been  stated  that  melanin  occurs  occasionally  in  the  urine  in  cases  where 
no  melanotic  growth  is  present,  but,  as  Garrodf  has  shown,  this  is  a  mis- 
take and  is  due  to  large  quantities  of  indican  in  the  urine.  It  is,  therefore, 
important  to  be  on  the  outlook  for  the  fallacy  of  inistaking  indican  for 
melanin.  Urines  which  contain  an  excess  of  indican  give  with  HNO3  a 
reaction  like  that  for  melanin,  but  there  is  no  colour  reaction  with  ferric 
chloride,  and  in  this  way  the  two  can  be  distinguished.  The  spontaneous 
darkening  of  the  urine  must  be  distinguished  from  that  of  alkaptonuria 
by  the  tests  already  given.  In  addition,  the  urine  in  alkaptonuria  re- 
duces Fehling's  solution,  but  does  not  contain  sugar,  as  shown  by  the 
phenylhydrazin  test. 

The  toxicity  of  the  urine  has  been  found  to  be  increased  (Charrin  J). 

(Edema  of  the  feet  is  comparatively  frequent  in  the  later  stages  ojf 
the  disease.  It  may  be  due  to  several  causes,  such  as  cardiac  debility, 
or  to  a  toxsemdc  state  resulting  from  hepatic  insufficiency;  in  the  latter 
case  the  oedema  is  analogous  to  that  occurring  in  cirrhosis.  CEdema, 
not  only  of  the  legs,  but  of  the  genitals,  scrotum,  and  lower  part  of  the 
tnmk,  may  be  mechanical  and  due  to  direct  pressure  exerted  by  gro\\i:h, 
either  in  the  liver  or  in  the  adjacent  lymphatic  glands,  on  the  inferior 
vena  cava  and  other  venous  channels,  or  to  thrombosis  of  the  inferior 
vena  cava.  {Vide  case  on  p.  519.)  It  maj''  also  be  due  to  the  pressure 
of  ascites  on  the  inferior  vena  cava. 

*  Hilton  Fagge:  Trans.  Path.  Soc,  vol.  xxviii,  p.  172. 
t  St.  Bartholomew's  Hospital  Reports,  vol.  xxxviii,  p.  25. 
t  Charrin:  Sem.  Med.,  1892,  p.  80. 


512  DISEASES    OF   THE    LIVER. 

Thoracic  Signs  and  Symptoms. — The  large  size  of  the  liver  may 
encroach  on  the  thorax  and  thus  lead  to  collapse  and  hypostatic  engorge- 
ment of  the  bases  of  the  lungs,  with  signs  of  bronchitis.  Concomitant 
ascites  will  tend  to  displace  the  thoracic  viscera  and  to  compress  the 
lungs  and  produce  pulmonary  embarrassment;  this  may  be  temporarily 
reheved  by  tapping  the  abdomen.  When  the  growth  involves  the  cap- 
sule of  the  liver  or  the  diaphragm,  it  may  give  rise  to  the  symptoms 
of  pleurisy. 

SYMPTOMS. 

Great  weakness,  of  which  complaint  is  not  infrequently  made  by 
patients,  may  be  explained  on  one  of  the  following  hypotheses :  It  may 
be  the  result  of  such  extensive  destruction  of  the  liver  substance  that  the 
organ  fails  to  do  its  work  of  stopping  poisons  which  in  the  ordinary 
course  of  events  are  absorbed  from  the  ahmentary  canal  and  then  de- 
stroyed or  rendered  innocuous.  This  condition  of  hepatic  inadequacy 
leads  to  general  toxaemia  and  so  to  great  feebleness  and  loss  of' appetite. 
Hepatic  inadequacy  would  also  interfere  with  the  absorption  and  proper 
assimilation  of  food. 

Gastric  disturbance  is  frequent,  there  being  loss  of  appetite, 
or  even  a  marked  distaste  for  food,  especially  for  meat.  In  very  rare 
instances  there  is  great  exaggeration  of  appetite,  while  in  some  cases  the 
appetite  remains  unaffected  or  is  sustained  by  a  sort  of  auto-suggestion 
to  counteract  the  wasting.  (Hanot.*)  Nausea  is  often  present,  and 
there  may  be  actual  vomiting,  probably  reflex  in  origin.  Symptoms 
of  chronic  gastritis  may  for  a  time  be  the  chief  or  only  manifestations. 
The  bowels  are  usually  confined,  and  considerable  difficulty  may  be  ex- 
perienced in  the  late  stages  in  getting  them  to  act  without  disturbing  the 
patient  too  much.  Diarrhoea  is  very  exceptional.  In  the  late  stages 
obstinate  hiccough  may  supervene,  and  may  be  very  resistant  to  treat- 
ment. 

Hepatic  Pain. — ^The  presence  of  growth  in  the  liver  gives  rise  to 
tension  and  stretching  of  the  capsule  and  so  to  tenderness  and  to 
pain;  this  is  further  increased  by  perihepatitis  set  up  by  growths  involving 
the  capsule  of  the  liver;  when  the  growth  is  deep-seated  in  the  substance, 
as  in  some  examples  of  primary  carcinoma,  pain  may  be  httle  marked 
or  even  absent.  The  pain  may  be  almost  constant  in  the  right  hypo- 
chondrium,  but  is  often  especially  felt  in  the  back,  in  the  shoulder,  or 
in  the  loins.  It  is  more  marked  on  exertion,  and  is  worse  at  night.  Pain 
is  not  always  present,  but  it  has  some  bearing  on  the  diagnosis,  since 
there  is  comparatively  little  pain  in  cirrhosis,  while  in  malignant  disease 
of  the  liver  it  is  usually  both  persistent  and  severe.  Secondary  growths 
in  the  diaphragm  or  an  extension  of  the  growth  from  the  liver  into  the 
diaphragm  may  set  up  pleurisy  and  so  give  rise  to  a  good  deal  of  pain. 
Attacks  of  pain  resembling  those  of  biliary  colic,  but  not  due  to  the  pas- 
sage of  gall-stones,  are  occasionally  met  with  when  the  common  duct  is 
pressed  upon  from  without. 

*  Hanot:  Mercredi  MMical,  1S93,  p.  417. 


MALIGNANT    DISEASE   OF  THE   LIVER.  513 

V.  Schultz  *  describes  attacks  of  pseudo-gall-stone  colic  in  a  man,  aged  forty- 
seven,  who  had  secondary  growths  in  the  portal  fissure  compressing  the  duct  and 
setting  up  jaundice.     The  primary  growth  was  in  the  rectum. 

Pruritus,  or  itching  of  the  skin,  the  result  of  hepatic  insufficiency, 
may  be  very  troublesome,  and  a  patient  who  is  semicomatose  may  be  con- 
tinually scratching  himself.  Pruritus  is  usually  seen  in  association  with 
jaundice  and  comparatively  late  in  the  course  of  the  disease.  Bou- 
chard f  speaks  of  it  as  occurring  sometimes  early  in  the  disease,  before 
sufficient  data  for  the  diagnosis  are  forthcoming. 

It  is  only  very  rarely  that  peripheral  neuritis  can  be  referred  solely 
to  failure  of  the  detoxicating  function  of  the  liver.  In  most  cases  where 
peripheral  neuritis  complicates  malignant  disease  of  the  liver  it  is  due  to 
concomitant  alcoholism. 

Hayem  J  observed  the  acute  onset  of  neuritis  in  both  arms  and  legs  in  a  case 
of  primary  carcinoma  of  the  liver,  which  may  have  been  due  either  to  hepatic  in- 
sufficiency or  possibly  to  toxines  derived  from  the  growth. 

In  primary  malignant  disease  the  liver  may  be  so  extensively  infil- 
trated with  the  growth  that  hepatic  insufficiency  is  estabhshed.  This 
form  of  auto-intoxication  accounts  for  the  occurrence  of  haemorrhages, 
somnolence,  and  delirium  in  the  last  stages  of  the  disease,  and  may  render 
the  diagnosis  from  cirrhosis  difficult. 

Charrin§  described  an  exceptional  case  where  mental  delusions  occurred  in  an 
early  stage  of  carcinoma  of  the  liver  and  were  thought  to  be  due  to  toxaemia,  as 
the  toxicity  of  the  urine  was  increased. 

DURATION. 

In  primary  malignant  disease  of  the  liver  the  disease  runs  a  rapid 
course,  and  sometimes  justifies  the  description  "acute  cancer." || 

From  an  analysis  of  his  cases  Hale  White**  concluded  that  the  disease 
probably  never  lasts  more  than  four  months.  In  exceptional  cases 
symptoms  do  not  exist  for  as  many  weeks. 

In  secondary  malignant  disease  of  the  liver  the  duration  of  life  is  vari- 
able. Much  depends  on  the  nature  and  situation  of  the  primary  tumor. 
This  may  kill  the  patient  before  the  growths  in  the  liver  have  become 
manifest.  On  the  other  hand,  if  the  primary  growth  has  been  removed 
or  remains  entirely  latent,  life  may  be  prolonged  for  a  year,  or,  in  ex- 
treme instances  even  longer,  after  signs  of  a  growth  in  the  liver  have  ap- 
peared. Usually,  however,  death  occurs  within  six  months  of  the  first 
sign  of  hepatic  enlargement. 

Sometimes  the  liver  may  be  considerably  enlarged  and  nodular,  and 
the  patient  remains  for  weeks  in  much  the  same  condition  and  tlien  sud- 
denly goes  rapidly  down  hill.  It  is  often  suiprising  how  comparati^'el3• 
latent  the  disease  may  remain  for  a  time.     In  other  instances  the  liver 

*  Schultz:  BerUn.  klin.  Wochen.,  Feb.  5,  1S94,  B.  132. 
t  Bouchard:  Congress  at  Rome,  1S94. 
t  Quoted  in  Levi's  Paris  These,  1896. 
§  Charrin:  Sem.  med.,  1892,  p.  310. 

II  Rioufol,  Thfise  de  Lyon,  1899.     Acute  Cancer  of  Li\or. 
**  Hale  White:  Guy's  Hospital  Reports,  1890. 
33 


514  DISEASES    OF   THE    LIVER. 

steadily  enlarges,  and  'pari  passu  the  patient's  condition  deteriorates. 
It  has  been  stated  that  secondary  growths  in  the  hver  grow  with  greater 
virulence  during  hot  weather.     (Fenwick.*) 


DIAGNOSIS  OF   MALIGNANT  DISEASE. 

The  diagnostic  signs  of  malignant  disease  in  the  liver  are  rapid  and 
progressive  enlargement,  with  evidence  of  definite  tumor  formation  in 
the  organ,  pain,  loss  of  weight  and  of  constitutional  strength,  and,  when 
the  disease  is  not  primary  in  the  liver,  evidence  of  mahgnant  disease 
elsewhere.  As  has  been  pointed  out  already,  the  primary  growth  is 
latent  in  about  half  the  cases  of  secondary  malignant  disease  of  the  liver. 

As  a  rule,  malignant  disease  of  the  liver,  whether  primary  or  secondary, 
gives  rise  to  some  hepatic  enlargement  and  pain,  so  that  disease  of  the 
Hver  is  at  least  suspected.  When  the  growths  are  of  small  size  and  the 
liver  is  not  enlarged,  there  may  be  no  clinical  evidence  that  the  hver  is 
affected;  this  occurs  in  a  certain  proportion  of  cases  of  secondary  ma- 
lignant disease  of  the  liver,  and  is  easily  explained  inasmuch  as  the 
patient  dies  from  the  effects  of  the  primary  growth. 

In  primary  malignant  disease  of  the  liver  it  is  rare  for  the  growi:h 
to  remain  entirely  latent.  It  may,  however,  happen  that  the  observer's 
attention  is  exclusively  directed  to  secondary  results  or  concomitant 
affections. 

Thus  Sokoloff  t  describes  the  case  of  a  man  aged  seventy  who  had  ascites  and 
dropsy  and  was  regarded  as  having  arteriosclerosis.  After  death  a  primary  columnar- 
celled  carcinoma  of  the  liver  was  found.  Gouget  J  narrates  a  very  similar  case  in 
a  man  aged  fifty-three  years,  thought  to  have  arteriosclerosis  and  bronchitis.  At 
the  autopsy  the  liver  was  of  normal  size  and  contained  numerous  growths  of  col- 
umnar-celled carcinoma;  there  were  no  other  growths  in  the  body.  To  the  na*ked 
eye  the  growths  closely  resembled  gummata.  H.  G.  Wells  §  reported  a  case  of 
primary  carcinoma  with  cirrhosis  which  was  latent,  the  patient  dying  from  uraemia. 

Hale  White  ||  records  the  case  of  a  woman  aged  thirty-nine  who  was  thought  to 
be  suffering  from  the  vomiting  of  pregnancy,  but  who  died  after  premature  labour 
had  been  induced.  Primary  malignant  disease  of  the  liver,  weighing  126  ounces, 
was  found. 

DIFFERENTIAL  DIAGNOSIS. 

Under  this  head  the  diagnosis  of  malignant  disease  in  the  liver  sub- 
stance, whether  primary  or  secondary,  from  other  conditions  will  first  be 
considered,  and  then  the  distinction  between  primary  and  secondary 
malignant  disease  will  be  dealt  with. 

Portal  Cirrhosis. — When  a  patient  comes  under  observation  with 
the  abdomen  full  of  ascitic  fluid  it  is  often  difhcult  to  form  a  reliable 
opinion  as  to  whether  there  is  cirrhosis  in  a  late  stage  or  malignant  disease 
of  the  liver.  The  diagnosis  must  then  remain  in  doubt  until  the  fluid  is 
withdrawn;  when  this  has  been  done,  the  liver  can  be  carefully  examined. 

*  Fenwick:  Cancer  and  Other  Tumors  of  the  Stomach,  p.  18.3. 

t  Sokoloff :  Virchow's  Archiv,  Bd.  clxii,  S.  1. 

i  Gouget:  Bull.  Soc.  Anat.  Paris,  1898,  p.  605. 

§  Wells,  H.  G.:  American  Journ.  Med.  Sciences,  vol.  cxxvi,  p.  403,  1903. 

I!  Hale  White:  Trans.  Path.  Soc,  vol.  x.xxvi,  p.  251. 


MALIGNANT    DISEASE    OF   THE    LIVER.  515 

A  small  or  moderately  enlarged  liver,  when  associated  with  enlargement 
of  the  spleen,  points  to  cirrhosis,  while  a  large  and  nodular  liver,  espe- 
cially when  combined  with  iimbilication  of  the  surface,  indicates  malig- 
nant disease.  Emaciation  and  pain  are  more  prominent  in  malignant 
disease,  but  wasting  may  be  very  considerable  in  cirrhosis.  A  large 
cirrhotic  liver,  when  associated  with  some  jaundice  and  ascites,  closely 
imitates  carcinoma,  but  in  cirrhosis  the  enlargement  is  more  uniform, 
and  affects  both  lobes,  while  the  spleen  is  often  enlarged  and  cachexia 
is  less  rapid.  The  association  of  well-marked  Jaundice  and  ascites,  how- 
ever, should  always  suggest  secondary  malignant  disease.  Progressive 
increase  in  size  is  in  favour  of  malignant  disease,  more  especially  if  it 
affect  one  lobe  only.  In  the  following  case  primary  carcinomata  imi- 
tated cirrhosis: 

A  cook  aged  forty-three  years  was  admitted  under  Dr.  Penrose  into  St.  George's 
Hospital  with  "a  lump  in  the  middle  of  the  abdomen,"  vomiting  in  the  morning, 
loss  of  appetite,  and  emaciation.  She  had  had  piles  for  fifteen  years.  Alcohol 
had  been  taken  in  inoderation.  On  admission  she  was  thin,  had  an  enlarged, 
roughened  liver,  and  some  ascites,  which  rapidly  increased  in  amount  and  required 
tapping.  She  became  jaundiced  and  passed  into  a  "typhoid"  condition,  with 
dry  tongue,  muttering  delirium,  and  running  pulse.  At  the  autopsy,  except  for 
a  few  minute  growths  in  the  lungs,  there  was  no  new-growth  in  any  part  of  the 
body,  except  in  the  liver,  which  weighed  106  ounces;  there  was  no  growth  in  the 
gall-bladder  or  ducts;  the  right  lobe  contained  extensive  areas  of  whitish-yellow 
growth  of  firm  consistency,  and  also  small  separate  umbilicated  growths;  the  left 
lobe  was  a  thin,  small  cake  of  about  the  size  of  a  child's  hand,  and  was  nearly  sepa- 
rated from  the  rest  of  the  liver,  and  moved  on  a  hinge;  it  also  contained  much 
growth.     The  liver  was  not  cirrhotic.     There  was  chronic  gastritis. 

In  the  rare  condition,  primary  carcinoma  supervening  on  cirrhosis, 
a  diagnosis  from  cirrhosis  is  usually  imi^ossible,  though  in  a  few  cases 
where  the  liver  is  large  the  nodules  of  growths  can  be  felt.  Pain  over 
the  liver  is  often  a  more  prominent  feature  in  these  cases  than  in  cirrhosis, 
and  jaundice,  though  not  always  present,  may  be  very  marked. 

From  the  large  hver  of  hypertrophic  biliary  cirrhosis  primary  malig- 
nant disease  differs  in  its  more  rapid  growth,  in  the  absence  of  splenic 
enlargement,  and  in  the  character  of  the  jaundice.  In  malignant  disease 
it  is,  generally  speaking,  either  absent  or,  if  present,  obstiiictive,  so  that 
no  bile  passes  into  the  blood.  In  biliary  cirrhosis  jaundice  is  constant, 
but  not  complete,  and  the  faeces  are  not  devoid  of  bile.  Hypertrophic 
biliary  cirrhosis  is  met  with  much  earlier  in  life  than  malignant  disease. 

Syphilitic  Disease  of  the  Liver. — Gummata  and  gummatous  enlarge- 
ment of  the  liver,  especially  when  the  patient  is  markedly  cachectic, 
very  closely  imitate  malignant  disease  of  the  liver.  In  cases  where  the 
liver  is  hard  and  enlarged  and  the  patient's  general  condition  is  good, 
gummata  should  be  thought  of  and  vigourous  antisyphilitic  treatment 
should  be  employed.  In  all  cases  of  doubt  iodides  in  large  doses  should 
be  given.  If,  after  a  full  coiu'se,  the  enlargement  is  still  progressive,  the 
case  is  almost  certainly  malignant.  A  history  of  syphilis  is,  of  course, 
important,  but  the  most  decisive  point  is  the  effect  of  antisyphilitic  treat- 
ment adeciuately  carried  out. 

A  large,  firm,  lardaceous  liver  in  a  cachectic  patient  might  be  mis- 


516  DISEASES    OF   THE    LIVER. 

taken  for  primary  massive  carcinoma  of  the  liver  at  first  sight,  but  the 
evidence  of  lardaceous  disease  elsewhere,  as  shown  by  albuminuria  and 
diarrhoea,  the  absence  of  pain  and  of  rapid  and  progressive  enlargement 
of  the  liver,  together  with  a  history  of  past  suppuration  or  of  syphilis, 
should  enable  the  practitioner  to  come  to  a  correct  diagnosis.  When 
gummata  are  combined  with  the  lardaceous  change,  the  liver,  being 
nodular  and  enlarged,  may  resemble  that  of  secondary  mahgnant  disease. 
The  history  and  evidence  of  syphiHs  are  important,  but  the  effect  of 
treatment  is  the  only  really  reliable  means  of  definitely  deciding  the 
point;  if  the  fiver  progressively  enlarges  under  full  doses  of  iodide  of 
potassium,  malignant  disease  is  almost  certainly  present.  A  lardaceous 
liver  with  syphilitic  cicatrices  and  copious  adhesions  sometimes  feels  so 
irregular  through  the  abdominal  wall  that  mahgnant  disease  is  fikely  to 
be  diagnosed;  other  evidences  of  lardaceous  disease,  such  as  albuminuria, 
should  always  be  looked  for  in  doubtful  cases  of  malignant  disease  of 
the  liver.     Albuminuria  is  decidedly  rare  in  the  latter  disease. 

A  hydatid  cyst  may  imitate  malignant  disease  of  the  liver,  especially 
a  primary  massive  carcinoma,  in  a  comparatively  early  stage  before 
marked  constitutional  symptoms  have  arisen,  while  multiple  hydatid 
cysts  may  simulate  the  nodules  of  secondary  malignant  disease. 

In  hydatid  the  enlargement  is  slow  and  constitutional  symptoms  are 
absent.  In  malignant  disease  the  tumor  usually  grows  rapidly,  other 
nodules  may  be  felt,  and  cachexia  is  Hkely  to  supervene.  Generally 
speaking,  malignant  disease  occurs  later  in  life  than  hydatid ;  caution  is, 
therefore,  necessary  before  diagnosing  a  hydatid  cyst  of  the  fiver  in 
elderly  persons.  These  points  are  illustrated  in  the  following  case  of 
primary  massive  carcinoma  of  the  liver: 

A  man  aged  sixty-five  was  admitted  under  my  care  in  St.  George's  Hospital 
in  September,  1900,  with  a  lump  in  the  situation  of  the  left  lobe  of  the  liver,  dull 
pain  of  three  months'  standing  in  the  epigastrium,  which  was  getting  worse,  and 
loss  of  flesh.  There  was  no  history  of  syphihs  and  no  evidence  of  growth  elsewhere. 
The  diagnosis  lay  between  malignant  disease,  gumma,  and  hydatid.  A  full  course 
of  iodides  did  no  good,  and  in  the  middle  of  October  the  liver  was  bigger  and  definite 
nodules  could  be  felt  on  the  surface.  The  liver  rapidly  enlarged  in  size,  and  the 
patient  lost  flesh  and  weight.  Pain  was  pretty  constant  over  the  liver,  which 
eventually  nearly  filled  the  abdomen.  There  was  never  any  ascites,  and  jaundice 
only  occurred  three  days  before  death.  No  rise  of  temperature  was  ever  observed. 
During  the  last  twenty-four  hours  of  life  only  3  ounces  of  urine  were  passed.  At 
the  autopsy  the  liver  showed  a  massive  growth  in  the  left  lobe,  of  firm  consistence 
and  bright  yellow  colour,  which  involved  the  capsule  and  was  firmly  adherent  to 
the  stomach.  There  were  numerous  secondary  gro'w'ths  in  the  right  lobe,  which 
was  smaller  than  the  left.  The  gall-bladder  was  very  small  and  collapsed,  but  not 
involved  in  the  growth.  There  was  considerable  enlargement  of  the  glands  in  the 
portal  fissure,  but  no  obstruction  of  the  portal  vein  or  bile-ducts.  The  liver  weighed 
8  pounds.  No  gro^-t,!!  could  be  found  in  any  other  part  of  the  body.  Microscopically 
the  growth  was  a  spheroidal-celled  carcinoma  and  probably  arose  from  the  fiver  cells. 
The  fibrous  tissue  of  the  growth  was  in  places  very  profuse,  and  the  epithehal  cells 
were  much  compressed;  it  resembled  a  slow-growing  carcinoma  of  the  breast.  The 
fibrous  tissue  showed  advanced  hyaline  change. 

When  the  fiver  contains  several  hydatid  cysts,  some  difficulty  in 
arriving  at  a  correct  diagnosis  must  be  expected. 

Thus  in  a  case  diagnosed  as  hydatid  of  the  liver  and  operated  upon,  the  appear- 
ances so  closely  resembled  multiple  malignant  growths  that  the  operation  was 


MALIGNANT    DISEASE    OF   THE    LIVER.  517 

abandoned;  at  the  autopsy  they  were  found  to  be  multiple  hydatids  after  all.  (Sarg- 
non.*)  The  coincidence  of  carcinoma  and  hydatid  cysts  in  the  same  liver  has 
several  times  been  met  with.      (Habran,t  Longuet,t  Florand.§) 

Multilocular  or  alveolar  hydatid  has  often  been  mistaken  for 
malignant  disease,  both  clinically  and  even  when  found  after  death. 
It  has  not  been  described  as  occurring  in  England,  and  it  is  rare  anywhere. 
In  most  cases  of  the  disease  the  spleen  is  enlarged,  while  the  course  of 
the  disease  is  much  slower  than  in  mahgnant  disease. 

From  Intra-hepatic  Suppuration. — In  rare  instances  the  soft 
character  of  a  rapidly  growing  tumor,  or  the  formation  of  false  cysts 
from  necrosis  or  haemorrhage,  may  give  rise  to  fluctuation,  while  fever, 
which  is  not  very  uncommon  in  malignant  disease  of  the  liver,  may 
further  increase  the  resemblance  to  some  form  of  intra-hepatic  suppura- 
tion, such  as  abscess,  pylephlebitis,  etc.  An  exploratory  laparotomy  may 
be  the  only  means  of  distinguishing  between  growth  and  suppuration. 
Suppuration  may  indeed  be  superimposed  on  malignant  disease. 

In  the  following  case  abscess  seemed  clinically  to  be  more  probable 
than  growth  or  cirrhosis : 

A  man  aged  forty-one  years  began  to  suffer  from  sick  headaches  three  months 
before  his  death;  a  month  later  he  had  flatulence  and  epigastric  pain.  When 
admitted  into  St.  George's  Hospital  on  Feb.  12,  1902,  under  my  colleague,  Dr. 
Ewart,  the  patient,  who  was  well  nourished  and  free  from  jaundice,  presented 
great  enlargement  of  the  liver,  which  projected  markedly  in  the  epigastrium.  After 
admission  the  temperature  became  raised,  and,  an  abscess  being  suspected,  the  liver 
was  aspirated,  but  nothing  but  blood  was  withdrawn.  As  the  temperature  con- 
tinued to  rise.  Sir  W.  Bennett  opened  the  abdomen  and  found  numerous  growths 
on  the  surface  of  the  liver.  A  small  piece  was  removed,  and  found  to  be  a  spheroidal- 
celled  carcinoma.  The  patient  died  a  week  later.  At  the  autopsy  the  liver  weighed 
11  pounds  7  ounces;  the  left  lobe  was  almost  uniformly  infiltrated  by  new-growth, 
while  the  right  lobe  contained  a  number  of  discrete  growths.  The  only  other  growth 
was  one  in  the  middle  of  the  body  of  the  pancreas. 

Howard  Marsh  ||  reported  the  case  of  a  soldier  aged  forty-three,  who  had  been 
in  India,  and  had  an  enlarged  liver  extending  two  inches  below  the  ribs  and  forming 
a  prominent  swelling  in  the  epigastrium,  with  exactly  the  appearance  of  an  abscess 
pointing;  it  was  soft,  fluctuating,  and  the  skin  over  it  was  dusky-red.  Aspiration 
only  brought  away  a  little  blood,  and  at  the  necropsy  cancer  of  the  liver  was  found. 
In  Bramwell  and  Leith's  **  case  of  primary  sarcoma  of  the  liver  an  abscess  was 
diagnosed  and  53  ounces  of  chocolate-coloured  fluid  were  removed  by  aspiration. 
There  was  a  primary,  irregular-celled  sarcoma  of  the  liver,  which  weighed  nine 
pounds.     Hawthorne  ft  has  published  a  somewhat  similar  case. 

In  the  following  case  there  was  some  resemblance  to  pylephlebitis : 

A  man  aged  twenty  was  admitted  under  my  care  at  St.  George's  Hospital  on  May 
15,  1902,  with  anaemia,  fever,  and  a  large  and  tender  liver.  His  history  pointed 
to  an  attack  of  appendicitis  five  weeks  before,  followed  by  two  rigors  and  by  vomit- 
ing. It  was  thought  that  he  had  either  a  large  abscess  in  connexion  with  the 
vermiform  appendix  and  tracking  up  to  the  liver  by  the  side  of  the  colon,  or  pyle- 
phlebitis. It  was  decided  to  give  him  the  benefit  of  the  doubt  and  he  was  advised  to 
submit  to  operation.  At  the  operation  by  Mr.  Jaffrey  there  was  no  abscess,  but  the 
liver  was  large  and  bled  readily  when  punctured;  on  the  convexity  of  the  liver  there 

*  Sargnon:  Lyon  Medical,  1S9S,  p.  254. 

t  Habran:  Bull.  Soc.  Anat.,  1868,  p.  437. 

t  Longuet:  Gaz.  hebdom.,  1874,  p.  774. 

§  Florand:  Bull.  Soc.  Anat.,  1886,  p.  677. 

II  Marsh,  H.:  St.  Bartholomew's  Hospital  Reports,  vol.  xxiii,  p.  148. 
**  B.  Bramwell  and  Leith:  Lancet,  1897,  vol.  i,  p.  170. 
ft  Hawthorne,  C.  O.:  CUn.  Jour.,  vol.  viii,  p.  361. 


518 


DISEASES    OF    THE    LIVER. 


was  a  raised  area,  thought  to  be  either  an  early  stage  of  an  abscess  or  new-growth. 
It  was  punctured,  but  nothing  came  out.  The  age  of  the  patient  mihtated  against 
new-growiih.  The  abdomen  was  closed,  and  the  patient  survived  for  five  weeks; 
during  the  greater  part  of  this  period  the  temperature  was  intermittent,  going  up 
to  101°  at  night  and  becoming  normal  in  the  morning;  during  the  last  week  of 
hfe  the  temperature  was  almost  normal.  (Edema  of  the  legs  and  back  developed 
some  weeks  before  death. 

At  the  autopsy  the  liver  was  occupied  by  numerous  white  gro'tt'ths  showing 
cystic  degeneration,  and  weighed  18  pounds.  The  primary  growth  was  in  the  left 
kidney.  There  was  thrombosis  of  the  inferior  vena  cava  close  to  its  bifurcation, 
thus  accounting  for  the  cedema.     The  portal  vein  was  normal. 

Microscopically  the  growth  was  an  endothelioma  "ttith  much  myxomatous 
change. 

A  large  cystic  sarcoma  of  the  liver,  such  as  is  described  on  page  517, 
may  very  closely  imitate  an  abscess  or  a  sanguineous  peritoneal  cyst. 
If  opened,  the  fluid  from  a  cystic  sarcoma  will  probably  contain  growth 
which,  when  examined,  microscopically,  T^dll  show  evidence  of  mahgnancy. 


MONTH 

:M:aj-  ir)03 

June                                        1 

DAY 

I's  1 1's  1  i? 

18  I  10 !  20  '  21 

22  !  22  !  2- 1  ;  25  !  21;  '  ?7  j  28 

20 

30    31 

1      2UI, 

i\i\i 

3 

9  1  10  1 11  1 

l'2  1  13  1 1'l  :  15  i  I'c  !  17    IS 

19  !  20 

21 

22  1 23  1 24    25  1 

F       f  < 
1C9 

108' 

107' 

loc' 
lo; 

101 
103' 
102' 

im' 

100 
'J8 

or 

OS 
96 

>i:e  «:E  .«:£ 

>tE).E'..t-L 

MI  -IE  ML  .lU  MEME.n-E 

,.E 

HE 

HE 

»E 

ME 

He 

XE 

aE 

«.E 

ai:E 

rfE 

ME 

IE 

MEMEMEMEMEME 

ME;JIE 

«E 

«e«em;e| 

i    ;      i 

=  :  '  i 

i 

: 

; 

i 

;  1  1  i  :  i  ;  !  1  !  ; 

i  1  ! 

: 

:  =■    ; 

:       ■- 

-    =       ■','.•/'. 

•■ 

;  1  i 

;  ;i::; 

^rl^$^M 

s 

: 

; 

: 

: 

= 

i       = 

i 

- 

: 

I 

; 

= 

:• 

i 

i=   i 

1 

: 

; 

: 

; 

■■ 

;  1  ;  ■  :    ;    :  '  :; 

- 

; 

;■= ! 

: 

: 

■■ 

: 

;  !  ;                  i 

:  j  ;  n  1  : 

1    :_j    1 

; 

; 

= 

; 

\  .\  '  ^         t  ■ 

':\\\\    \\ 

i  1  ; 

ifl 

;     ; 

i^ 

: 

i 

i      i 

;  i ;  1 ;  i  : 

: 

f\l\f\f\ 

K '      .J^ 

K  A-'-  '  i\  ',-  t'  ', 

':    1    :        1\    ]        : 

"M    r"            -  - 

A/\aA/    ■ 

\m.mM 

•^,A/Vf-^ 

-N^^   -irA  ' 

;    ;  1  :  !  i  M 

''~\j '■ 

.  Y — V  u  V 

i/ V:  ,  :  .'*.  .V:- 

:  \^l}i.  V 

Y— 

■l^  :  ^^  M 

!j.V-    . 

— :— 

— r- 

:       V  1   ■ 

m: 

;  i  i 

: 

Hi 

1r^ 

;  1 ; 

l|; 

i|; 

i 

■.fir 

^. 

%ivf 

\f 

: 

MM; 

=  M 

iM 

•: 

; 

:  1; 

= 

;  M    ; 

\  1; 

i  1  i 

: 

: 

1 

ill 

i  li 

ih  i 

PULSE 

^ 

RESP. 

BO. 

n 

1 

0 

i'' 

0 

0 

1 

2 

5 

6 

5 

2 

1 

1 

i^ 

lA 

4 

0  i2 

4i4 

2  (3 

4 

4 

2 

4 

4 

5 

4     4 

s 

3 

4 

3 

3il|2 

2 

iA 

72  44 

48148146138 

54  00141 

35 

46t34 

36 

34|30  4G 

30|28 

28  20 

30'22|35 

24 

WEIGHT 

.    !    M 

,      j 

1 

1 

:     1 

1 

1 

1       J..;,      I 

1 

!     1 

1      1 

Fig.  71. — Temperature  Chart  of  Man,  Aged  Twenty  Years,  with  Secondary  Endothelioma 
OF  Liver  Imitating  Pylephlebitis.     Primary  Growth  in  the  Left  Kidney. 


but  even  then  it  may  be  impossible  to  say  whether  the  growth  arose  in 
the  liver  or  invaded  it,  as  a  suprarenal  or  other  retroperitoneal  tumor 
might  do.  The  diagnosis  during  hfe  in  these  cases,  which  luckily  are  rare, 
is  extremely  difficult.  Conversely,  slow  abscess  formation  in  the  hver 
may  be  regarded  as  mahgnant  disease  and  not  operated  upon  for  this 
reason. 

Chronic  Venous  Engorgement. — ^The  enlarged  and  tender  liver  of 
chronic  venous  engorgement,  especially  in  the  late  stage  of  mitral  disease, 
has,  in  rare  instances,  been  regarded  as  malignant.  This  mistake  is  not 
likely  to  occur  often,  as  the  general  aspect  of  the  two  diseases  is  so  different. 
Difficulty  is  more  likely  to  arise  in  cases  of  marked  dilatation  of  the  left 
ventricle  without  any  mitral  murmur.  The  presence  of  '  obstructive 
cardiac  or  pulmonary  disease,  and  the  effect  of  treatment  by  digitalis, 
strophanthus,  purgatives,  etc.,  in  diminishing  the  size  of  the  li^'er  are 
points  in  the  diagnosis  on  which  further  insistence  is  unnecessary. 


MALIGNANT    DISEASE    OF    THE    LIVER.  519 

A  woman,  aged  forty  years,  but  looking  fifteen  years  older,  was  admitted  under 
my  care  in  St.  George's  Hospital  in  January,  1903,  in  great  pain  and  respiratory 
distress.  Her  appearance  suggested  morbus  cordis  or  a  large  pleural  effusion, 
b'Jt  the  heart  appeared  healthy  and  there  was  only  a  little  dulness  at  the  right 
base.  There  was  much  resistance  in  the  epigastrium  and  great  pain  on  pressure, 
and  as  she  had  frequent  retching,  it  was  thought  she  might  have  malignant  disease 
of  the  stomach  and  liver.  Her  condition  prevented  a  thorough  examination,  and 
she  was  kept  under  the  influence  of  morphine,  but  the  pain  seemed  very  severe. 
Three  days  before  death  she  became  jaundiced.  At  the  autopsy  there  was  no  growth 
of  any  kind.  The  liver  was  enlarged  and  showed  some,  but  not  advanced,  chronic 
venous  engorgement.  The  heart  weighed  15  ounces  and  showed  extensive  fibroid 
disease.  The  orifices  of  the  coronary  arteries  were  extremely  small,  and  the  ascend- 
ing part  of  the  aorta  showed  gelatinous  thickening,  suggesting  syphilitic  or  acute 
aortitis.  There  were  a  pulmonary  apoplexy  in  the  right  lung  and  a  pleural  effusion. 
It  is  probable  that  the  pain  was  cardiac  and  of  the  nature  of  angina. 

Impacted  Gall-stone  in  the  Common  Bile-duct;  Intermittent 
Hepatic  Fever. — Impaction  of  a  gall-stone  in  the  common  bile-duct 
may  occur  without  any  previous  attacks  of  biliary  colic.  When  this 
occurs  in  a  person  past  micldle  life,  it  may  resemble  very  closely  malignant 
disease  of  the  liver,  especially  that  form  arising  in  the  bile-ducts  (vide 
p.  683).  As  time  goes  on,  however,  the  jaundice  tends  to  diminish, 
whereas  in  malignant  disease  it  becomes  deeper.  In  impacted  gall-stone 
the  liver,  if  enlarged  at  first,  does  not  progressively  increase  in  size,  but 
rather  diminishes,  and  there  is  an  absence  of  irregularities  on  its  surface. 

A  man  aged  sixty-seven  became  jaundiced  at  the  beginning  of  1890  after  having 
felt  weak  for  ten  days;  there  had  been  no  pain  or  colic.  About  May  17th  he  con- 
sulted the  late  Sir  Andrew  Clark,  who,  according  to  the  patient,  diagnosed  cancer 
of  the  liver  and  gave  him  a  month  to  live.  When  admitted  to  St.  George's  Hospital 
under  the  late  Dr.  Cavafy  he  was  thin,  jaundiced,  and  weak.  The  hepatic  dulness 
began  at  the  fifth  rib  in  the  right  nipple  line,  and  extended  below  the  right  costal 
mar2;in,  where  there  was  a  rounded,  dull  swelling  extending  do-mawards  to  within 
one  inch  of  the  umbilicus.  No  pain  or  tenderness  existed.  With  rest  in  bed  the 
jaundice  cleared  away  and  the  tumor  in  the  right  hypochondrium  receded,  until, 
at  the  beginning  of  August,  the  skin  was  almost  natural  in  colour.  He  then  had 
spells  of  diarrhoea,  which,  however,  were  easily  controlled  by  treatment.  On 
September  20th  and  October  8th  he  had  definite  rigors,  his  temperature  was  raised 
at  intervals,  and  he  was  losing  flesh  and  strength  from  attacks  of  diarrhoea.  On 
November  17th  a  severe  bout  of  diarrhoea  began;  on  the  19th  he  had  a  rigor,  and 
on  the  following  morning  he  died  rather  suddenly.  At  the  autopsy  I  found  a  large 
calculus  in  the  common  loile-duct,  close  to  the  duodenum;  "it  was  loose  and  allowed 
bile  to  flow  past  it  into  the  duodenum,  as  was  proved  by  pressure  on  the  gall-bladder. 
There  was  catarrhal  cholangitis,  to  which  the  fever  and  occasional  rigors  were  due; 
the  liver  showed  secondary  pericholangitic  fibrosis  and  there  were  numerous  old 
adhesions  around  the  gall-bladder  and  liver.  There  was  no  trace  of  maUgnant 
disease  in  the  body. 

A  displaced  or  a  wandering  liver  very  rarely  imitates  malignant 
disease.  In  Crawfurd's  *  case  of  anteverted  wandering  liver  malignant 
disease  was  diagnosed  during  life.  The  association  of  jaundice  and 
ascites  with  hepatoptosis  is  most  unusual,  but  it  may  occur  from  kinking 
of  the  portal  vein  and  bile-duct.  The  freely  movable  state  of  the  liver 
should  direct  attention  to  the  real  condition.  The  severe  constitutional 
symptoms  in  malignant  disease  and  their  absence  in  wandering  and 
displaced  livers  should  help  to  ])rcvent  any  chance  of  confusion. 

A  large  renal  tumor  on  the  right  side  may  appear  to  be  in  direct 

*Crawfurd,  R.  P.:  Lancet,  1897,  vol.  ii,  p.  1182. 


520  DISEASES    OF   THE    LIVER. 

continuity  witii  the  liver.  In  some  cases  of  extensive  cystic  disease  of 
the  kidneys  the  tumor  may  imitate  a  distended  gall-bladder,  or  possibly, 
if  tense  cysts  project  from  the  surface  of  the  kidney,  secondary  growths 
in  the  liver.  A  bimanual  exainination  will  show  that  the  renal  tumor 
definitely  bulges  into  the  loin.  The  presence  of  bowel  in  front  of  the 
renal  tumor  is  important;  this  may  be  made  more  manifest  by  filhng 
the  colon  with  air  after  removing  its  solid  contents  by  means  of  an  enema. 
Tumors  of  the  right  suprarenal  body,  by  growing  forwards,  may 
very  closely  resemble  hepatic  growths.  In  some  cases  the  liver  may 
become  invaded  by  continuity  and  secondary  growths  often  occur  in 
the  hver. 

In  a  large  cystic  sarcoma  of  the  right  suprarenal  body,  which  I  examined  post- 
mortem in  1891,  the  diagnosis  was  first  hydatid  of  the  liver,  and  subsequently 
malignant  disease;  in  this  case  there  were  secondary  growths  in  the  liver,  as  well 
as  direct  invasion  of  that  organ. 

Inflammatory  thickening  around  the  gall-bladder  may  be  palpable 
as  a  hard  mass,  and  thus  may  give  rise  to  physical  signs  resembhng  car- 
cinoma. The  history  of  gaU-stones  and  the  fact  that  the  patient's 
general  state  is  not  so  grave  as  in  carcinoma  are  important  points  to 
bear  in  inind. 

Occasionally  faecal  accumulation  in  the  transverse  colon  may  imi- 
tate malignant  disease;  here  the  tumors  may  vary  in  position  from 
time  to  time,  can  be  indented  by  pressure,  are  capable  of  removal  by 
purgatives  or  abdoixiinal  massage,  and,  when  a  careful  examination  is 
made,  if  need  be  under  an  anaesthetic,  other  masses  can  be  made  out  in 
the  course  of  the  colon. 

Improbable  as  it  may  appear,  difficulty  has  arisen  in  distinguishing 
between  'pregnancy  and  secondary  malignant  disease  of  the  hver. 

In  the  following  case*  both  conditions  existed  at  the  same  time  and  the  ab- 
dominal enlargement  was  naturally  thought  to  be  explained  by  pregnancy.  A 
married  woman  aged  thirty-nine  years,  who  had  had  several  children,  was  thought 
to  be  pregnant.  She  died,  and  a  six-months  foetus  was  found  in  the  uterus.  The 
liver  weighed  17J  pounds  and  contained  numerous  secondary  growths;  the  primary 
growth  appears  to  have  been  in  the  colon. 

A  case  was  reported  by  Hale  White  f  in  which  a  woman  was 
thought  to  be  suffering  from  the  vomiting  of  pregnancy  until  a  pri- 
mary carcinoma  of  the  liver  was  found  at  the  autopsy. 


DIAGNOSIS  BETWEEN  PRIMARY  AND   SECONDARY  MALIGNANT  DISEASE  OF  THE 

LIVER  DURING  LIFE. 

In  secondary  malignant  disease  of  the  liver  the  primary  growth  may 
remain  latent  and  not  give  rise  to  any  symptoms  during  life.  In  such 
cases  there  are  often  no  means  of  arriving  at  a  correct  diagnosis  of  sec- 
ondary, rather  than  primary,  mahgnant  disease  of  the  liver.  These  cases, 
which  are  clinically  described  as  "malignant  disease  of  the  liver,"  tend, 
when  included  in  statistics,  to  make  primary  malignant  disease  appear 

*  Robinson:  Trans.  Path.  Soc,  vol.  ii,  p.  167. 

t  Hale  White:  Trans.  Path.  Soc,  vol.  xxxvi,  p.  251. 


MALIGNANT    DISEASE    OF  THE   LIVER.  521 

less  rare  than  it  really  is.  According  to  Hale  White,*  in  about  half  the 
cases  of  secondary  carcinoma  of  the  liver  the  j^rimary  site  cannot  be 
determined  during  life. 

The  primary  growth  may  remain  latent  when  it  is  in  the  stomach,  pan- 
creas, oesophagus,  kidney,  and,  in  exceptional  instances,  when  in  the  colon. 

In  the  following  case  the  primary  growth  was  entirely  latent,  the  liver 
was  greatly  enlarged,  and  nodules  were  easily  felt;  the  disease  of  the  liver 
was  regarded  as  secondary,  possibly,  to  a  gastric  carcinoma. 

A  wasted  old  man  aged  sixty-two  years  was  admitted  under  my  care  in  St. 
George's  Hospital  on  June  22,  1899,  complaining  of  pain  over  the  liver,  inability 
to  lie  on  his  left  side,  shortness  of  breath,  difficulty  in  digestion,  and  constipation. 
Six  weeks  previously  his  legs  began  to  swell;  this  was  followed  by  swelling  of  the 
abdomen.  He  had  ascites  which  required  tapping.  The  liver  was  much  enlarged, 
and  extended  nearly  down  to  the  umbilicus;  nodules  which  seemed  to  be  umbilicated 
were  readily  felt.  On  the  skin  over  the  free  edge  of  the  liver  there  was  a  nieshwork 
of  dilated  vessels.  There  was  dulness  in  both  flanks.  The  urine  was  free  from 
albumin;  two  days  before  his  death,  when  his  conjunctivae  became  jaundiced, 
bile-pigment  appeared  in  the  urine.  He  got  steadily  weaker,  had  little  or  no  pain, 
completely  lost  his  appetite,  and  died  after  being  in  a  drowsy  condition  for  forty- 
eight  hours  on  July  6th.  At  the  autopsy  the  liver  weighed  9  pounds  14-^  ounces, 
and  was  packed  with  nodules  of  soft  white  growth  which  were  not  umbilicated. 
The  right  kidney  weighed  8  pounds  5  J  ounces  and  was  transformed  into  a  large 
haemorrhagic  growth  which  had  broken  down  into  pseudo-cysts.  Some  of  the  cysts 
contained  cholesterin  crystals.  Microscopically  the  growth  was  a  beautiful  villous 
carcinoma.     (Vide  Fig.  66.) 

Kelynackf  has  described  an  almost  exactly  similar  case  in  a  woman,  but  the 
left  kidney  was  affected  and  there  was  hsematuria,  so  that  the  primary  growth 
did  not  remain  latent  as  in  this  case.  The  liver  contained  numerous  cystic  growths 
and  weighed  111  ounces. 

I  have  seen  two  other  cases  in  which  the  primary  growth  in  the  kidney  remained 
quite  latent;  this  is  very  likely  to  happen  when  the  right  kidney  is  affected,  and  is 
under  cover  of  the  enlarged  liver,  but  it  may  occur  when  the  gro'n'th  in  the  left 
kidney  is  small. 

From  extreme  sensibility  and  a  mistaken  sense  of  clehcacy  a  woman 
may  conceal  the  fact  that  she  has  carcinoma  of  the  breast  and  only  com- 
plain of  symptoms  pointing  to  malignant  disease  of  the  liver. 

Such  a  case  is  recorded  by  Pearson  and  Howes  J  where  an  ulcerating  carcinoma 
of  the  mamma  was  only  discovered  after  death  in  a  woman  aged  sixty  who  during 
life  had  been  under  treatment  for  a  tumor  in  the  liver  with  pain  and  ascites. 

Carcinoma  of  the  stomach  may  remain  quite  latent  when  there  are 
extensive  secondary  growths  in  the  liver.  According  to  Fenwick,§  the 
changes  in  the  liver  are  most  marked  when  the  gro\A^h  in  the  stomach 
is  comparatively  insignificant.  Inasmuch  as  a  pyloric  gro^vth  is  likely 
to  lead  to  obstruction  and  symptoms,  the  latent  growths  are  more  often 
in  the  body  or  cardiac  end  of  stomach. 

Secondary  growths  in  the  liver  are  not  uncommon  when  carcinoma 
attacks  the  lower  half  of  the  oesophagus,  but  dysphagia  is  nearly  always 
present. 

In  a  man  aged  fifty-five  years  who  died  in  St.  George's  Hospital  with  carcinoma 
of  the  oesophagus  and  numerous  secondary  growths  in  a  liver  weighing  14  pounds, 
there  was  nothing  more  definite  than  a  distaste  for  solid  food. 

*  Hale  White:  Allbutt's  System  of  Medicine,  vol.  iv,  p.  197. 

t  Jour.  Path,  and  BacterioL,  vol.  iv,  p.  236. 

j  Trans.  Path.  Soc,  vol.  xxvi,  p.  185. 

§  Fen  wick:  Cancer  and  Other  Tumors  of  the  Stomach,  p.  182. 


522  DISEASES    OF    THE    LITER. 

The  presence  of  an  enlarged  gland  (Virchow's  gland)  above  the 
clavicle  should  suggest  the  possibility  of  oesophageal  carcinoma,  but  it 
may,  of  course,  occur  in  other  cases  of  generalised  new-gro-v\i:h.  Enor- 
mous enlargement  of  the  liver  may  be  due  to  melanotic  sarcoma  arising 
secondarily  to  a  primar}^  growth  in  the  uveal  tract;  in  such  cases  the 
seat  of  the  primarj^  gro'\\^h  may  easily  be  overlooked  if  the  patient  wears 
a  glass  eye  and  does  not  call  attention  to  the  fact  that  his  eye  has  been 
removed. 

Multiplicity  of  nodules  on  the  surface  of  an  enlarged  liver  is  much 
in  favour  of  secondarj^  growth,  but  unless  there  is  definite  evidence  of 
primary  growth  in  the  body,  or  of  one  having  been  removed,  the  diagnosis 
of  secondary  growths,  though  most  probable,  cannot  be  made  with  abso- 
lute certainty,  since  primar}^  malignant  disease  may  occur  in  a  multiple 
nodular  form.  Deep  jaundice  and  the  association  of  ascites  with,  jaimdice 
are  in  favour  of  secondary  malignant  disease,  while  verj^  rapid  enlarge- 
ment of  the  Hver  without  emaciation  is  more  frequent  in  primarj^  malig- 
nant disease.  It  is  true  that  the  hver  may  increase  in  size  very  rapidly 
in  secondary  malignant  disease,  but  since  the  primarj^  growth  is  usually 
in  the  ahmentary  canal,  there  is  generally  considerable  emaciation  on 
this  account  before  the  hver  is  much  or  at  all  affected.  Wlien  the  primarv- 
groT\i:h  is  in  the  kidneys  or  in  the  uveal  tract,  emaciation  is  not  so  marked. 
In  the  enlargement  of  the  hA^er  due  to  melanotic  sarcoma  a  clue  to  the 
nature  of  the  disease,  even  in  the  absence  of  any  history^  of  an  intra-ocular 
gro^i:h,  may  be  obtained  by  finding  melanin  in  the  urine. 

To  summarise  the  differential  diagnosis  of  primar}'  and  secondary' 
mahgnant  disease  of  the  liA^er: 

Primary.  Secondary. 

No  sign  or  symptom  of  growth  else-       Some  evidence  of  gro'W'th  elsewhere. 

where  in  the  body. 

A  single  tumor.  Multiple  tumors. 

Very  rapid  growth.  Less  rapid  growth. 

Jaundice  rare  and  slight.  Jaundice  common. 

Ascites  infrequent.  Ascites  common. 

Emaciation  not  so  marked.  Emaciation  marked. 

Course  rapid.  Course  not  so  acute. 

Pepere  *  has  attempted  to  draw  a  clinical  distinction  between  primarj^ 
carcinoma  and  primary  sarcoma  of  the  hver.  According  to  his  observ^a- 
tions,  primary  sarcoma  nms  a  more  rapid  course  and  is  less  frequently 
accompanied  by  jaundice  or  ascites  than  primary  carcinoma. 


PROGNOSIS. 

When  the  diagnosis  of  mahgnant  disease  of  the  hver  can  be  made  at 
the  bedside,  the  prognosis  is  always  hopeless.  It  is  true  that  when 
laparotomy  reveals  the  presence  of  early  primaiy  malignant  disease  of 
the  liver,  malignant  disease  limited  to  a  constriction  lobe,  or  malignant 
disease  of  the  gall-bladder  invading  the  liver,  there  is  a  chance  that  re- 

*  Pepere:  Archiv.  de  Med.  experiment,  et  d'anat.  path.,  tome  xiv.  p.  805,  Nov., 
1902. 


MALIGNANT    DISEASE    OF   THE    LIVER.  523 

moval  mil  not  be  followed  b}"  recurrence.  But  even  in  these  cases,  wliich 
can  hardly  be  diagnosed  with  any  certainty  before  the  abdomen  is  opened, 
the  disease  usually  returns  and  kills  the  patients.  Operation  for  removal 
of  malignant  gro'v\'ths  from  the  liver,  whether  from  its  substance  or  when 
starting  in  the  gall-bladder,  is  the  only  means  at  our  disposal  at  present 
of  mitigating  the  otherwise  absolute^  fatal  prognosis.  The  prognosis 
is  better  when  a  growth  originating  in  the  gall-bladder  is  removed  than 
in  resection  of  the  liver  for  a  primar}^  neoplasm.  Death  is  more  rapid 
in  primary  malignant  disease  than  in  the  more  famiHar  secondary-  growths 
in  the  hver. 

How  long  life  may  be  prolonged  with  secondary'  gro'^i:hs  in  the  liver 
is  uncertain.  In  most  cases  death  follows  within  six  months  of  definite 
e\aclence  of  hepatic  enlargement.  It  must  be  remembered  that  in  some 
instances  the  liver  may  have  been  previously  enlarged  from  some  inde- 
pendent cause;  a  floating  lobe  or  tight-laced  liver  might  thus  give  rise 
to  a  fallacy. 

In  a  case  of  secondary  melanotic  sarcoma  of  the  liver  recorded  by  Litten  there 
was  evidence  of  hepatic  enlargement  for  four  years  before  death,  a  period  quite 
incompatible  mth  the  view  that  a  secondary  growth  was  present  all  the  time. 

On  the  analogy  of  the  spontaneous  disappearance  of  solid  and  in- 
operable groTviihs  in  the  abdomen  having  the  appearance  of  mahgnancy 
— a  remarkable  event  to  which  the  late  Professor  Greig  Smith  *  drew 
attention — ^it  is  conceivable  that  mahgnant  disease  of  the  Hver  might  oc- 
casionally disappear.  Undoubted  carcinomatous  secondars^  growths  in  the 
skin  have  in  A'ery  rare  instances  been  known  to  disappear  spontaneously,t 
and  in  a  similar  case  enlargement  of  the  liver  has  been  noticed  to  pass 
away.     (A.  P.  Gould. J) 

Campbell  quotes  a  case  §  in  which  influenza,  supervening  in  the  course  of 
malignant  disease  of  the  liver,  was  followed  by  rapid  diminution  in  the  size  of  the 
liver.  The  patient  indeed  seemed  to  get  well,  but  in  one  and  a  half  years'  time  the 
growth  returned  and  proved  fatal.  It  is  possible  that  in  this  instance  a  secondary 
streptococcal  infection  on  the  influenza  attack  may  have  manufactured  a  toxine 
that  acted  on  the  hepatic  gro^vi^h,  much  in  the  same  way  as  Coley's  fluid  does  on 
sarcomata. 

The  only  bright  side  to  the  prognosis  of  malignant  disease  of  the  liver 
is  the  possibility  that  the  diagnosis  may  be  wrong  and  that  the  actual 
condition  is  gummatous  or  hydatid  disease  of  the  hver. 


TREATMENT. 
The  medical  treatment  is  purely  palhative,  and  directed  chiefly 
to  the  relief  of  pain  and  discomfort  by  morphine,  opium, .  and  chloral. 
H\i3odermic  injection  of  morphine  is  preferable  to  opium  by  the  mouth, 
inasmuch  as  it  is  more  surely  absorbed,  disturbs  digestion  less,  and  its 
effects  can  be  more  accurately  estimated.     From  the  necessarily  fatal 

*  Greig  Smith:  Medico-f'hirurg.  Trans.,  vol.  Lxxvii,  p.  139. 
t  Gould,  A.  P.:  Trans.  Clin.  Soc,  vol.  xxx,  p.  205. 
t  Gould,  A.  P.:  Clinical  Journ.,  1902,  May  28,  p.  96. 
§  Campbell,  H.:  Brit.  Med.  Journ.,  1898,  vol.  i,  p.  1126. 


524  DISEASES    OF   THE    LIVER. 

nature  of  the  disease  morphine  may  be  given  without  any  qualms  of 
conscience  as  to  morphinomania.  Measures  should  be  taken  to  combat 
the  excessive  constipation  induced  by  morphine,  and  it  is  often  advisable 
to  combine  the  morphine  with  a  little  atropine. 

Pain  over  the  liver  may  be  to  some  extent  relieved  by  the  local  appli- 
cation of  a  plaster  made  up  of  the  pharmacopceial  plasters  of  opium  and 
of  belladonna.  Hot  fomentations  or  poultices  may  be  given  a  trial. 
The  pain  and  tenderness  are,  of  course,  aggravated  by  examination, 
which  should,  therefore,  not  be  unnecessarily  repeated. 

If  there  is  jaundice,  itching  may  be  the  chief  thing  that  the  patient 
complains  of,  and,  to  relieve  it,  chloride  of  calcium  by  the  mouth  should 
be  tried,  while  warm  alkaline  baths,  bathing  the  skin  with  carbolic  acid 
1  :  40,  or  the  hypodermic  injection  of  pilocarpine,  may  give  relief;  proba- 
bly morphine  will  be  found  to  be  the  most  generally  successful  means  of 
combating  it. 

Vomiting  should  be  treated  by  ice,  morphine,  bismuth,  and  dilute 
hydrocyanic  acid.     Washing  out  the  stomach  may  be  very  useful. 

Flatulence  and  distension  of  the  intestine  should  be  treated  by  various 
carminatives,  by  minute  doses  (4V  gr.)  of  calomel,  creasote  perles,  and 
by  gentle  purges.  Constipation  should  be  met  by  saline  purges  and  mild 
laxatives,  such  as  cascara. 

The  diet  is  largely  determined  by  the  patient's  inclinations ;  usually 
there  is  want  of  appetite  and  dislike  for  meat,  so  that  liquid  food,  milk, 
jelHes,  tea,  and  coffee  are  all  that  he  cares  to  take.  Milk  has  the  ad- 
vantage of  being  easily  digested  and  giving  rise  to  a  minimum  of  putre- 
factive products.     Stimulants  are  usually  desirable. 

If  ascites  gives  rise  to  abdominal  distension  and  discomfort,  tapping 
should  be  performed. 

Operative  Treatment. — Removal  of  the  growth  is,  of  course,  the 
ideal  method  of  treatment,  but  is  only  to  be  thought  of  for  a  primary 
and  single  growth.  A  number  of  cases  have  been  operated  upon  and 
excision  of  the  mahgnant  growth  performed. 

In  a  tabular  statement  of  76  cases  in  which  resection  of  the  hver  had  been  per- 
formed for  growths  or  other  conditions,  Keen*  gives  18  carcinomata,  5  sarcomata, 
and  1  endothelioma. 

Removal  of  a  mahgnant  growth  in  the  gall-bladder  is  much  less 
difScult  than  excision  of  a  primary  mahgnant  growth  from  the  substance 
of  the  liver.  Another  grave  practical  difficulty  is  that  of  arriving  with 
any  certainty  at  a  diagnosis  of  a  primary  hepatic  growth  before  it  has 
become  too  extensive  for  satisfactory  removal. 

Success  is,  therefore,  more  likely  to  occur  in  cases  where  the  ex- 
ploratory operation  was  undertaken  under  the  idea  that  there  were  con- 
ditions other  than  malignant  disease  present,  such  as  a  hydatid  cyst.  It 
is  very  probable  that  good  results  might  follow  in  cases  where  a  small 
secondary  growth  is  excised  at  the  same  time  as  a  primary  carcinoma  of 
the  stomach  or  of  the  gall-bladder,  as  in  Mayo  Robson's  case,t  where 

*  Keen:  Annals  of  Surgery,  Sept.,  1899,  p.  276. 

t  Mayo  Robson:  Medico-Chirurg.  Trans.,  vol.  Ixxix,  p.  159. 


:\IALIGNANT    DISEASE    OF   THE    LIVER.  525 

complete  recoveiy  followed,  is  removed.  But  in  such  cases  there  is, 
unfortunately,  the  danger  of  the  liver  being  more  ^ddely  infected  than 
appears  to  the  naked  eye. 

Laparotomy,  with  a  view  of  removing  a  diagnosed  growth,  would 
often  be  only  an  exploratory  incision,  for  the  extent  of  the  disease  and 
the  presence  of  secondary  growths  would,  in  a  large  number  of  cases, 
render  any  operative  treatment  impracticable.  At  the  present  time, 
however,  the  surgery-  of  the  liver  is  advancing  by  such  leaps  and  bounds 
that  the  value  of  resection  of  the  liver  for  new-gro\\i:hs  is  hkely  to  be 
more  extensively  tested.  According  to  H.  J.  Waring,*  most  of  the  cases 
that  have  been  operated  upon  have  died  from  a  recurrence  of  the  growth. 

*  Waring,  H.  J.:  Diseases  of  Liver,  Gall-bladder,  etc.,  p.  195. 


JAUNDICE. 

Definition. — Jaundice  is  the  condition  due  to  the  presence  of  bile- 
pigment  in  the  blood,  and  is  recognised  clinically  by  staining  of  the  skin, 
conjunctivae,  mucous  membranes,  blood-serum,  and,  as  a  rule,  of  the 
urine,  by  bile-pigment. 

Like  albuminuria,  it  is  a  symptom  and  not  a  disease,  and  may  be  met 
T\ith  in  a  number  of  different  conditions,  the  common  and  essential  factor 
being  obstruction  at  some  point  to  the  passage  of  bile  along  the  bile 
capillaries  or  ducts. 

Etymology. — The  word  jaundice  is  derived  from  the   French  Jaune,  yellow. 

Wickham  Legg  *  gives  a  number  of  possible  derivations  for  icterus,  such  as  Iktu, 
the  yellow-breasted  martin,  which  probably  was  the  equivalent  in  ancient  Greek 
households  of  our  domestic  cat;  'inrtijoc,  the  golden  oriole,  the  sight  of  which  was 
supposed  to  cure  jaundice,  while  the  bird  died  (Phny);  and  from  li^nvog,  a  kite, 
from  the  colour  of  its  eyes. 

INTRODUCTION. 

The  formation  of  bile-pigment  from  hsemoglobin  is  limited  to  the  cells 
of  the  liver  and  cannot  be  vicariously  carried  out  elsewhere  in  the  body, 
for,  as  shown  by  experiments  on  animals,  this  transformation  does  not 
take  place  when  the  liver  is  removed  or,  and  this  comes  to  the  same  thing, 
when  all  the  vessels  going  to  it  are  ligatured. 

Moleschott  t  showed  that  after  excision  of  the  liver  in  frogs  there  was  no  forma- 
tion of  bile  in  any  part  of  the  body ;  while  by  excluding  the  Hver  of  pigeons  from 
the  circulation  by  ligature  of  its  vessels  Stern  J  and  Minkowski  and  Naunyn,§  in 
ducks,  proved  that  the  same  was  true  in  birds. 

It  was,  however,  formerly  thought  that  since  hsematoidin,  which  is 
chemically  identical  with  bilirubin,  is  formed  in  old  hsemorrhages,  etc., 
from  haemoglobin,  bile-pigment  was  similarly  manufactured  in  other 
parts  of  the  body. 

Jaundice,  or  the  presence  of  bile-pigment  in  the  blood,  is  due  to  the 
passage  of  bile,  manufactured  bj^  the  liver,  into  the  circulation  instead 
of  into  the  intestines.  This  miscarriage  of  the  bile  may  occur  either 
directly  the  bile-pigment  is  formed  by  the  liver  cells — i.  e.,  before  the 
bile  enters  the  bile-ducts — or  later,  after  it  has  passed  into  the  ducts. 
In  cases  of  long-standing  biliary  obstruction,  in  which  the  dilated  intra- 
hepatic ducts  only  contain  mucus,  the  bile  formed  by  the  liA'er  cells 
passes  almost  directly  into  the  adjacent  lymphatics,  and  thence  into  the 
thoracic  duct,  and  so  reaches  the  general  circulation.     Cases  of  this  kind, 

*  Lesg,  J.  Wickham:  Bile,  Jaundice,  and  Bilious  Diseases,  p.  22.5. 
t  Moleschott:  Archiv  f.  phvsiol.  Heilk.,  Bd.  xi,  S.  479,  1852. 
J  Stern:  Archiv  f.  exper.  Path.  u.  Pharmak.,  Bd.  xix,  S.  39. 
§  Minkowski  and  Naunyn:  Archiv  f.  exper.  Path.  u.  Pharmak.,  Bd.  xxi,  S.  1. 

526 


JAUNDICE.  527 

in  which  no  bile  is  visible  in  the  ducts,  were  formerly  thought  to  prove 
that  jaundice  might  result  from  suppression  of  the  bile-secreting  function 
of  the  liver,  and  might  be  due  to  the  resulting  accumulation  in  the  blood, 
of  bile-pigments  formed  in  the  circulation  from  haemoglobin.  This, 
hoAvever,  is  erroneous,  for  the  presence  of  bile-pigment  in  the  liver  cells 
in  such  cases  shows  that  the  formation  of  bile  still  continues.  When 
there  is  obstmction  in  the  ducts  the  bile  passes  from  the  bile  capillaries 
or  ducts  into  the  lymphatic  vessels  of  the  liver  and  not  into  the  blood- 
vessels. This  has  been  shown  by  the  experiments  of  Saunders  *  early  in 
the  last  century  (1803),  and  later  by  Fleischl  f  (1874),  V.  Harley  J  (1892), 
and  Szubinski  §  (1899).  It  has  also  been  shown  that  jaundice  due  to 
ligature  of  the  bile-duct  may  be  removed  or  prevented  by  ligature  of  the 
thoracic  duct. 

It  was  thought  by  Frerichs,  and  quite  recently  by  Szubinski,  that  under  certain 
conditions  the  normal  mechanism  of  secretion  of  bile  by  the  hver  cells  may  be  so 
disordered  that,  instead  of  turning  sugar  into  the  blood  and  bile  into  the  bile  capil- 
laries, the  bile  is  discharged  directly  into  the  blood. 

Obstruction  to  the  flow  of"  fDile  through  the  ducts  leads  to  a  rise  in 
the  pressure  of  the  bile,  which  is  normally  low,  and,  as  a  result,  the  bile 
passes  into  the  lymphatics  and  so  into  the  general  circulation.  This 
clearly  explains  the  production  of  jaundice  in  cases  where  there  is  a  gross 
mechanical  obstruction  in  the  ducts,  but  it  is  necessary  to  consider 
further  the  method  of  causation  of  jaundice  in  those  cases  where  there  is 
no  manifest  obstruction  in  the  larger  bile-ducts. 


PATHOLOGY  OF  JAUNDICE. 

Jaundice  was  formerly  divided  into :  (i)  Hepatogenous  or  obstructiA-e, 
due  to  manifest  obstruction  in  the  larger  bile-ducts,  and  (ii)  so-cahed 
non-obstructive,  where  there  was  no  gross  obstruction  in  the  course  of 
the  bile-ducts.  This  form  included  (a)  jaundice  thought  to  be  due  to 
hsemolytic  changes  in  the  blood,  which  consisted  in  the  hberation  of 
hsemoglobin  and  its  transformation  in  the  circulation  into  bile-pigment ; 
this  was  spoken  of  as  hcematogenous  jaundice,  (h)  Jaundice  from  poly- 
cholia,  in  which  an  excessive  secretion  of  bile  was  followed  by  such  free 
absorption  of  bile  by  the  raucous  membrane  of  the  intestine  and  bile- 
passages  that  some  of  it  overflowed  into  the  general  circulation,  (c) 
Jaundice  by  suppression,  in  which  the  cells  of  the  hver  were  supposed 
to  strike  work  and  no  longer  form  bile.  As  a  result  an  accumulation  of 
bile-pigments,  manufactured  in  the  general  circulation,  was  thought  to 
occur.  As  in  the  first-mentioned  form  (hsematogenous  jaundice),  this 
explanation  was  based  on  the  erroneous  assumption  that  bile-pigments 
could  be  formed  elsewhere  in  the  body  than  in  the  liver. 

*  Saunders:  A  Treatise  on  the  Structure,  Economy,  and  Diseases  of  the  Liver, 
1803,  p.  3,  3d  ed. 

t  Fleischl:  Arbeiten  aus  d.  Anstalt  zu  Leipsig,  1874,  Jalirg.  ix,  S.  24. 
t  Harley,  V.:  Archiv  f.  Anat.  u.  Phys.,  1893,  S.  291. 
§  Szubinski:  Ziegler's  Bcitnige,  Bd.  xxvi,  S.  446,  1899. 


528  DISEASES    OF   THE    LIVER. 

"  Haematogenous  "  Jaundice. — InA'arioiis  toxic  and  infective  condi- 
tions of  the  blood  in  -^'hich  the  haemoglobin  is  hberated  from  the  red 
blood-corpuscles  jaundice  of  a  shght  degree  of  intensity  is  often  seen. 
A  good  example  of  this  "toxaemic"  jaundice  is  pro^dded  in  the  experi- 
ments of  Stadelmann*  and  Hunter  j  with  tolujdendiamin.  This  poi- 
son, when  introduced  into  the  circulation,  gives  rise  to  destruction  of 
the  red  blood-corpuscles  -^-ith  liberation  of  haemoglobin  (haemolysis)  and 
to  jaimdice.  After  its  administration  the  flow  of  bile  is  at  first  increased, 
and  there  is  an  increase  in  the  bile-pigments  poured  out  (poly chromic), 
o-^dng  to  an  augmented  amount  of  free  haemoglobin,  the  antecedent  of 
bile-pigments,  reaching  the  hver.  After  a  time  the  amount  secreted 
diminishes  and  the  bile  becomes  more  viscid,  until  finally  the  flow  of 
bile  becomes  almost  arrested.  This  sloving  and  diminution  in  the  flow 
of  bile  depend  on  inflammation  of  the  smaller  intra-hepatic  bile-ducts, 
which  become  swollen,  secrete  tliick  mucus,  and  are  in  a  condition  of 
catarrhal  cholangitis  due  to  the  toxic  effects  of  the  toluylenchamin.  The 
jaundice,  therefore,  is  really  due  to  obstruction,  which,  being  situated 
in  the  small  intra-hepatic  ducts,  is  readity  overlooked.  This  explanation 
accounts  for  the  comparatively  shght  jaundice  seen  in  septicaemia, 
pyaemia,  haemoglobinuric  fever,  pernicious  anaemia,  phosphorus  and 
other  forms  of  poisoning,  and  snake-bite.  The  jaundice  is,  therefore, 
toxaemic,  and  is  dependent  on  changes  (inflammation  and  obstruction) 
in  the  small  intra-hepatic  bile-ducts,  produced  by  poisons  in  the  general 
circulation.  It  maybe  appropriately  spoken  of  as  intra-hepatic  orhaemo- 
hepatogenous  jaundice,  but  not,  as  it  formerly  was,  as  "haematogenous" 
jaundice.  Experiment  shows  that  the  presence  of  free  haemoglobin  in 
the  blood,  though  it  leads  to  an  increased  secretion  of  bile-pigment  in  the 
bile  (polychromia),  does  not  of  itself  give  rise  to  jaundice.  In  practice 
jaundice  is  often  seen  in  cases  ^s^here  extensive  haemolysis  or  destruction 
of  red  blood-corpuscles  is  taking  place.  The  two  phenomena  are  the 
associated  but  independent  results  of  infective  or  toxic  influences  which 
destroy  the  red  blood-corpuscles,  on  the  one  hand,  and,  on  the  other 
hand,  set  up  catarrhal  inflammation  of  the  intra-hepatic  bile-ducts. 

Paroxysmal  haemoglobinuria,  though  usuaU}',  is  not  necessarily,  asso- 
ciated with  jaundice.  In  pernicious  anaemia  haemolysis  in  the  portal 
area  is  a  Tery  marked  feature,  but  the  jaimdice  is  shght  and  may  be 
practically  absent.  On  careful  microscopic  examination  of  the  hver  in 
pernicious  anaemia  catarrhal  inflammation  of  the  smaU  bile-ducts  may  be 
seen  in  some  instances. J 

The  Question  of  So-called  Jaundice  from  Polycholia.— When  jaun- 
dice was  found  to  be  associated  -^dth  bile  in  the  faeces,  it  was  supposed  that 
there  was  such  a  profuse  secretion  of  bile  (polycholia)  that  an  excessive 
amount  of  bile  was  absorbed  from  the  mucous  membrane  of  the  intestines 
and  bile-passages  and  passed  through  the  liver  into  the  general  circulation. 

*  Stadelmann:  Der  Icterus  u.  seine  verscheidenen  Formen,  Stuttgart,  1S91. 
t  Hunter,  W.:  Journ.  Path,  and  Bacteriol.,  vol.  iii,  p.  259,  1896,  and  Allbutt's 
System,  vol.  iv. 

X  Compare  Bret  and  Cade:  Lyon  Medical,  tome  xcix,  p.  461. 


JAUNDICE.  529 

Bile  maybe  present  in  the  fgeces  of  jaimcliced  patients  under  various  con- 
ditions ;  thus  in  obstruction  of  one  hepatic  duct  icterus  results,  but  the  other 
hepatic  duct  pours  bile  into  the  duodenum.  When  a  calculus  hes  in  the 
common  duct  it  may  act  Hke  a  ball-valve  and  allow  bile  to  escape  into 
the  bowel  at  intervals;  and  in  bihary  cirrhosis  bile  is  usually  present  in 
the  faeces.  In  none  of  these  examples  is  there  any  suggestion  to  the 
effect  that  an  excessive  secretion  of  bile  exists.  In  haemohepatogenous 
or  toxaemic  jaundice  there  is  in  the  early  stage  a  secretion  of  bile  rich 
in  bile-pigment  (polychroixiia)  and  poor  in  bile  acidS;  the  pigment  appear- 
ing in  the  excreta;  obstruction  in  the  small  ducts  subsequently  occurs 
and  produces  jaundice.  This  is  the  explanation  of  so-called  jaundice 
from  polycholia.  But  it  should  be  pointed  out  that,  strictly  speaking, 
there  is  not  an  excessive  secretion  of  normal  bile  (polychoha),  but  only 
of  bile-pigment  (polychromia),  and  that  the  bile  salts,  far  from  being 
increased,  are  diminished. 

The  Question  of  the  So-called  Jaundice  from  Suppression  of  the 
Bile-secreting  Function  of  the  Liver. — It  was  formerly  supposed  that 
the  hver  might,  from  nervous  or  other  influences,  cease  to  secrete  bile, 
and  that  an  accumulation  of  refuse  blood-pigment  in  the  circulation 
resulted,  which  became  changed,  without  the  intervention  of  the  liver, 
into  bile-pigment. 

Auld  *  has  recently  argued  in  favour  of  jaundice  due  to  excessive  haemolysis, 
set  up  experimentally  and  regarded  by  him  as  chiefly  occurring  in  the  spleen,  being 
independent  of  any  bile  foriuation  in  the  liver,  and,  therefore,  htematogenous. 
He  found  the  liver  cells  degenerate  and  free  from  pigment,  but  his  results  are  not 
convincing,  as  there  was  no  proof  that  the  pigment  in  the  skin  was  bile. 

There  is  no  proof  that  in  jaundice  the  hver  does  strike  work,  and, 
moreover,  inasmuch  as  experimental  research  has  shown  that  bile  is  only 
formed  in  the  liver,  jaundice  could  not  result  if  the  formation  of  bile  there 
completely  ceased.  This  last  argument,  indeed,  is  fatal  to  the  idea  of 
jaundice  from  suppression  of  the  bile-forming  function  of  the  Hver. 
In  acute  yellow  atrophy  and  phosphorus  poisoning  the  jaundice 
is  almost  certainly  due  to  obstruction  in  the  small  intra-hepatic  ducts 
from  inflammation,  and  to  the  passage  of  bile  into  the  lymphatics,  which 
results  as  a  natural  consequence.  In  long-continued  biliary  obstruction 
the  ducts  contain  clear  mucous  fluid  devoid  of  bile,  and  it  might  be,  and 
indeed  has  been,  thought  that  the  liver  ceased  to  secrete  bile  under  these 
conditions;  but  here  the  hver  cells,  as  shown  by  the  presence  of  bile- 
pigment  inside  them,  still  manufacture  bile,  which  passes  almost  directly 
into  the  lymphatic  vessels  and  so  into  the  circulation. 

"Urobilin"  Jaundice. — {Synonyms:  Hcemophoeic  Jaundice;  Acholuric 
Jaundice.) — These  terms  have  been  apphed  to  cases  where  the  skin  is 
yellow,  but  where  bile-pigment  is  not  present  in  the  urine.  It  has  been 
thought  that  staining  of  the  skin  indistinguishable  from  jaundice  may  be 
due  to  some  pigments  other  than  those  of  l)ile — either  urol)ilin  or  a  hypo- 
thetical product  of  haemoglobin  called  haemophein  (Gubler).  The  reason 
for  supposing  the  pigmentation  of  the  sldn  to  be  due  to  urobilin  was  that 

*  Auld:  Selected  Researches  in  Pathology,  1901. 
34 


530  DISEASES    OF   THE    LIVER, 

in  such  cases  the  urine  often  contained  an  excess  of  urobihn.  If  the 
blood-serum  in  such  cases,  obtained  from  a  bhster  or  from  other  sources, 
is  examined,  it  is  found  to  contain  bile-pigment  in  small  quantities  and 
not  urobihn;  hence  the  condition  is  one  of  true  jaundice,  and  the  terms 
"urobihn"  and  " hsemophceic"  jaundice  are  erroneous  and  misleading. 
Excessive  urobilinuria  may  occur  in  cases  of  toxsemic  jaundice  in  which 
bile-pigment  is  temporarily  absent  from  the  urine.  To  this  condition  the 
term  "acholuric  jaundice"  has  been  apphed  (Gilbert  and  Herscher*). 
Cases  formerly  caUed  urobilin  jaundice  are,  therefore,  mild  cases  of 
jaundice  in  which  a  sufficient  amount  of  bile-pigment  passes  into  the 
circulation  to  stain  the  skin,  but  not  enough  to  be  present  constantly  in 
the  urine.  The  excess  of  urobihn  in  the  urine  is  probably  due  to  the 
action  of  bacteria  on  bile-pigment  in  the  intestine.  Gilbert  and  Herscher, 
however,  consider  that  the  urobihn  is  manufactured  by  the  kidneys  from 
bile-pigment  present  in  the  blood-serum.  This  form  of  jaundice  is  some- 
times seen  in  portal  cirrhosis  and  in  gastritis,  and  may  be  due  to  a  slight 
secondary  infection  of  the  ducts  from  the  duodenum  (Hayemf).  On  the 
other  hand,  it  may  be  a  mild  form  of  toxsemic  jaundice.  The  condition 
is  very  closely  alhed,  according  to  Gilbert  and  Herscher,  to  simple  family 
cholsemia  (vide  p.  39),  described  by  Gilbert,  and  Lereboullet,J  and  differs 
from  it  in  the  urine  being  more  concentrated. 

Classification. — Jaundice  may  be  divided,  therefore,  into — (1)  Ex- 
tra-hepatic or  "obstructive,"  where  there  is  a  gross  obstruction,  usually 
involving  the  large,  extra-hepatic  bile-ducts,  to  the  flow  of  bile  along 
the  bile-ducts.  (2)  Toxcemic,  intra-hepatic,  or  hcemohepatogenous,  where 
there  is  obstrviction  in  the  small  intra-hepatic  bile-ducts.  The  obstruc- 
tion is  due  to  cholangitis  or  inflammation  of  the  minute  ducts,  depending 
on  the  irritating  effect  of  poisons  derived  from  the  blood  circulating 
through  the  hver. 

Jaundice  is,  therefore,  always  due  to  obstruction,  and  is  a  symptom, 
not  a  disease  in  itself.  It  may  be  the  result  of  a  purely  local  condition, 
viz.,  a  tumor  pressing  on  the  large  extra-hepatic  bile-ducts ;  or,  on  the  other 
hand,  it  may  primarily  depend  on  a  general  infective  or  toxsemic  process 
which  sets  up  angiocholitis  and  thus  obstruction  in  the  small  intrahepatic 
bile-ducts. 

TOXAEMIC,  INTRA-HEPATIC,  OR    HAEMOHEPATOGENOUS  JAUNDICE. 

This  form  of  jaundice,  where  there  is  no  gross  obstruction  to  the  flow 
of  bile  through  the  larger  bile-ducts,  is,  as  has  already  been  pointed  out, 
obstructive  and  due  to  inflammation  of  the  small  intra-hepatic  bile- 
ducts  (angiocholitis)  set  up  by  poisons  reaching  the  liver  b}'  the  blood- 
stream. Hsemohepatogenous  jaundice  is  met  with  in  a  variety  of  con- 
ditions which  may,  for  convenience,  be  divided  into  two  groups:  (i) 
A^arious  infections;  (ii)  as  the  result  of  certain  poisons  or  drugs. 

*  Gilbert  and  Herscher:  La  Presse  Medicale,  Dec.  27,  1902,  p.  1239. 
t  Hayem:  Soc.  Med.  des  Hop.,  Mav  14,  1897. 

J  Gilbert  and  Lereboullet:  Gaz.  Hebdom.  de  Med.  et  de  Chirurg.,  Sept.  21, 
1902,  p.  889. 


JAUNDICE.  531 

(i)  It  may  occur  in  a  number  of  diseases,  especially  hsemic  infections, 
such  as  pyaemia,  septicaemia,  relapsing  fever,  haemoglobinuric  fever,  and 
may  be  seen  in  pneumonia,  typhoid  fever,  pernicious  anaemia.  In  some 
instances,  as  mentioned  above,  jaundice  may  occur  in  association  with 
haemolysis,  for  example,  in  paroxysmal  haemogiobinuria;  the  jaundice, 
however,  is  not  a  necessary  result  of  haemolysis,  but  a  concomitant  effect 
of  a  common  toxic  or  infective  cause.  In  the  diseases  enumerated  above 
jaundice  is  an  incidental,  and  in  most  instances  not  a  constant,  symptom 
of  a  well-recognised  disease,  but  in  some  instances,  as  Weil's  disease  (or 
infectious  jaundice)  and  acute  yellow  atrophy,  it  is  one  of  the  most 
characteristic,  if  not  the  most  essential,  of  the  clinical  features. 

(ii)  Some  of  the  poisons  which  give  rise  to  toxaemic  jaundice  have 
been  already  referred  to,  such  as  toluylendiamin,  phosphorus,  snake-bite. 
In  addition,  jaundice  occasionally  follows  large  doses  of  chloroform, 
chloral,  antifebrin  (acetanilide)  (P.  K.  Brown  *),  santonin,  Fihx  mas, 
poisoning  by  arseniuretted  hydrogen,  anilin,  mushrooms,  and  even  in  fatal 
cases  of  sulphate  of  copper  poisoning. 

General  Characters  and  Distinctions  from  Obstructive  Jaundice. 
— Haemohepatogenous  or  toxaemic  jaundice  is  essentially  a  sign  of  some 
underlying  infection  or  intoxication,  and  is  usually  subordinate  to  the 
constitutional  symptoms.  The  patient  suffers  comparatively  Uttle  from 
the  presence  of  bile  in  the  general  circulation,  but  is  definitely  and  often 
severely  ill  from  the  primary  disease  or  intoxication.  The  jaundice  is, 
as  a  rule,  slight,  though  in  acute  yellow  atrophy  and  icterus  gravis  it 
is  bright  yellow,  and  the  dark-green  tint  of  chronic  obstructive  jaundice 
does  not  occur.  There  may  be  manifest  signs  of  toxaemia;  as  shown  by 
cutaneous,  nasal,  gingival,  and  gastro-intestinal  haemorrhages,  and  by 
nervous  symptoms.  The  urine  contains  less  bilirubin  than  in  obstructive 
jaundice,  but,  owing  to  the  fact  that  bile  reaches  the  intestine  and  is 
there  exposed  to  putrefactive  and  fermentative  changes,  urobiHn  is 
formed,  absorbed,  and  excreted  into  the  urine.  In  obstructive  jaundice, 
where  bile  is  excluded  from  the  bowel,  there  is  no  urobilinuria.  In  both 
toxaemic  and  obstructive  jaundice  bile  acids  are  present  in  the  urine  for 
the  first  few  days,  but  not  after  this ;  the  amount  of  the  bile  acids  found 
in  the  urine  during  these  early  days  is  rather  less  in  toxaemic  than  in 
obstructive  icterus.  It  may  be  pointed  out  that  little  importance  can 
be  attached  to  results  obtained  by  Pettenkoffer's  well-known  test,  since, 
as  employed  in  ordinary  clinical  practice,  it  is  quite  unreliable.!  As  the 
result  of  the  general  haemic  infection  or  intoxication  there  are  often 
changes  in  the  renal  epithelium  leading  to  albuminuria. 

The  faeces  contain  bile-pigments,  sometimes  even  in  excess;  this  is 
due  to  increased  secretion  of  bile-pigments  (polychromia)  as  a  result 
of  the  toxaemia  augmenting  the  supply  of  haemoglobin  to  the  liver  cells. 
The  motions  in  toxaemic  jaundice  thus,  differ  markedly  from  the  clay- 

*  P.  K.  Brown:  American  Journ,  Med.  Sciences,  vol.  cxxii,  1901,  p.  770. 
t  Hay's  sulphur  test  or  O.K. F.  Griinbaum's  method  of  estimating  bile  salts 
sliould  be  eni])I()yetl. 


532  DISEASES   OF  THE   LIVER. 

coloured  dejecta  of  cases  where,  from  complete  obstruction  of  the  ducts, 
bile  is  excluded  from  the  intestines. 

The  course  of  the  disease  is  more  acute,  as  a  nde,  than  in  obstructive 
icterus,  and  is  not  accompanied  by  the  itching  of  the  skin,  xanthopsia 
or  yellow  vision,  and  slow  pulse  which  may  accompany  obstructive 
jaundice.  Signs  of  constitutional  disturbance,  such  as  enlarged  spleen, 
fever,  and  albuminuria,  are  common,  while  grave  symptoms  develop 
sooner  and  more  frequently  than  in  obstructive  jaundice,  where  they  only 
occur  late  or  at  the  termination  of  long-continued  jaundice.  In  severe 
cases  of  hsemohepatogenous  jaundice  the  "typhoid  state,"  with  dry- 
tongue,  dehrium,  coma,  and  multiple  haemorrhages,  may  rapidly  develop. 
The  important  features,  therefore,  are  the  slight  degree  of  jaundice  and 
the  presence  of  marked  constitutional  symptoms,  the  want  of  proportion 
between  the  icterus  and  the  symptoms,  and  the  evidence  of  hsemic 
infection  or  intoxication. 


OBSTRUCTIVE  JAUNDICE. 

Signs. — Jaundice  appears  first  in  the  conjunctiva,  then  successively 
on  the  face,  neck,  body,  and  extremities.  The  ''whites"  of  the  eyes  are 
the  first  part  to  show  the  bile-pigment,  but  bile-pigment  appears  in  the 
urine  a  day  or  two  before  there  is  any  manifest  jaundice.  The  masses  of 
fat  (Pingueculae)  often  seen  under  the  conjunctiva  frequently  have  a 
slightly  yellow  colour  and  may  mislead  a  careless  observer  into  the  belief 
that  jaundice  is  present.  A  shght  degree  of  icterus  is  more  readily  de- 
tected in  a  fair-skinned  patient  than  in  one  of  a  dark  complexion,  in 
whom  the  skin  is  often  somewhat  sallow.  It  should  also  be  remembered 
that  jaundice  is  easily  overlooked  in  artificial  light.  The  mucous  mem- 
brane of  the  lips  and  palate  shows  an  icteric  tint,  if  looked  for,  which 
appears  almost  as  soon  as  in  the  conjunctiva.  When  jaundice  has 
existed  for  a  long  time,  the  bile-pigment  in  the  skin  turns  of  a  dark-green 
colour  (bihverdin),  and  so  alters  the  skin  that  the  condition  is  often 
spoken  of  as  "black  jaundice."  After  recovery  from  severe  jaundice  the 
skin  is  often  left  discoloured  for  a  very  considerable  period. 

In  chronic  jaundice,  usually  of  some  years'  duration,  the  skin  occa- 
sionally shows  multiple  xanthelasma.  The  relation  between  chronic 
icterus  and  this  rare  skin  disease  is  not  known.  Xanthelasma  may 
occur  in  the  absence  of  jaundice,  and  it  is,  of  course,  in  only  a  small 
percentage  of  the  cases  of  chronic  jaundice  that  xanthelasma  develops. 
In  chronic  jaundice  there  is  a  tendency  to  the  formation  of  stigmata,  or 
spider  angiomata,  on  the  skin  of  the  face  and  elsewhere.  "V^^len,  as  the 
result  of  complete  biliary  obstruction  or  from  other  causes,  the  protective 
function  of  the  liver  fails,  and  toxines,  manufactured  in  the  alimentary 
canal,  pass  into  the  circulation  and  give  rise  to  cholremia  or  biliary 
toxaemia,  haemorrhages  may  take  place  into  the  skin  and  nmcous  mem- 
branes, giving  rise  to  epistaxis,  melaena,  etc. 

The  urine  is  acid  in  reaction,  and  is  somewhat  diminished  in  amount. 
It  becomes  bile  stained  with  bihrubin  before  the  conjunctivae  or  the  skin 


JAUNDICE.  533 

show  the  icteric  tint.  As  mucli  as  twenty-four  hours  may  elapse  between 
the  appearance  of  bile  in  the  urine  and  in  the  conjunctiva.  The  colour 
of  the  urine  varies  in  different  cases  and  at  different  times  from  an  intense 
yellow,  to  brown,  olive,  or  a  very  dark  brown.  When  shaken  up,  the 
froth  becomes  yellow.  The  colour  must  be  distinguished  from  that  in 
urobihnuria,  hsematuria,  melanuria,  and  the  alterations  due  to  rhubarb, 
chrysophanic  acid,  senna,  and  santonin,  by  Gmehn's  test  for  bile-pigment. 

Occasionally,  especially  in  convalescence  from  obstructive  jaundice, 
the  urine  contains  no  bilirubin,  although  the  skin  is  still  jaundiced. 
When  bile  is  completely  excluded  from  the  bowel,  there  is  no  urobilin 
in  the  urine;  but  when  the  obstruction  is  incomplete  and  allows  some 
bile  to  escape  into  the  duodenum,  urobihnuria  may  appear.  This  depends 
on  the  fact  that  urobihn  is  manufactured  from  bihrubin  in  the  intestine 
as  the  outcome  of  microbic  activity.  Bile  salts  are  present  in  the  urine 
for  the  first  few  days  of  jaundice,  but  then  disappear;  the  same  holds 
good  in  toxsemic  jaundice;  but  the  quantity  of  bile  salts  in  the  urine 
is  larger  in  obstructive  than  in  toxsemic  jaundice.  The  disappearance 
of  bile  salts  from  the  urine  probably  depends  on  a  diminished  production 
of  bile  acids  in  all  forms  of  icterus. 

As  a  result  of  the  bacterial  decomposition  of  proteids  (putrefaction) 
in  the  alimentary  tract  the  ethereal  sulphates  in  the  urine  are  increased 
and  a  considerable  amount  of  indican  may  be  found.  It  must,  however, 
be  remembered  that  drugs  like  creasote  and  salol,  which  are  frequently 
given  to  control  flatulence,  are  themselves  capable  of  increasing  the 
amount  of  ethereal  sulphates  present  in  the  urine.* 

When,  in  the  late  stages  of  obstructive  jaundice,  a  marked  toxsemic 
condition — cholsemia — has  supervened,  the  renal  epithehum  may  suffer 
and  albuminuria  may  occur.  Casts,  if  carefully  looked  for,  are  almost 
always  present;  they  depend  on  the  jaundice,  and  are  not  necessarily 
accompanied  by  albuminuria. 

Experimental  ligature  of  the  bile-duct  has  been  found  to  give  rise  to  casts  in 
the  urine  without  albuminuria.     (WaUerstein.f) 

The  Fceces. — ^There  is  usually  constipation,  and  the  motions  are  often 
extremely  offensive.  In  the  absence  of  bile  the  fseces  are  pale  and  are 
devoid  of  urobilin;  the  ''clay-coloured"  appearance  is  partly  due  to  the 
absence  of  these  pigments  and  partly  to  an  excess  of  finely  divided  fat 
and  bubbles  of  gas.  The  presence  of  fat  in  excess  probably  interferes 
with  absorption  of  proteids  and  favours  fermentation.  It  has  been 
estimated  by  Miiller  |  that  when  bile  is  excluded  from  the  bowel  the 
undigested  fat  may  rise  from  7  to  10  per  cent.,  which  is  the  normal,  to 
55  or  78.5  per  cent.  In  exceptional  cases,  when  obstruction  is  not  com- 
plete, bile  enters  the  bowel  and  the  fseces  are  of  a  fairly  normal  colour 
and  contain  urobihn.  This  may  occur  when  one  of  the  two  hepatic  ducts 
is  obstructed,  or  when  a  "floating"  gall-stone  in  the  common  duct  allows 
some  bile  to  escape  into  the  duodenum. 

*  Vide  Herter:  Lectures  on  Chemical  Pathology,  p.  205. 
fWallerstein:  Berlin,  klin.  Wochen.,  Bd.  xxxix,  S.  310,  1902. 
+  Muller:  Zeitschrift  f.  klin.  Med.,  Bd.  xii,  1889. 


534  DISEASES    OF  THE   LIVER. 

Conditions  of  the  Other  Secretions. — ^There  has  been  a  good  deal  of 
discussion  and  discrepancy  of  opinion  about  the  condition  of  the  various 
secretions  in  jaundice.  The  majority  of  the  secretions,  such  as  the  sahva, 
the  mucus  of  the  mouth  and  alimentary  canal,  are  not  bile-stained. 
The  perspiration  is  usually  free  from  bile,  but  not  uncommonly  bile  is 
present  in  the  secretions  of  the  axilla.  Tears  and  women's  milk  are  more 
often  free  from  bile  than  jaundiced.  Although  the  bile-pigments  do  not 
appear  in  the  sahva,  the  sahvary  glands  themselves,  like  other  organs, 
are  deeply  bile-stained.  In  inflammatory  conditions  the  pathological 
secretions  and  exudations  become  icteric,  as  shown  by  pneumonic  sputum, 
pleural  and  peritoneal  effusions,  and  saliva  in  mercurial  salivation. 

Circulatory  System. — In  the  absence  of  pain  and  fever  the  pulse  tends 
to  be  slow.  This  is  generally  true,  but  some  observers  have  doubted 
whether  it  is  a  universal  rule:  thus  Mackenzie*  has  never  met  with  a 
slow  pulse  in  jaundice.  It  is  especially  in  catarrhal  and  recent  jaundice 
that  slowing  of  the  heart's  beat  is  most  marked.  In  this  connexion  it 
is  interesting  to  note  that  it  has  been  ascribed  to  the  inhibitory  action 
of  bile  salts  on  the  cardiac  ganglia;  for  bile  acids  pass  into  the  blood  in 
the  early  stage  of  jaundice,  but  are  produced  in  very  small  quantities 
when  jaundice  is  estabhshed.  The  pulse  is  frequently  observed  to  vary 
very  considerably  with  position;  sitting  up  may  increase  the  pulse-rate 
by  twenty  beats.  The  arterial  blood  pressure  is  low.  From  muscular 
incompetence  a  mitral  systohc  murmur  may  become  audible,  and  from 
increased  pressure  in  the  pulmonary  circulation  due  to  this  cause,  or 
possibly  to  reflex  constriction  of  the  pulmonary  vessels  referred  from 
the  bile-ducts,  the  second  sound  over  the  pulmonary  artery  becomes 
accentuated. 

The  blood-serum  is  stained  of  a  greenish-yellow  tint.  The  specific 
gravity  of  the  blood  as  a  whole  is  increased,  but  that  of  the  serum  is 
unaffected.  The  coagulation  time  is  prolonged,  a  fact  of  importance 
in  conjunction  with  the  great  tendency  to  haemorrhage  in  marked  jaun- 
dice. The  blood  may  take  fifteen  to  twenty  minutes  to  coagulate 
instead  of  the  normal  four  minutes.  (Osler.t)  In  severe  cases  the 
alkalinity  of  the  blood  has  been  found  to  be  diminished. 

There  is  very  little  anaemia  except  in  severe  cases;  this  is  rather 
curious,  inasmuch  as  considerable  haemolysis  from  the  action  of  the  bile 
acids  inight  natural^  have  been  expected.  This  absence  of  haemolysis 
in  jaundice  is  explained  by  the  hypothesis  that  in  jaundice  the  manu- 
facture of  bile  acids  is  inhibited.  In  cases  of  advanced  obstructive 
jaundice  with  cholaemia  granular  degeneration  of  the  red  blood-corpuscles 
is  a  prominent  feature.  In  cholaeiriia  there  is  usually  leucocytosis.  In 
jaundice  of  no  great  intensity  and  without  grave  toxaemic  symptoms 
leucocytosis  does  not  occur  unless  there  is  some  other  responsible  cause, 
such  as  inflammation  or  suppuration. 

A.  S.  Griinbaum,f  in  1896,  pointed  out  that  the  undiluted  blood- 

*  Mackenzie,  J.:  The  Study  of  the  Pulse,  p.  134,  1902. 

t  Osier,  W.:  Johns  Hopkins  Hosp.  Bull.,  vol.  xii,  p.  264,  1901. 

X  Griinbaum,  A.  S.:  Lancet,  1896,  vol.  ii,  p.  806. 


JAUNDICE.  535 

senim  of  jaundiced  patients  in  manj^  cases  agglutinated  typhoid  bacilli, 
but  that  when  diluted,  the  falhng-off  in  the  agglutinative  power  of  the 
serum  was  out  of  all  proportion  to  the  dilution.  Eckardt  *  has  recently 
drawn  attention  to  this  subject.  Dr.  Harold  Spitta  has  kindly  given 
me  some  unpubhshed  observations  on  the  relative  agglutinative  proper- 
ties of  icteric  sera  on  the  colon,  Gaertner,  and  typhoid  bacilli.  In  ten 
cases,  eight  of  which  were  catarrhal  jaundice,  Gaertner's  bacillus  was  not 
agglutinated  in  any;  there  was  shght  clumping  of  BaciUus  typhosus, 
dilution  1  :  10,  in  two  cases,  no  clumping  in  dilution  1  :  100.  Nine 
cases  agglutinated  Bacillus  coH  in  dilution  of  1  :  10,  and  six  cases  in  dilu- 
tion of  1  :  100. 

The  respiration  is  usually  normal,  but  the  rate  may  be  slowed.  The 
temperature,  like  the  functions  of  the  body  generally,  is  depressed.  This 
is  probably  due  to  the  action  of  toxines  on  the  tissues  and  also  to  the 
diminished  intake  of  food  and  assimilation.  Fever,  when  present,  is 
either  due  to  the  same  cause  that  is  responsible  for  the  jaundice,  as 
hepatic  abscess,  gumma,  or  cirrhosis,  or  is  the  result  of  some  complica- 
tion, such  as  cholangitis  in  gall-stone  obstruction. 

The  liver  is  often  enlarged  from  damming-up  of  the  bile,  and  may  be 
tender.  In  mahgnant  disease  and  in  cirrhosis  its  surface  may  be  knobby 
or  irregular. 

Enlargement  of  the  gall-bladder  is  a  valuable  sign  of  obstruction  of 
the  common  duct.  When  chronic  jaundice  is  due  to  gall-stones,  the 
gall-bladder  is  collapsed  from  previous  cholecystitis,  while  in  cases  of 
malignant  disease  pressing  on  the  cormnon  bile-duct  the  gall-bladder 
may  form  a  tense,  pear-shaped  tumor.  If  a  calculus  be  impacted  in  the 
cystic  duct,  the  gall-bladder  may  be  distended  with  mucus,  and  occa- 
sionally is  enlarged  from  the  presence  of  numerous  calculi;  there  are 
exceptions  to  the  general  rule  enunciated  by  Courvoisier  that  in  jaundice 
due  to  gaU-stones  the  gall-bladder  is  collapsed,  while  in  jaundice  due  to 
malignant  disease  it  is  dilated. 

The  spleen  is  usually  not  enlarged,  but  if  it  is,  it  points  to  biliary 
cirrhosis,  some  septic  or  toxic  process,  such  as  Weil's  disease  or  infective 
jaundice,  to  syphilis,  or  to  that  extremely  rare  condition,  alveolar  hydatid. 

Symptoms.— Apart  from  the  independent  effects  of  underlying  dis- 
eases the  symptoms  accompanying  jaundice  are  due  partly  to  the  presence 
of  bile  in  the  circulation,  which  acts  as  a  depressing  poison,  partly  to  a 
secondary  toxaemia  produced  by  the  failure  of  the  hver  to  perform  its 
important  protective  function  of  stopping  poisons  brought  to  it  from  the 
ahmentary  canal,  and  partly  to  the  absence  of  bile  from  the  ahmentary 
canal.  These  distinctions  in  the  causation  of  the  symptoms  must  not 
be  pressed  too  far,  but  it  will  be  convenient  to  consider  the  symptoms 
under  the  following  heads: 

Symptoms  Due  to  Bile  in  the  Circulation. — ^The  normal  constituents  of 
bile,  the  bile  salts,  the  bile-pigments,  and  the  cholesterin,  must  be  con- 
sidered from  the  point  of  view  of  their  toxic  action  on  the  tissues  of  the 
body. 

*  Eckardt:  Miinchen.  med.  Wochen.,  Bd.  xlix,  S.  1129. 


536  DISEASES   OF  THE   LIVER. 

The  bile-salts  exert  a  well-marked  li8emol3i;ic  action  on  red  blood- 
corpuscles  outside  the  body,  but  it  is  plain  that  bile  acids  are  not  present 
in  the  blood  in  sufficient  amounts  in  jaundice  to  produce  haemolysis. 
If  hsemolysis  due  to  this  cause  occurred,  there  should  be  marked  anaemia 
and  escape  of  blood-pigment  in  the  urine  in  cases  of  obstructive  jaundice. 
Neither  of  these  events  occurs.  Anaemia  may  be  associated  "uith  jaundice, 
but  is  not  specially  related  to  it.  Haemoglobinuria  does  not  occur  in 
obstructive  jaundice;  it  is  seen  in  some  cases  of  toxaemic  jaundice,  such 
as  haemoglobinuric  fever,  and  experimentally  in  toluylendiamin  poison- 
ing, but  here  the  haemolysis  precedes  the  development  of  jaundice,  and, 
hke  it,  is  due  to  the  action  of  a  poison.  The  absence  of  anaemia  and 
haemoglobinuria  in  obstructive  jaundice  and  the  fact  that  bile  salts  are 
only  found  in  the  urine  during  the  first  few  days  of  jaundice  show  that 
the  production  of  bile  salts  by  the  Uver  cells  is  inliibited  during  the 
existence  of  jaundice.  The  toxic  effects  of  the  bile  salts  are  shght  com- 
pared with  what  might  naturally  have  been  expected.  The  symptoms 
referable  to  the  action  of  the  bile  salts  are  slowing  of  the  pulse  and  dila- 
tation of  the  peripheral  vessels.  The  headache  and  mental  depression 
may  in  part  be  due  to  a  similar  toxic  effect  on  the  brain. 

Bihrubin  was  thought  by  Bouchard  to  be  ten  times  more  toxic  than 
bile  salts,  and  the  comparative  inmiunity  from  severe  symptoms  in 
ordinar}^  jaundice  was  explained  by  the  consideration  that  much  of  this 
pigment  was  fixed  in  the  skin  and  other  jaundiced  tissues.  It  appears, 
however,  that  bihrubin  is  a  comparatively  feeble  poison;  the  subjective 
symptoms  which  have  been  referred  to  it  are  xanthopsia  and  pruritus. 

Yellow  vision,  or  xanthopsia,  has  been  explained  as  the  result  of  the 
retina  and  media  having  become  so  infiltrated  "^"ith  bihrubin  that  the 
blue  and  %'iolet  raj's  are  absorbed.  As  a  result,  the  patient  suffers  from 
blue  bhndness.  There  is  a  want  of  relationship  between  the  degree  of 
jaundice  and  yellow  vision;  it  may  be  absent  in  advanced  icterus  and 
present  when  it  is  but  shghtly  marked.  Yellow  A-ision  is  seldom  a  suffi- 
cient source  of  amioyance  to  lead  to  a  definite  complaint  on  the  patient's 
part,  but  on  enquir}^  it  is  not  infrequently  found.  It  is.  therefore,  not 
an  important  or  prominent  symptom.  The  yellow  vision  which  follows 
the  administration  of  santonin  is  more  noticeable. 

Pruritus,  or  itching  of  the  skin  -without  any  local  lesion,  may  be  due 
to  the  irritating  action  of  the  bile  on  the  sensory  endings  of  the  nen-es 
in  the  skin;  on  the  other  hand,  it  may  appear  before  jaundice  has  begim 
to  show  itself;  possibly  it  is  then  the  first  effect  of  an  altered  blood 
condition.  In  a  case  of  HaA-iUand  HaU's  *  of  carcinoma  of  the  ampulla 
of  Vater,  itching  of  the  skin  came  on  a  week  before  jaundice  was  detected. 
Such  cases  raise  a  doubt  whether,  after  aU,  the  itcliing  is  due  entirely  to 
the  presence  of  bihrubin;  it  is  possible  that  other  concomitant  poisons 
may  give  rise  to  it,  or  that  the  dr}-,  iU-nourished  condition  of  the  skin 
is  the  cause.  The  itcliing  is  usually  associated  "U'ith  well-developed 
jaundice.  The  irritation  msiy  be  excessive  and  prevent  sleep ;  the  scratch- 
ing may  induce  traumatic  eczema.  Urticaria  and  Hchen  are  sometimes 
*  Havilland  HaU:  Lancet,  1902,  vol.  i,  p.  1102. 


JAUNDICE.  537 

seen  on  a  jaundiced  skin.  Urticaria  has  a  very  curious  appearance,  the 
bile-stained  exudation  making  the  bullae  look  much  more  jaundiced  than 
the  surrounding  skin. 

Cholesterin  was  thought  by  Flint  *  to  be  the  cause  of  the  grave  nerv-ous 
symptoms  occurring  late  in  the  course  of  obstructive  jaundice,  and  the 
term  cholesteraemia  was  employed  in  the  sense  that  cholsemia  often 
is  now.  There  is  no  satisfactory  evidence  that  cholesterin  exerts  a 
toxic  action  on  the  body.  It  is  true  that  experimental  injection  of  cho- 
lesterin into  the  body  has  been  followed  by  bad  results.  But  these  were 
probably  either  mechanical  and  due  to  obstruction  of  small  blood-vessels, 
or,  according  to  Herter,t  caused  by  the  glycerin  in  which  the  cholesterin 
was  suspended. 

Symptoins  Due  to  the  Presence  of  Poisons  Other  than  Bile  in  the  Circu- 
lation.— Owing  to  the  failure  of  the  liver  to  stop  poisons  received  from 
the  alimentary  canal,  a.uto-intoxication  results,  and  if  the  kidneys  do  not 
compensate  for  this  by  free  diuresis,  a  toxsemic  condition,  analogous  to 
that  of  uraemia,  results.  The  increased  fermentation  and  putrefactive 
changes  consequent  on  the  exclusion  of  bile  from  the  bowel  render  the 
process  of  auto-intoxication  one  of  considerable  importance.  In  a  minor 
degree  mental  depression,  incapacity  for  continued  mental  effort,  drowsi- 
ness, headache,  and  general  debility  are  the  results  of  this  hepatic  toxse- 
irda,  while  in  more  marked  degrees  there  may  be  dehrium,  somnolence, 
and  coma.  A  bitter  taste  in  the  mouth  is  often  complained  of,  although 
the  saliva  does  not  contain  bile-pigment;  this  bitter  flavour  may  depend 
on  the  presence  of  toxic  bodies,  which,  owing  to  hepatic  insufficiency, 
have  escaped  into  the  general  circulation  and  passed  into  the  saliva. 
There  is  often  considerable  impairment  of  appetite,  with  a  special  distaste 
for  fatty  food. 

The  tendency  to  haemorrhage  in  chronic  obstructive  jaundice  is  a 
noticeable  fact,  and  one  of  great  importance  when  any  surgical  operation 
has  to  be  performed,  inasmuch  as  fatal  haemorrhage  may  result.  Haemor- 
rhages into  the  skin  are  common,  while  epistaxis  is  sometimes  a  cause 
of  great  anxiety.  The  frequent  oozing  from  the  gums  is  accompanied 
by  an  offensive  character  of  the  breath.  The  coagulation  time  of  the 
blood  in  chronic  jaundice  shows  marked  retardation;  instead  of  coagu- 
lating in  four  minutes  it  may  take  fifteen  or  twenty  minutes  (Osier  J). 
This  blood  change  may  be  due  to  hepatic  insufficiency ;  it  may  reasonably 
be  supposed  that  the  liver  fails  to  stop  poisons  and  bodies  alHed  to  pep- 
tones absorbed  from  the  alimentary  canal.  The  poisons  would  damage 
the  walls  of  the  blood-vessels,  while  the  peptone-like  bodies  would  inter- 
fere with  the  coagulation  of  the  blood.  It  has,  however,  been  suggested 
by  Mayo  Robson  ^  that  the  haemorrhagic  tendency  is  pancreatic  in 
origin,  and  that  it  may  depend  on  a  diminution  of  lime  salts  in  the  blood 
due  to  a  profuse  excretion  of  lime  salts  in  the  urine  in  pancreatitis. 

*  Austin  Flint,  Jr.:  American  Journ.  Med.  Sciences,  Oct.,  1862,  p.  305. 
t  Herter:  Lectures  on  Chemical  Pathology,  p.  331. 
i  Osier,  W.:  Johns  Hopkins  Hosp.  Bull.,  vol.  xii,  p.  264,  Aug.,  1901. 
§Mayo  Robson:  Brit.  Med.  Jour.,  1901,  vol.  i,  p.  1131,  and  Lancet,  March  19, 
1904. 


538  DISEASES    OF   THE    LIVER. 

The  absorption  into  the  blood  of  glycerin  from  associated  fat  necrosis  is 
a  possible  cause  of  haemorrhage,  especially  for  local  extravasation  of 
blood  in. the  neighbourhood  of  the  pancreas.  In  two  cases  the  blood 
plates  were  greatly  diminished.     (Cammidge.*) 

Symptoms  Due  to  the  Absence  of  Bile  from  the  Intestinal  Tract. — Con- 
stipation is  very  common,  and  is  usually  explained  as  due  to  the  absence 
of  the  natural  purgative,  bile.  Excessive  fermentation  leading  to  flatu- 
lence and  extremely  offensive  motions  is  very  common.  The  excessive 
decomposition  in  the  bowel  may  account  for  transient  attacks  of  diarrhoea. 
It  is  probable  that  absorption  of  the  poisonous  bodies  produced  in  the 
intestine  lead  to  headache,  mental  depression,  and  other  symptoms. 
The  interference  with  the  absorption  of  fat  is  an  important  factor  and 
leads  to  considerable  loss  of  weight.  The  finely  diffused  fat  probably 
favours  fermentative  changes  in  the  bowel  in  addition  to  interfering  with 
absorption  of  the  other  food  elements. 


DIAGNOSIS  OF  JAUNDICE. 

As  has  already  been  pointed  out,  jaundice  may  be  overlooked  alto- 
gether if  the  patient  is  seen  only  by  yellow  artificial  fight,  such  as  gas 
or  candle  illumination.  No  serious  difficulty  should  arise  in  distinguish- 
ing jaundice  from  other  pigmentary  changes  in  the  skin.  The  yeUow 
colour  of  patients  with  slight  icterus  is  hardly  likely  to  be  confused  with 
the  bronzing  of  sunburn,  with  the  natural  hue  of  the  yeUow-skinned 
races  of  mankind,  or  with  the  tint  of  the  skin  in  the  advanced  cachexia 
of  mafignant  disease;  but  should  any  question  arise,  examination  of 
the  conjunctivse  and  of  the  urine,  or  of  blood-serum  obtained  from  a 
blister,  for  the  presence  of  bile-pigment  will  quickly  settle  the  matter. 
The  dark-green  colour  of  the  skin  in  ''black"  jaundice  of  long-continued 
biliary  obstruction  might  conceivably  be  confused  with  the  pigmentation 
of  the  skin  in  Addison's  disease,  hsemochromatosis,  malarial  melanaemia, 
argyria,  etc.,  but  here  again  examination  of  the  conjunctivse,  urine,  and 
blood-serum  will  prevent  error. 

The  past  effects  of  severe  jaundice  may  give  rise  to  some  difficulty, 
but  further  investigation  and  the  history  of  the  case  should  make  matters 
clear. 

In  a  case  reported  by  Cavafy  f  a  man  aged  twenty-nine,  who  had  had  syphiHs, 
had  abnormal  pigmentation  and  itching  of  the  skin  left  behind  by  jaundice  eight 
years  previously.  A  committee  of  the  Pathological  Society  were  appointed  to 
consider  the  case  and  reported  that  it  was  leucoderma. 

Feigned  Jaundice. — The  skin  may  be  coloured  yellow  by  malingerers 
in  order  to  escape  active  work  or  punishment ;  saffron  and  turmeric  may 
be  emplo5^ed  for  this  purpose. {  The  fraud  should  be  readily  detected  by 
the  absence  of  any  bile-pigment  in  the  conjunctivse  and  urine.  If  an 
attempt  is  made  to  darken  the  urine  by  taking  rhubarb   or  santonin, 

*  Cammidge,  P.  J. :  Quoted  by  Mayo  Robson. 

t  Cavafy,  J.:  Trans.  Path.  Soc,  vol.  xxxii,  p.  25S. 

X  Wickham  Legg:  Jaundice,  etc.,  p.  375. 


JAUNDICE.  539 

Gmelin's  reaction  with  nitric  acid  is  absent,  and  the  addition  of  alkahs 
turns  the  urine  red  instead  of  brown. 


DIFFERENTIAL  DIAGNOSIS  OF    JAUNDICE  DUE  TO  VARIOUS  CAUSES. 

Since  the  distinction  between  obstructi\'e  jaundice  and  toxseniic 
(or  hsemohepatogenous)  jaundice  has  already  been  considered  (p.  531), 
it  is  now  only  necessary  to  refer  to  the  differential  diagnosis  and  the 
various  causes  of  obstructive  jaundice.  The  causes  of  obstructive  jaun- 
dice are  very  numerous,  but  for  convenience  they  may  be  grouped  into 
three  classes: 

(1)  Where  the  obstruction  is  inside  the  lumen  of  the  bile-ducts,  such 
as  a  gall-stone  or  parasites.  (2)  Where  the  obstruction  depends  on 
changes  originating  in  the  walls  of  the  larger  bile-ducts,  e.  g.,  catarrhal 
cholangitis.  (3)  Where  obstruction  is  produced  by  processes  arising 
outside  the  larger  ducts.  Thus  tumors  or  adhesions  may  mechanically 
compress  the  ducts.  Malignant  tumors  may  either  merely  compress  or 
may  actually  invade  the  ducts;  the  former  is  more  frequent. 

I.  Jaundice  Due  to  Obstruction  Inside  the  Lumen  of  the  Duct. — 
These  causes  of  obstructive  jaundice  are  considered  elsewhere,  (a)  Gall- 
stones are  described  on  page  703.  It  is  possible  that  inspissated  mucus 
may  obstruct  the  ducts,  but  the  cause  of  the  excessive  amount  of  mucus 
is  inflammation  of  the  ducts  and  gall-bladder  and  need  not  be  separately 
described  here.  Inflammation  of  the  minute  intra-hepatic  ducts  occurs 
in  toxsemic  jaundice,  in  biliary  cirrhosis  (p.  306),  and  possibly  in  simple 
family  cholsemia  (vide  p.  39). 

(fe)  Parasites  may  gain  access  to  the  ducts  and  mechanically  occlude 
the  lumen.  A  hydatid  cyst  may  discharge  into  the  ducts,  and,  as  a  result, 
pieces  of  membrane  or  daughter  cysts  may  block  the  ducts  and  give  rise' 
to  biliary  colic,  jaundice,  and  often  to  infective  cholangitis.  The  diag- 
nosis depends  on  the  history  that  the  patient  has  either  had  a  cyst  which 
has  disappeared,  or  that  an  existing  one  has  grown  smaller  about  the 
time  that  the  symptoms  appeared;  or,  still  better,  on  the  presence  of 
bile-stained  pieces  of  hydatid  membrane  in  the  fseces  or  possibl}'  even 
in  the  vomit.     The  subject  is  considered  more  at  length  on  page  415. 

Round-worms  (Ascaris  lumbricoides)  may  enter  the  common  bile- 
ducts  from  the  duodenum  and  give  rise  to  jaundice.  Of  this  rare  con- 
dition Mertens  *  has  collected  48  examples.  Distomum  hepaticum,  the 
liver  fluke  so  fatal  to  sheep,  has  been  found  in  the  ducts  of  the  human 
liver,  as  have,  in  rare  instances,  Distomum  sinense  and  Distomum  con- 
junctivum.  In  these  cases  the  diagnosis  depends  on  the  recognition  of 
the  worms  or  their  ova  in  the  faeces.  Reference  is  made  to  this  subject 
in  the  section  on  Parasitic  Affections  of  the  Bile-ducts  (p.  677). 

(c)  As  pathological  curiosities  some  authors  have  referred  to  the 
presence  of  foreign  bodies,  such  as  fruit-seeds,  small  cherry-stones,  and 
needles,  in  the  bile-ducts  (Graham  f),  l)ut  suspicion  as  to  the  nature  of 

*  Mertens:  Deutsch.  med.  Wochcn.,  Bd.  xxiv,  S.  358,  1S9S. 

t  Graham,  J.  E.:  Loomis  and  Thompson's  System  of  Medicine,  vol.  iii,  p.  428. 


540  DISEASES   OF  THE   LIVER. 

such  foreign  bodies  must  always  arise  unless  the  absence  of  the  constitu- 
ents of  gall-stones  has  been  definitely  proved. 

(d)  In  most  exceptional  instances  new  growth  may  extend  along  the 
lumen  of  the  common  bile-duct  and  occlude  it  without  necessarily  in- 
vading the  walls  of  the  duct  except  at  the  point  where  it  originates  or 
gains  entrance  into  the  lumen  of  the  duct.  This  has  been  observed  in 
primary  mahgnant  disease  of  the  gall-bladder — a  cylinder  of  growth 
projecting  into  the  common  bile-duct  (Bohnstedt  *) — and  in  primary  car- 
cinoma of  the  hver.     (Gilbert  and  Claude. f) 

II.  Jaundice  Due  to  Changes  in  the  Walls  of  the  Larger  Ducts. — 
(a)  Catarrhal  jaundice  due  to  inflammatory  swelling  of  the  mucous 
membrane  of  the  common  bile-duct,  either  inside  the  biliary  papilla  or 
in  the  lower  part  of  the  duct,  is  described  elsewhere  (p.  655)  under  the 
heading  of  Acute  Catarrhal  Cholangitis.  It  is  due  to  the  spread  of  in- 
flammation from  the  duodenum,  and  is  preceded  by  gastro-intestinal 
disturbance — ^vomiting  and  diarrhoea.  It  is  usually  of  short  duration, 
and  is  not  accompanied  by  the  fever,  enlarged  spleen,  albuminuria,  and 
jaundice  seen  in  infectious  jaundice. 

(6)  The  infective  and  suppurative  forms  of  cholangitis  are  usually 
associated  with  gall-stones  or  the  rupture  of  an  hydatid  cyst  into  the 
ducts,  but  comparatively  often  complicate  the  rare  condition  of  mahgnant 
disease  of  the  duodenum  involving  the  papilla.  Infective  cholangitis 
presents  the  symptoms  of  intermittent  hepatic  fever  {vide  p.  750),  while 
in  suppurative  cholangitis  (vide  p.  663),  where,  however,  jaundice  is  by 
no  means  constant,  the  clinical  picture  is  that  of  intra-hepatic  suppura- 
tion and  may  closely  resemble  suppurative  pylephlebitis.  It  may  be 
pointed  out  that  jaundice  in  the  roseolous  stage  of  syphilis  may  possibly 
be  due  to  a  specific  change,  resembhng  the  cutaneous  rash,  in  the  bile- 
ducts.     (Vide  p.  348.) 

(c)  Simple  stricture  of  the  large  bile-ducts  may  be  congenital  (vide 
p.  639,  Congenital  Obliteration  of  the  Ducts)  or  acquired,  and  due  to 
cicatrization  of  an  ulcer  in  the  ducts.  Apart  from  the  cystic  duct, 
stricture  of  which  does  not  give  rise  to  jaundice,  simple  stricture  of  the 
ducts,  such  as  might  conceivably  follow  cicatrization  of  an  ulcer  set  up 
by  a  gall-stone,  is  extremely  rare.  Hence  in  practice  cases  of  jaundice 
following  biliary  colic  should  be  regarded  as  due  either  to  fresh  gall-stone 
impaction  or  to  malignant  disease.  Simple  stricture  of  the  ducts  is 
described  on  page  653. 

(d)  Primary  growths  of  the  ducts  may  be  carcinomatous,  or  in  rare 
instances  innocent;  the  malignant  growths  (vide  p.  683)  occlude  the 
lumen  and  give  rise  to  deep,  progressive  jaundice  and  usually  to  enlarge- 
ment of  the  gall-bladder.  At  first,  since  there  is  often  colic,  it  may 
resemble  cholelithiasis,  except  for  the  dilated  gall-bladder,  while  later  it 
resembles  malignant  disease  of  the  head  of  the  pancreas.  Innocent 
tumors,  such  as  papillomata,  are  really  curiosities  (vide  p.  681).  Xanthel- 
asma has  been  described  as  arising  in  the  mucous  membrane  of  the  ducts 

*  Bohnstedt,  quoted  by  Devic  and  Gallavardin:  Rev.  de  Med.,  July,  1901,  p. 
569.  t^^il'^ert  and  Claude:  Archiv.  general,  de  Med.,  1895,  clxxv,  p.  53. 


JAUNDICE.  541 

and  causing  jaundice,  but  there  is  some  reason  to  doubt  whether  this  is 
the  true  interpretation  of  these  cases. 

(e)  Spasm  of  the  muscular  coats  of  the  ducts  seems  to  be  a  very 
reasonable  explanation  of  emotional  jaundice,  but  it  has  not  received 
much  support..  It  also  explains  jaundice  in  hysterical  subjects  when 
there  is  no  evidence  of  catarrh  or  other  causal  factor.  The  occurrence 
of  jaundice  in  cases  of  lead  poisoning  might,  in  the  absence  of  any  other 
satisfactory^  cause,  be  referred  to  spasm  of  the  ducts.  I  have  seen  recur- 
rent attacks  of  painful  jaundice  in  a  worker  in  lead  which  did  not  appear 
to  be  due  to  gall-stones. 

III.  Jaundice  Due  to  Pressure  Exerted  on  the  Bile-ducts  from 
Without. — Synopsis. — 1.  By  intrahepatic  tumors. 

2.  By  enlarged  glands  in  the  portal  fissure — 

Gummata,  malignant,  tuberculous,  sj^hilitic. 

3.  In  lesions  of  the  stomach — 

Carcinoma. 

Gastric  ulcer;   perigastric  adhesions. 

4.  In  duodenal  lesions — 

Ulcer. 
Carcinoma. 

5.  By  peritoneal  adhesions. 

6.  By  renal  and  suprarenal  tumors — 

In  nephroptosis. 

7.  By  retroperitoneal  tumors. 

8.  In  pancreatic  lesions — 

Carcinoma.     Cysts.     Chronic  pancreatitis.     Gumma. 

9.  By  aneurysm  of  the  aorta,  hepatic,  mesenteric  arteries. 

10.  In  gastroptosis. 

11.  In  hepatoptosis. 

12.  By  uterine  and  ovarian  tumors.     Pregnant  uterus. 

13.  Constipation. 

(1)  Intrahepatic  Tumors,  etc. — ^Tumors  inside  the  liver,  such  as  car- 
cinoma, may  press  on  the  intrahepatic  branches  of  the  bile-ducts,  and 
if  the  obstructed  area  is  a  large  one,  such  an  amount  of  bile  stasis  may 
result  as  to  lead  to  absorption  of  bile  by  the  lymphatics  and  so  to  jaun- 
dice. In  these  cases  bile  may  pass  from  the  other  lobe  of  the  liver  into 
the  duodenum,  so  that  the  faeces  retain  their  normal  colour.  A  hj^datid 
cyst  or  a  gumma  in  the  liver  may  act  in  a  similar  fashion. 

Primary  or  secondary  malignant  disease  of  the  liver  may  project 
into  the  portal  fissure  and  press  upon  the  hepatic  ducts,  the  common 
hepatic  or  common  bile-ducts,  and  so  give  rise  to  jaundice.  Hydatid 
cysts  or  gummata,  when  projecting  from  the  liver,  may  exert  pressure 
on  the  bile-ducts  in  a  similar  manner. 

In  a  case  recorded  bj^  Legg  *  a  hydatid  cyst  projecting  from  the  liver  com- 
pressed the  common  hepatic  duct  and  gave  rise  to  persistent  jaundice  with  xanthel- 
asma multiplex.  Bristowe  t  described  obstruction  of  both  hepatic  ducts  by  gum- 
mata. 

*  Legg,  J.  W. :  Trans.  Path.  Soc,  vol.  xxv,  p.  155. 

t  Bristowe,  J.  S. :  Trans.  Path.  Soc,  vol.  ix,  p.  233 


542  DISEASES    OF   THE    LIVER. 

(2)  Enlargement  of  the  glands  in  the  -portal  fissure  may  be  due  to  vari- 
ous causes,  such  as  intra-hepatic  inflammation,  malignant  disease,  and 
occasionally  to  tubercle  and  syphilis.  Malignant  infiltration  of  the 
glands,  which  is  the  most  frequent  cause  of  jaundice,  may  be  secondary 
to  disease  in  the  liver,  gall-bladder,  stomach,  pancreas,  intestine,  or  peri- 
toneum. 

Tuberculous  glands  in  the  portal  fissure  may  in  rare  cases  press  on 
the  bile-ducts  and  give  rise  to  obstructive  jaundice.  Cases  have  been 
recorded  by  Florand,*  Kester,t  Knight, J  Hodenpyl.g  The  rarity  of 
tuberculous  disease  of  the  glands  in  the  portal  fissure  depends  on  the 
fact  that  they  receive  the  lymphatics  from  the  liver,  and  not  from  the 
intestine  and  peritoneum.  Tuberculous  enteritis  and  peritonitis,  there- 
fore, give  rise  to  tuberculous  enlargement  of  the  portal  glands  in  a  round- 
about manner,  viz.,  by  producing  tuberculous  infection  of  the  portal 
spaces  in  the  liver — the  bacilli  travelling  by  the  portal  vein.  The  lymph- 
atics of  the  liver  then  become  involved  and  convey  the  infection  to  the 
portal  glands.  It  is  conceivable  that  tuberculous  infection  might  ex- 
tend along. the  lymphatic  trunks  against  the  flow  of  lymph  and  so  spread 
to  the  portal  fissure  from  the  abdominal  cavity.  Tuberculous  enlargement 
of  the  portal  glands  is,  therefore,  closely  bound  up  with  tuberculosis  of 
the  liver  {vide^.  336),  in  which,  however,  jaundice  is  most  exceptional.  A 
tuberculous  gland  in  the  portal  fissure  has  been  known  to  open  into  the 
common  bile-duct  (Kester),  much  in  the  same  way  that  tuberculous 
bronchial  glands  have  been  found  to  open  into  the  trachea.  Tubercu- 
lous glands  may  become  adherent  to  the  structures  in  the  portal  fissure 
and  render  any  attempt  at  removal  both  difficult  and  dangerous.  In 
Florand's  case  removal  of  tuberculous  glands  compressing  the  common 
bile-duct  was  followed  by  fatal  haemorrhage  from  the  portal  vein. 

Tuberculous  retroperitoneal  lymphatic  glands  may  compress  the 
common  bile-duct  near  its  entrance  into  the  duodenum  and  give  rise  to 
obstructive  jaundice.  The  glands  may  so  indent  the  pancreas  as  to 
look  at  first  like  tuberculosis  of  that  organ. 

Syphilitic  Adenitis. — It  has  been  tentatively  suggested  that  enlarge- 
ment of  the  glands  in  the  portal  fissure  may  be  the  cause  of  the  specific 
jaundice  seen  in  rare  instances  at  the  same  time  as  the  roseola  in 'syphilis, 
but  this  is  extremely  doubtful.  It  is  possible  that  gummatous  change 
or  syphilitic  adenitis  later  in  the  course  of  the  disease  may  involve  lymph- 
atic glands  in  the  neighbourhood  of  the  bile-clucts,  and,  by  pressure, 
give  rise  to  obstructive  jaundice.  This  condition  is  closely  allied  to 
gummatous  infiltration  about  the  head  of  the  pancreas  {vide  p.  549). 

A  man  aged  thirty-two  years  was  under  my  care  with  chronic  jaundice;  as  he 
did  not  improve,  an  exploratory  operation  was  done  by  Mr.  A.  M.  Sheild,  and  some 
hard  masses  were  felt  along  the  course  of  the  common  bile-duct.  Although  there 
was  no  manifest  evidence  of  syphilis,  he  was  put  on  iodides  and  mercury  and  became 
cornpletely  cured.     The  absence  of  any  roseola,  or,  indeed,  of  any  history  of  syphilis, 

*  Florand:  La  Semaine  Medicale,  1899,  p.  20. 

t  Kester:  Centralblatt  f.  inn.  Med.,  1896,  S.  213. 

X  Knight:  Quarterly  Med.  Journ.  (Sheffield),  Julv,  1895. 

§  Hodenpyl:  Medical  Record  (N.  Y.),  Nov.  12,  1898. 


JAUNDICE,  543 

made  it  unlikely  that  this  case  was  one  of  jaundice  in  the  early  stages  of  syphilis 
(vide  p.  348),  and  it  may  have  been  due  to  gummatous  adenitis. 

A  gumma  in  the  portal  fissure  may  press  on  or  involve  the  bile-ducts 
and  so  give  rise  to  jaundice. 

S.  AVest  *  recorded  a  remarkable  example  of  a  large  gumma  extending  from 
the  diaphragm  to  the  neck  of  the  gall-bladder,  measuring  4^  X  2^  inches.  The 
patient,  a  girl  aged  fifteen  years  with  jaundice,  was  the  subject  of  congenital  syphilis. 

Cases  of  tardiye  hereditary  syphilis  with  jaundice  and  clue  to  constriction  of 
the  bile-ducts  by  dense  adhesions  have  been  put  on  record  by  Mackenzie  f  and 
Lazarus-Barlow.l 

(3)  Lesions  of  the  Stomach. — Jaundice  occurs  in  from  6  to  13  per 
cent,  of  all  cases  of  gastric  carcinoma.  It  occurs  more  often  in  cases  where 
the  lesser  curvature  and  the  pylorus  are  affected,  and  is  less  frequent 
when  the  cardiac  end  of  the  stomach  is  involved. 

Jaundice  was  present  in  4  per  cent,  of  Osier  and  Macrae's  §  cases,  in  5.5  per 
cent,  of  Brinton's  ||  cases,  and  in  13.7  per  cent,  of  Fenwick's.** 

Usually  jaundice  is  due  to  pressure  exerted  by  enlarged  lymphatic 
glands  on  the  ducts,  either  in  the  portal  fissure  or  close  to  the  head  of 
the  pancreas.  In  some  cases  of  carcinoma  of  the  pylorus  or  of  the  lesser 
curvature  of  the  stomach  the  growth  spreads  by  direct  continuity  into 
the  lesser  omentum  and  may  thus  surround  the  common  bile-duct  and 
compress  and  invade  its  walls. 

This  was  well  shown  in  a  remarkable  case  of  spheroidal-celled  carcinoma  of 
the  pylorus  in  a  boy  aged  sixteen  years  who  died  in  St.  George's  Hospital  with 
marked  jaundice. 

It  is  noteworthy  that  in  secondary  malignant  disease  of  the  liver 
jaundice  is  more  frequent  when  the  primary  growth  is  in  the  stomach 
than  when  it  is  in  some  more  distant  part  of  the  abdomen,  such  as  the 
rectum.  This  depends  on  the  fact  that  jaundice  is  less  often  due  to  the 
actual  metastasis  in  the  liver  itself  than  to  glandular  infection  in  the 
immediate  neighbourhood  of  the  ducts  or  to  the  direct  spread  of  growth 
into  the  lesser  omentum. 

In  Gastric  Ulcer  and  Perigastritis.— J awndice  due  to  the  spread  of  in- 
flammatory adhesions  from  a  gastric  ulcer  near  the  pylorus  must  be  a 
very  rare  event,  as  it  is  not  mentioned  by  Murchison,  Habershon,  Brin- 
ton,  or  by  Dreschfeld.ft 

That  it  may  occur  is  shown  by  the  following  case.  J  | 

A  man  aged  twenty-seven  came  under  my  care  in  St.  George's  Hospital  with 
no  definite  history  whatever  of  gastric  ulcer,  but  with  dyspepsia  and  occasional 
\'omiting  of  six  weeks'  duration  and  jaundice  of  two  weeks'  standing.  The  stomach, 
was  dilated  and  a  definite  pyloric  tumor  with  what  was  tliought  to  be  thickening 

*  West,  S.:  Trans.  Path.  Soc,  vol.  xli,  p.  155. 

t  Mackenzie,  H.  W.  G. :  Ibid.,  vol.  xliii,  p.  84. 

X  Lazarus-Rarlow,  W.  S. :  Ibitl.,  vol.  1,  p.  158. 

§  Osier  and  Macrae:  Cancer  of  the  Stomach,  p.  55,  1900. 

!|  Brinton :  Diseases  of  the  Stomach,  p.  211,  1864. 
**  Fenwick,  S. :  Cancer  and  Tumors  of  the  Stomach,  p.  69,  1902. 
tt  Dreschfeld,  J. :  Allbutt's  System  of  Medicine,  vol.  iii. 
it  Kolleston:  Practitioner,  Nov.,  1897. 


544  DISEASES   OF  THE   LIVER. 

of  the  adjacent  curvatures  -^-as  palpable.  The  case  was  regarded  as  carcinoma  of 
the  pylorus,  but  as  iinsuitable  for  gastrojejunostomy.  At  the  postmortem  there 
was  no  mahgnant  disease,  but  a  cicatrising  ulcer  at  the  pylorus  giving  rise  to  marked 
narrowing  of  that  orifice  and  extensive  peripyloric  adhesions  involving  the  common 
duct.  The  head  of  the  pancreas,  which  was  enlarged  from  chronic  interstitial 
pancreatitis,  had  been  felt  in  life  and  regarded  as  thickening  of  the  curvatures  of 
the  stomach  near  the  pylorus. 

A  case  of  jaundice  and  ascites  in  a  man  aged  thirty-nine  years  due  to  fibrosis 
spreading  from  an  ulcer  near  the  pjdorus  to  the  portal  fissure  is  recorded  by  James.* 
The  common  bile-duct  was  normal,  but  the  two  hepatic  ducts  were  compressed  by 
cicatricial  tissue  which  spread  into  the  liver  along  the  portal  spaces. 

The  converse  condition,  viz.,  pericholecystitic  adhesions  prochicing 
pyloric  obstrviction^  has  been  fully  recognised  and  is  much  less  rare. 

(4)  Duodenal  Lesions. — Duodenal  ulcer  may  in  verj^  rare  instances  be 
associated  vith  jaundice  either  (i)  as  a  complication  or  (ii)  as  an  after- 
result. 

(i)  Ulceration  of  the  duodenum  is  almost  always  hmited  to  the  first 
part  of  the  duodenum  and  hardly  ever  extends  sufficiently  far  into  the 
second  part  to  invade  the  biliary  papilla.  Concomitant  duodenal  ca- 
tarrh, however,  may  spread  to  the  bihar}^  papilla. 

Perry  and  Shaw  f  record  several  cases  of  duodenal  ulcer  with  jaundice.  Mur- 
chison  X  describes  a  case  in  a  man  aged  sixty-nine,  but  there  is  a  strong  suspicion 
that  there  was  malignant  disease  of  the  duodenmn  in  the  region  of  the  biliary 
papilla. 

(ii)  As  a  sequela  from  the  results  of  cicatrization  and  heahng  of  the 
ulcer.  If,  as  rarely  happens,  the  ulcer  is  in  the  second  portion  of  the 
duodenum  and  involves  the  papilla,  cicatricial  contraction  may  give 
rise  to  permanent  obstructive  jaundice. 

Budd  §  described  a  case  of  this  kind,  and  Perry  and  Shaw  ||  refer  to  4  cases 
examined  after  death  where  a  cicatrised  duodenal  ulcer  obstructed  the  outflow  of 
bile  from  the  biliarj^  papilla.  Zoia  **  records  cicatrisation  of  a  duodenal  ulcer 
obstructing  the  bile  and  pancreatic  ducts  and  imitating  caxcinoma  of  the  head  of 
the  pancreas. 

Inflammatory  adhesions  may  sj^read  out  from  a  duodenal  ulcer  in 
the  first  part  and  compress  the  common  bile-duct  as  it  runs  towards  the 
bihary  papilla.  This  mechanism  is  exactty  like  that  already  described 
in  peripyloric  adhesions. 

]\Iorgantt  has  recorded  the  details  of  a  case  in  which  the  common  bile-duct  was 
firmly  bound  to  the  base  of  a  duodenal  ulcer  by  dense  adhesions  and  its  lumen 
much  constricted.     The  patient,  a  man  aged  fifty-two  years,  died  deeply  jaundiced. 

Carcmoma  of  the  duodenum  is  not  a  connnon  disease,  and  need  not 
cause  any  interference  -^-ith  the  outflow  of  bile  unless  the  gro-u-th  is 
situated  in  the  second  part  of  the  duodenum  and  involves  the  bihary 
papilla  by  extension  or  actually  starts  in  the  intestinal  mucous  mem- 

*  James:  Scottish  Medical  and  Surgical  Journal,  vol.  ii,  p.  511. 

t  Perry  and  Shaw :  Guy's  Hosp.  Reports,  vol.  1,  1S93. 

X  Murchison:  Diseases  of  the  Liver,  p.  422,  3d  ed.,  1SS5. 

§  Budd:  Diseases  of  the  Liver,  p.  204,  1857. 

II  Perry  and  Shaw:  Guy's  Hospital  Reports,  vol.  1,  p.  273,  1893. 
**  Zoia:  Gaz.  med.  di  Torino,  May  11,  1S99. 
tt  Morgan,  J.  H. :  Trans.  Path.  Soc,  vol.  xxvii,  p.  176 


JAUNDICE.  545 

brane  of  the  biliary  papilla.  This  latter  form  of  duodenal  carcinoma — 
juxta-ampuUary  or  perivaterian,  as  it  is  sometimes  called — imitates 
cancer  of  the  head  of  the  pancreas,  and,  like  it,  should  present  the  sign 
of  Bard  and  Pic,  viz.,  deep  jaundice  and  distension  of  the  gall-bladder, 
but  in  addition  it  has  a  special  tendency  to  set  up  infective  cholangitis, 
multiple  foci  of  suppuration  in  the  liver,  and  fever.  Specimens  of  this 
condition  are  to  be  found  in  the  museums  of  St.  Bartholomew's,  Guy's, 
and  St.  Thomas'  Hospitals.  The  following  case  illustrates  this  sequence 
of  events: 

Carcinoma  of  Biliary  Papilla,  Jaundice,  Suppurative  Cholangitis,  Secondary 
Abscesses  in  Prostate  and  Kidneys. — A  man  aged  fifty-two  years  was  under  the  care 
of  my  colleague,  Sir  Isambard  Owen,  in  St.  George's  Hospital  with  jaundice  of 
ten  months'  duration,  which,  however,  had  disappeared  for  one  month  during 
this  period  of  ten  months,  loss  of  strength  and  flesh,  and  difficulty  in  passing  water. 
The  liver  was  much  enlarged,  but  not  tender;  there  was  no  ascites.  The  urine 
contained  bile  and  an  excess  of  ethereal  sulphates  and  indican.  There  were  pus 
in  the  urine,  a  greatly  enlarged  prostate,  and  some  diarrhoea.  There  was  a  hectic 
temperature  during  the  last  five  weeks  of  life.  The  tentative  diagnosis  was  malig- 
nant disease  of  the  prostate  with  a  secondary  growth  in  the  portal  fissure  producing 
jaundice.  At  the  autopsy  there  was  a  carcinomatous  growth  Involving  the  duodenal 
surface  of  the  biliary  papilla,  with  great  dilatation  of  the  common  and  of  all  the 
bile-ducts  in  the  liver;  there  were  universal  suppurative  cholangitis  and  empyema 
of  the  gall-bladder.  The  liver  was  green,  not  fibrosed,  and  contained  some  secon- 
dary nodules  of  white  growth.  The  pancreatic  duct  was  dilated.  The  enlarge- 
ment of  the  prostate  was  due  to  an  abscess ;  there  were  numerous  abscesses  in  the 
two  kidneys. 

Cases  of  perivaterian  carcinoma  of  the  duodenum  without  marked 
jaundice  have  been  recorded  by  Lannois  and  Courmont*  and  by  Descos 
and  Beriel.t 

Carcinoma  of  the  duodenum  may  give  rise  to  jaundice  in  another 
way,  viz.,  by  inducing  gastroptosis,  which,  if  there  are  adhesions  around 
the  ducts,  may  induce  kinking  and  jaundice.  (Vide  Gastroptosis,  p. 
550.) 

Mackie  Whyte  %  has  put  a  case  on  record  where  cancer  of  the  duodenum,  not 
involving  the  biliary  papilla,  led  to  great  distension  of  the  stomach  and  so  to  kinking 
of  the  common  bile-duct  and  jaundice. 

(5)  Peritoneal  adhesions  around  the  hepatic  or  common  bile-ducts  may 
produce  kinking  of  the  ducts  and  thus  lead  to  jaundice.  Such  adhesions 
may  be  due  to  local  peritonitis  set  up  in  various  ways,  such  ,as  by  gall- 
stones in  the  gall-bladder,  perigastric  inflammation  (p.  543),  adhesions 
around  a  duodenal  ulcer  (p.  544),  adhesions  to  inflamed  retroperitoneal 
glands  (B.  Robinson  ^),  or  possibly  by  adhesions  due  to  perihepatitis 
(S.  Phillips  II).  It  is,  however,  remarkable  how  seldom  perihepatitis  and 
chronic  peritonitis  are  accompanied  by  jaundice. 

(6)  New-growths  of  the  right  kidney  or  suprarenal  body  very  seldom 
press  on  the  bile-duct  and  so  directly  produce  jaundice,  but  secondary 
growths  in  the  portal  fissure  may  set  up  jaundice. 

*  Lannois  and  Courn\ont:  Rev.  de  M^d.,  1894,  p.  291. 

t  Descos  and  Reriel:  Rev.  de  Med.,  1899,  p.  633. 

t  Whyte,  M. :  Scottish  Med.  and  Surg.  Journ.,  vol.  i,  p.  361,  1897. 

§  Byron  Robinson :  American  Med.  and  Surg.  Bulletin,  April,  1896. 

I|  Phillips,  S. :  Lancet,  1903,  vol.  i,  p.  1796. 

35 


546  DISEASES    OF   THE    LIVER. 

In  26  cases  of  primary  malignant  disease  of  the  suprarenal  bodies  jaimdice 
was  not  present  in  any.     (RoUeston  and  Marks.*) 

That  a  floating  kidney  can  exert  direct  pressure  on  the  bile-ducts 
and  thus  lead  to  jaundice,  as  suggested  by  Littenf  and  others,  is  re- 
garded as  improbable  by  Macalister.J  The  colic,  jaundice,  and  vomit- 
ing induced  by  a  floating  kidney  on  the  right  side  may  be  explained  in 
the  following  way:  the  peritoneum  over  the  kidney  being  continuous 
with  that  covering  the  duodenum  and  common  bile-duct,  undue  mobility 
of  the  kidney  will  exert  traction  on  the  duodenum  and  common  bile- 
duct  and  will  lead  to  narrowing  of  the  bile-duct  and  duodenum.  It  has 
been  pointed  out  that  nephroptosis  may  also  lead  to  downward  displace- 
ment of  the  duodenum,  with  Stretching  of  the  common  bile-duct,  dis- 
placement of  the  gall-bladder,  with  sharp  kinking  of  the  cystic  duct, 
torsion  of  the  vertical  part  of  the  duodenum,  and  perhaps  even  of  the 
bile-duct.     (J.  Hutchinson,  Jr.§) 

A  floating  kidney  may  not  only  produce  symptoms  exactly  like  hepatic 
colic  and  induce  jaundice,  but  the  displaced  kidney  may  readily  be  mis- 
taken for  a  distended  gall-bladder.  Hutchinson  has  described  two  cases 
where  what  was  thought  to  be  the  gall-bladder  turned  out  to  be  a  float- 
ing right  kidney. 

Cases  of  jaundice  diagnosed  as  cholelithiasis  and  shown  to  be  due  to 
,  floating  kidneys  have  been  recorded  by  Maclagan  and  Treves  (3),  |!  bj^ 
Hale  White,**  Cordier,tt  Fenwick,tt  Lawrie.§§ 

The  diagnosis  depends  on  the  detection  of  a  floating  kidney,  for  the 
symptoms,  biliary  colic  and  jaundice,  are  the  same  as  those  of  chole- 
lithiasis. If  the  symptoms  persist  after  the  floating  kidney  has  been 
efficiently  and  successfully  treated,  it  is  probable  that  there  is  cholelithia- 
sis in  addition. 

(7)  Pressure  Exerted  hy  Retroperitoneal  Tumors. — In  rare  instances 
retroperitoneal  tumors  have  been  known  to  give  rise  to  jaundice  by  pres- 
sure on  the  common  bile-duct. 

Vander  Veer  ||  ||  recorded  a  large  retroperitoneal  myxosarcoma  (weight  6  pounds) 
arising  from  the  region  of  the  left  adrenal  body,  which  so  interfered  with  the  bile- 
duct  as  to  produce  jaundice. 

A  hydatid  cyst  arising  in  connexion  with  the  retroperitoneal  space 
near  the  head  of  the  pancreas  may  compress  the  common  duct.  This 
is  illustrated  by  a  specimen  (No.  2256)  in  St.  Bartholomew's  Hospital 
Museum. 

(8)  Lesions  of  the  Pancreas  Producing  Jaundice. — Malignant  disease, 

*  RoUeston  and  Marks:  American  Journ.  Med.  Sciences,  vol.  cxvi,  p.  398,  Oct., 
1898.  t  Litten:  Berlin.  Charite-Annalen,  1880,  S.  10. 

X  Macalister,  A. :  Allbutt's  System  of  Medicine,  vol.  iv,  p.  346. 
§  Hutchinson,  J.,  Jr.:  The  Practitioner,  1902,  vol.  Ixviii,  p.  186. 
II  Maclagan  and  Treves:  Lancet,  1900,  vol.  i,  p.  15. 
**  Hale  White:  Brit.  Med.  Journ.,  1892,  vol.  i,  p.  223. 
tt  Cordier:  American  Journ.  of  Obstet.,  1896,  a'oI.  xxxiv,  p.,  532. 
tt  Fenwick:  Lancet,  1899,  vol.  ii,  p.  1296. 
j§  Lawrie:  Brit.  Med.  Journ.,  1901,  vol.  i,  p.  15. 

nil  Vander  Veer:  American  Journ.  of  the  Medical  Sciences,  vol.  ciii,  ]>.  22,  Jan., 
1892. 


JAUNDICE.  547 

cysts,  chronic  interstitial  inflammation,  gummata,  and  calculi  in  Wir- 
sung's  duct  are  all  capable  of  compressing  the  common  bile-duct  and 
producing  obstructive  jaundice,  but  with  the  exception  of  the  first 
named  are  rarely  recognised  as  acting  in  this  manner. 

Malignant  disease  of  the  pancreas  may  be  primary  or  secondary,  but 
it  is  almost  entirely  with  primary  malignant  disease  that  we  are  at  pres- 
ent concerned.  It  is  practically  always  carcinoma,  and  usually  attacks 
the  head  of  the  gland — according  to  Hale  White,*  in  85  per  cent,  of  the 
cases.  When  in  this  situation,  the  growth  readily  compresses  the  com- 
mon bile-duct  near  its  termination,  but  when  the  growth  is  limited  to 
the  tail  or  body  of  the  pancreas,  jaundice  does  not  result  unless  a  second- 
ary growth  compresses  the  duct  or  there  is  some  other  cause  for  jaundice, 
such  as  a  calculus  in  the  common  duct.  Jaundice  is  met  in  a  majority 
of  cases  of  primary-  malignant  disease  of  the  pancreas. 

Mirallie  f  found  it  in  82  out  of  113  cases,  but  Hale  White  gives  a  lower  estimate, 
viz.,  in  "probably  more  than  half  the  cases,"  and  considers  that  the  incidence  of 
icterus  has  been  somewhat  exaggerated  by  previous  writers.  Oser  gives  two-thirds 
as  the  proportion  of  cases  in  which  jaundice  occurs. 

The  jaundice  may  come  on  gradually  and  painlessly,  or  be  accom- 
panied by  colic.  It  is  permanent  and  progressive,  and  becomes  intense, 
so  that  cholsBmia  develops  comparatively  early.  The  other  distinctive 
features  of  malignant  disease  of  the  head  of  the  pancreas  are  rapid  and 
extensive  wasting,  the  presence  of  a  tumor  in  the  position  of  the  pan- 
creas, which,  however,  is  only  palpable  in  a  small  minority  of  the  cases, 
and  distension  of  the  gall-bladder.  The  association  of  deep  jaundice  with 
a  large  gall-bladder  was  specially  insisted  upon  by  Bard  and  Pic,  J  and  is 
sometimes  spoken  of  as  the  sign  of  Bard  and  Pic.  It  illustrates  Cour- 
voisier's  law,  which  is  to  the  effect  that  biliary  obstruction  due  to  new- 
growth  is  accompanied  by  an  enlarged  gall-bladder,  while  in  gall-stone 
obstruction  of  the  common  duct  the  gall-bladder  is  small.  As  a  matter 
of  fact,  however,  the  gall-bladder,  even  though  enlarged  as  shown  by 
postmortem  examination,  is  not  always  palpable  during  life.  As  already 
pointed  out,  the  diagnosis  depends  on  the  intense  jaundice,  the  rapid 
loss  of  weight,  and  the  enlargement  of  the  gall-bladder.  It  is,  however, 
practically  impossible  to  distinguish  it  from  primary  carcinoma  of  the 
common  bile-duct.?  In  primary  carcinoma  of  the  ampulla  of  Vater 
(vide  p.  697)  and  of  the  duodenal  surface  of  the  biliary  papilla  the  jaun- 
dice may  intermit,  which  it  never  does  in  malignant  disease  of  the  pan- 
creas, and  fever  from  infective  cholangitis  may  supervene.  From  a 
calculus  in  the  common  duct  the  diagnosis  may  be  easy  when  the  cases 
are  typical,  but  sometimes  it  is  difficult,  as  attacks  of  pseudo-biliary 
colic  may  occur  about  the  time  of  the  onset  of  jaundice  in  malignant  dis- 
ease of  the  pancreas,  while  ]min  may  be  absent  in  some  cases  of  calculus 
in  the  conniion  duct.     The  history  of  the  cases  and  the  course  of  the 

*  Hale  White:  Guy's  Hosp.  Reports,  vol.  liv,  p.  17. 
t  Miralh^:  Gaz.  des  Hojx,  1893,  p.  889. 
t  Bard  and  Pic:  Rev.  de  M.6d.,  vol.  viii,  p.  257. 

§  Cammidge's  test,  however,  provides  a  means  of  distinguishing  between  tliese 
tAVO  conditions. 


548  DISEASES   OF  THE   LIVER. 

disease,  especially  the  character  of  the  jaundice,  progressive  or  inter- 
mittent, and  the  condition  of  general  nutrition  will  usually  clear  up  a 
diagnosis  which  at  first  was  doubtful. 

Cammidge's  Test. — By  treating  the  urines,  free  from  sugar,  of  cases  of  pancreatic 
disease  by  a  special  method,  which  cannot  be  described  further  here  except  to 
state  that  the  urine  is  first  boiled  with  HCl  and  then  with  sodiimi  acetate  and 
phenyl-hydrazin  hydrochlorate,  Cammidge  *  obtained  crystals  which  could  not  be 
got  from  normal  urine.  He  was  further  able  to  differentiate  between  the  crystals 
obtained  from  the  urine  of  (i)  malignant  disease,  (ii)  acute  inflammation,  and  (iii) 
chronic  inflammation  of  the  pancreas.  Jaundice  due  to  pancreatic  disease  could 
thus  be  distinguished  from  jaundice  due  to  other  causes,  and  further  malignant 
disease  could  be  diagnosed  from  inflammatory  affections  of  the  pancreas.  These 
results  have  been  freely  criticised,  and,  though  they  appear  valid,  the  subject  is 
stiU  open  for  discussion. 

Malignant  disease  of  the  pancreas  may  be  associated  with  chole- 
lithiasis, and  in  rare  instances  with  gall-stones  in  the  common  duct. 

Thus  a  woman  aged  fifty-eight,  under  my  care  in  St.  George's  Hospital  in  Sep- 
tember, 1899,  was  thought  to  be  suffering  from  gall-stone  obstruction  and  was 
accordingly  operated  upon;  a  gall-stone  was  felt,  and  on  manipulation  was  dis- 
placed, it  was  thought,  into  the  duodenum.  Death  occurred  on  the  third  day, 
largely  from  haemorrhage  at  the  site  of  operation.  At  the  autopsy  it  was  found 
that  the  calculus  had  been  pushed  back  into  the  gall-bladder,  and  that  all  the 
ducts  were  greatly  dilated.  The  gaU-bladder  was  small  and  contained  two  round 
large  cholesterine  calculi.  The  head  of  the  pancreas  contained  a  colloid  carcinoma 
which  did  not  involve  the  duct,  so  the  jaundice  was  probably  due  to  the  stone  in 
the  common  duct.  Microscopically  the  growth  was  a  spheroidal-celled  carcinoma 
undergoing  extensive  colloid  change. 

Pancreatic  Cysts,  etc.- — Jaundice  is  rarely  due  to  a  pancreatic  cyst, 
but  may  occur  when  the  cyst  is  situated  sufficiently  close  to  the  bile- 
duct  to  compress  it.  Pancreatic  and  peripancreatic  cysts  may  present 
in  various  situations:  (1)  Above  the  stomach  and  below  the  liver  (in- 
terhepatico-gastric  type).  (ii)  Between  the  greater  curvature  of  the 
stomach  and  the  transverse  colon;  this  is  the  commonest  form  (sub- 
hepatico-gastric  type),  (iii)  Below  the  transverse  colon,  so  that  the 
cyst  projects  near  the  umbilicus  (subhepato-gastro-colic  type). 

Cysts  which  pass  forwards  between  the  stomach  and  the  transverse 
colon  (subhepatico-gastric  type)  may  compress  the  common  bile-duct. 
Oser  t  has  collected  15  cases  in  which  jaundice  has  occurred. 

A  man  aged  thirty  with  jaundice  of  three  months'  duration  under  my  care  in 
St.  George's  Hospital  was  operated  upon  by  Mr.  G.  R.  Turner  and  a  pancreatic 
cyst  found  projecting  between  the  greater  curvature  of  the  stomach  and  the  trans- 
verse colon. f  After  drainage  the  jaundice  disappeared  and  the  man  recovered. 
Turney  and  Ballance  §  met  with  a  case  of  jaundice  in  a  man  aged  thirty-five  in 
whom  the  symptoms  were  thought  to  point  to  calculous  obstruction  of  the  common 
bile-duct;  laparotomy,  however,  proved  that  the  jaundice  was  due  to  the  pressure 
of  a  pancreatic  cyst.  Cases  have  also  been  described  by  Havilland  HaU,|| 
McPhedran.** 

A  hydatid  cyst  in  the  pancreas  is  a  pathological  curiosity. 

*  Lancet,  March  19,  1904. 

t  Oser :  Nothnagel's  Encyclopaedia  of  Practical  Medicine,  p.  195,  English 
Translation.  |  Vide  also  Trans.  Medical  Soc,  vol.  xxi,  p.  94. 

§  Turney  and  Ballance:  St.  Thomas'  Hospital  Reports,  vol.  xxvi. 
II  Havilland  Hall:  Trans.  Medical  Soc,  vol.  xxi,  p.  107. 
**  McPhedran:  Trans.  Associat.  American  Physicians,  vol.  xii,  p.  61. 


JAUNDICE.  549 

A  hydatid  cyst  in  the  head  of  the  pancreas  was  tlie  cause  of  jaundice  of  ten 
months'  duration  and  of  ascites  in  a  boy  aged  six  j^ears.  At  the  autopsy  the  gall- 
bladder was  dilated  and  the  bile-duct  and  portal  vein  were  stretched  over  the  cyst 
and  so  compressed  that  it  was  impossible  to  force  bile  from  the  distended  gall- 
bladder into  the  duodenum  before  the  cyst  was  opened.  The  liver  was  enlarged, 
granular  on  the  surface,  and  fibrosed.* 

Chronic  Interstitial  Pancreatitis. — Mayo  Robson  f  and  Barling  %  have 
drawn  attention  to  the  fact  that  chronic  inflammation  of  the  head  of  the 
pancreas  may  compress  the  common  bile-duct  and  produce  a  train  of 
symptoms — obstructive  jaundice,  colic,  and  wasting — strongly  suggest- 
ing mahgnant  disease  or  impacted  gall-stones.  This  chronic  fibrosis  may 
be  directly  due  to  gall-stones  in  the  common  duct  and  may  persist  after 
the  stone  is  expelled.  The  diagnosis  of  these  cases  is  veiy  difficult,  and 
the  moral  drawn  from  them  is  that  it  is  advisable  to  admit  such  cases  to 
operation.  In  some  instances  the  gall-bladder  has  been  drained,  either 
externally  or  into  the  small  intestine,  while  in  other  cases  the  abdomen 
has  been  closed  without  any  more  radical  measure  than  manipulation  of 
the  parts.  Recovery  has  followed  both  of  these  methods  of  surgical  treat- 
ment. It  is  possible  that  where  the  parts  have  merely  been  manipulated 
(Owen,§  Dalziel  ||)  a  calculus  in  the  orifice  of  the  biliary  papilla  may  have 
been  displaced  into  the  duodenum.  It  seems  highly  probable  that  cases 
of  chronic  interstitial  pancreatitis  have  been  regarded  not  only  during 
life,  but  even  after  death,  as  examples  of  carcinoma  of  the  head  of  the 
pancreas.  According  to  Hale  White,**  however,  chronic  interstitial  pan- 
creatitis is  a  rare  disease;  for  in  forty-one  years  there  were  19,000 
necropsies  at  Guy's  Hospital  with  only  four  cases  of  this  disease. 

In  cases  of  pancreatitis  the  secretion  of  the  gland  escapes  into  the  surrounding 
tissues  and  sets  up  fat  necrosis.  As  a  result  of  this  glycerine  and  fatty  acids  are 
liberated.  It  was  first  thought  that  the  tendency  to  haemorrhage,  both  in  acute 
inflammation  of  the  pancreas  and  in  cases  of  chronic  pancreatitis,  which  is  so  often 
accompanied  by  chronic  jaundice,  might  be  due  to  the  action  of  glycerine  (Mayo 
Robson  tt)>  but  more  recently  Mayo  Robson  ||  refers  it  to  a  diminution  of  the 
lime  salts  in  the  blood  depending  on  increased  excretion  of  lime  in  the  form,  of 
oxalates  in  the  urine. 

Closely  allied  to  chronic  interstitial  pancreatitis  is  the  extremely 
rare  condition  gummatous  infiltration  in  and  around  the  head  of  the 
pancreas. 

In  a  man  aged  thirty-three  who  had  had  syphilis  ten  years  previously,  and 
was  suffering  from  marked  obstructive  jaundice  H.  B.  Robinson  §§  opened  the 
abdomen,  felt  a  growth  in  the  situation  of  the  head  of  the  pancreas,  and  accordingly 
put  the  gall-bladder  into  communication  with  the  hepatic  flexure  of  the  colon. 
Under  iodide  of  potassium  the  mass  disappeared  and  there  was  a  gain  in  weight  of 

*  Guy's  Hospital  Museum,  No.  1475. 

t  Mayo  Robson:  Brit.  Med.  Journ.,  1900,  vol.  ii,  Epitome,  p.  26.    Lancet,  1900 
vol.  ii. 

X  Barling:  Brit.  Med.  Journ.,  1900,  vol.  ii,  p.  1766. 

§  Owen:  Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  1.311,  and  Hale  White:  Brit.  Med. 
Journal,  1903,  vol.  ii,  p.  126. 

II  Dalziel:  Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  1312. 
**  Hale  White:  Brit.  Med.  Journ.,  1903,  vol.  ii,  p.  126. 
tt  Mayo  Robson:  Philadelphia  .MecHcal  Journal,  June  1,  1901. 
%%  Lancet,  1904,  vol.  i,  March  7. 
§§  Robinson,  H.  B. :  Brit.  Med.  Journ.,  1900,  vol.  ii,  p.  1004. 


550  DISEASES    OF   THE    LIVER. 

two  stones.     A  similar  case  of  Da  Costa's  is  mentioned  in  Gould's  Year-book  of 
Surgery  for  1902,  p.  181.     ]Mo\Tiihan  *  has  also  described  this  condition. 

A  large  pancreatic  calculus  in  the  termination  of  Wirsimg's  duct  may 
compress  the  end  of  the  common  bile-duct  and  give  rise  to  jaundice. 

Pearce  Gould  t  has  recorded  a  case  where  a  pancreatic  calculus  the  size  of  a 
horse-bean  gave  rise  to  jaimdice. 

(9)  Aneurysms  of  the  Abdominal  Aorta,  etc. — An  aneurysm  of  the 
abdominal  aorta  near  the  cceliac  axis  may  exert  pressure  on  the  common 
bile-duct  and  so  give  rise  to  jaundice  and  dilatation  of  the  gall-bladder. 
Cases  have  been  recorded  by  Stokest  and  W.  L.  Dickinson. § 

In  a  man  aged  twenty-eight,  who  had  sj'philis  when  twenty  j^ears  of  age,  a 
sacculated  aneurysm  involving  the  origin  of  the  cceliac  axis  burst  into  the  second 
part  of  the  duodenum  a  short  distance  above  the  biliary  papilla.  The  common 
bile-duct  was  comjsressed  and  the  gall-bladder  distended.  Jaundice  occurred 
three  daj^s  before  death,  which  was  preceded  by  sudden  and  profuse  hsematemesis. 
(W.  L.  Dickinson.) 

Aneurysms  of  the  hepatic  artery  are  rare,  but  when  they  do  occur,  are 
frequently  accompanied  by  jaimdice.  The  aneurj^sm  may  compress  the 
bile-ducts  above  the  entrance  of  the  cystic  duct,  and  hence  the  gall- 
bladder need  not  be  dilated,  as  in  jaundice  due  to  an  aortic  aneuiysm. 
An  aneurysm  of  the  hepatic  artery  may,  by  interfering  \A\\\  the  blood- 
supply  to  the  bile-ducts,  dispose  to  infection,  cholangitis,  and  thus  give 
rise  to  suppuration  in  the  ducts.     {Vide  p.  44.) 

An  aneurysm  of  the  superior  mesenteric  artery  near  its  origin  from  the 
aorta  has  been  knovm  to  compress  the  bile-duct  and  give  rise  to  jaundice. 
Cases  have  been  pubhshed  by  Dr.  J.  A.  Wilson  ||  and  Sir  W.  T.  Gairdner.** 
The  majority  of  aneurysms  on  this  vessel,  however,  are  not  associated 
with  jaundice.  Those  on  the  peripheral  portions  of  the  artery  or  its 
branches  are  not  in  relation  with  the  bile-ducts,  and  therefore  do  not 
compress  them. 

(10)  Gastroptosis  is  not  infrequent,  but  its  association  ^dth  jaundice 
is  rare.  Steele  ft  states  that  gastroptosis  alone  camiot  produce  sufficient 
pressure  on  the  bile-ducts  to  obstruct  the  flow  of  bile  along  the  ducts; 
this  is  based  on  his  observ^ations  that  after  death  downward  displace- 
ment of  the  pylorus,  so  as  to  imitate  the  conditions  present  in  gastrop- 
tosis; though  it  stretched  the  gastrohepatic  omentum,  did  not  interfere 
with  the  passage  of  bile  into  the  duodenum:  If,  however,  there  were 
any  adhesions  involving  the  ducts  in  the  portal  fissure,  a  verj^  moderate 
amount  of  displacement  of  the  pylonis  produced  kinking  of  the  ducts 
and  obstruction.  It  would  thus  appear  that  if  there  are  any  adhesions 
around  the  ducts,  gastroptosis  Tvill  readily  produce  jaimdice. 

(11)  Hepatoptosis. — In  wandering  liver  jaundice  may  be  due  to  the 

*Movnihan:  Lancet,  1902,  vol.  ii,  p.  856. 

t  Gould,  A.  P. :  Trans.  Clin.  Soc,  vol.  xxxii,  p.  59. 

t  Stokes:  Diseases  of  Heart  and  Aorta,  1854,  p.  633. 

§  Dickinson,  W.  L. :  Trans.  Path.  Soc,  vol.  xlii,  p.  77. 

II  Wilson,  J.  A. :  Medico-(  hirurg.  Trans.,  vol.  xxiv,  p.  221. 
**  Gairdner,  W.  T. :  Clmical  Medicine.  1862,  p.  504. 
It  Dutton  Steele:  University  Medical  Magazine  (Penn.),  Feb.,  1901,  p.  838. 


JAUNDICE.  ■  551 

presence  of  gall-stones,  to  concomitant  catarrh  of  the  ducts,  to  a  floating 
right  kidney,  or  to  twisting  of  the  common  bile-duct. 

Dutton  Steele  *  has  collected  15  cases  of  hepatoptosis  in  which  there  were 
attacks  of  jaundice  witliout  gall-stones. 

In  Crawf urd's  t  case  of  anteverted  liver  the  bile-duct  had  apparently 
been  twisted,  so  as  to  give  rise  to  jaundice,  at  the  junction  of  the  common 
bile  and  cystic  ducts.  The  descent  or  dropping  of  the  liver  tends  to 
produce  this  twisting.  By  injection  experiments  in  the  dead  body 
Dutton  Steele  has  shown  that  the  more  the  liver  descends  towards  the 
pelvis,  the  more  difficult  it  is  to  drive  injection  from  the  biliary  papilla 
into  the  gall-bladder. 

(12)  Conditions  of  the  Uterus,  Ovarian  Tumors,  etc. — The  pressure  of 
a  pregnant  uterus  on  the  ducts  has  been  regarded  as  responsible  for 
jaundice  (MurchisonJ).  This  is  very  doubtful;  mild  jaundice  in  preg- 
nant women  is  usually  due  to  gastroduodenal  catarrh,  but  may  be  due 
to  gall-stones,  cholangitis,  or  toxsemic  inflammation  of  the  small  intra- 
hepatic ducts.  As  mentioned  elsewhere,  the  occurrence  of  acute 
yellow  atrophy  is  especially  favoured  by  pregnancy. 

Ovarian  tumors  may  exceptionally  give  rise  to  jaundice  by  pressing 
on  the  bile-duct.  Poynder  §  has  recorded  such  a  case.  On  the  other 
hand,  jaundice  may  be  merely  associated  with  the  presence  of  ovarian 
cysts  and  depend  on  catarrhal  inflammation  of  the  papilla,  infective 
cholangitis,  or  gall-stones.  The  abdominal  distension  caused  by  an 
ovarian  cyst  favours  stagnation  of  bile,  infection  of  the  ducts,  and  chole- 
lithiasis. Thus  suppurative  cholangitis  or  cholecystitis  may  complicate 
ovarian  cysts. 

(13)  Constipation  may  be  associated  with  jaundice.  SHght  jaundice 
may  possibly  be  due  to  absorption  of  poisons  from  the  intestine  produc- 
ing catarrh  of  the  intra-hepatic  bile-ducts,  or  in  other  cases  be  due  to 
the  spread  of  associated  duodenal  catarrh  to  the  common  duct.  In  this 
way  the  relief  of  jaundice  after  free  purgation  may  be  explained.  It 
seems  improbable  that  faecal  accumulation  by  direct  .pressure  can  give 
rise  to  jaundice.  But  in  rare  cases  where  the  colon  is  firmly  united  to 
the  under  surface  of  the  liver  by  adhesions,  faecal  accumulation  in  the 
transverse  colon  may  possibly  lead  to  kinking  or  compression  of  the 
common  bile-duct. 


GENERAL  REMARKS  ON  THE  DIAGNOSIS  OF  JAUNDICE. 

The  large  number  of  conditions  which  may  give  rise  to  jaundice 
makes  it  essential  that  a  careful  examination  should  be  made  for  any 
other  evidence  of  disease.  Thus  the  existence  of  a  tumor  in  the  abdo- 
men, breast,  or  rectum  will  suggest  malignant  disease,  while  the  co- 
existence of  sy]ohilis,  either  in  the  secondary  or  tertiary  stage,  should  be 

*  Dutton  Steele:  University  of  Pennsylvania  Med.  Bull.,  vol.  xv,  p.  424,  Jan., 
1903.  t  Crawfunl,  R.  P. :  Lancet,  1S97,  vol.  ii,  p.  1182. 

J  Murchison:  Lectures  on  Diseases  of  the  Liver,  2d  ed.,  1877,  p.  358. 
§  Poynder:  The  Indian  Med.  Gaz.,  June,  1899,  p.  208. 


552  DISEASES    OF   THE    LIVER. 

an  indication  for  specific  treatment.  The  following  jDoints  have  a  bear- 
ing on  the  nature  of  jaundice  in  a  given  patient. 

Age. — Shght  and  transient  jaundice  coming  on  v^dtliin  a  few  days 
of  birth  is  benign  or  physiological,  but  if  well  marked  and  accompanied 
by  constitutional  symptoms  and  fever,  should  suggest  a  grave  form  of 
jaundice  due  either  to  septic  infection  of  the  umbihcal  cord  or  to  some 
hsemic  infection.  (Vide  p.  561.)  Persistent  jaundice  from  birth  is  in 
favour  of  congenital  obstruction  in  the  larger  bile-ducts  {vide  p.  639) 
which  is  usually  rapidly  fatal,  but  in  rare  instances  jaundice  may  per- 
sist from  birth  into  adult  life  {vide  Hereditary  Jaundice,  p.  562).  In 
childhood  and  early  adult  life  catarrhal  jaundice  is  common.  Between 
the  ages  of  thirty  and  forty-five  years  gall-stones,  especially  in  women, 
are  the  most  probable  cause,  while  later  in  hfe  mahgnant  disease  and 
cirrhosis  must  be  taken  into  account. 

Sex. — ^Women  are  more  prone  to  gall-stones  and  to  mahgnant  dis- 
ease; men  to  cirrhosis  and  perhaps  to  the  infectious  forms  of  jaundice, 
such  as  Weil's  disease,  which  have  been  noticed  to  attack  soldiers  and 
butchers.  Pregnant  women  seem  more  susceptible  than  others  to  acute 
yellow  atrophy. 

Family  Tendency  to  Jaundice. — The  occurrence  of  jaundice  in 
several  members  of  the  same  family  may  be  clue  to  some  acute  infection, 
such  as  in  Weil's  disease,  and  is  seen  in  epidemic  jaundice.  Chronic 
jaundice  in  members  of  the  same  family  is  met  with  in  hj^Dertrophic 
bihary  cirrhosis  and  in  some  other  allied  and  rare  conditions  {vide  p. 
309).  The  disease  usually  spoken  of  as  congenital  obliteration  of  the 
bile-ducts  also  has  a  tendency  to  attack  infants  of  the  same  parents. 

Onset. — If  preceded  by  gastro-intestinal  disturbance,  catarrhal 
jaundice  should  be  thought  of;  if  by  severe  cohc,  gall-stones.  A  gradual 
onset  with  no  special  or  striking  symptoms  should  suggest  the  pressure 
of  a  tumor  on  the  ducts.  Repeated  and  transient  attacks  are  in  favour 
of  gall-stones. 

Occurrence  of  Pain. — Constant  pain  is  suggestive  of  mahgnant 
disease;  intermittent  attacks  point  to  gall-stones.  Attacks  of  bihar}^ 
cohc  may  also  occur  when  hydatid  membranes  are  passed  through  the 
ducts  and  occasionally  when  mahgnant  disease  involves  the  ducts — 
pseudo-gall-stone  colic.  Absence  of  pain  is,  however,  no  proof  against 
mahgnant  disease,  though  it  is  the  rule  in  catarrhal  jaundice  and  com- 
mon in  cirrhosis. 

Duration  and  Progress.— Jaundice  of  short  duration  is  most  com- 
monly catarrhal  or  due  to  the  passage  of  gall-stones.  If  continued  for 
more  than  six  months,  it  is  highly  unlikely  that  malignant  disease  is 
present,  and  biliary  cirrhosis  or  impacted  gall-stone  should  be  thought 
of.     Jaundice  lasting  for  years  is  probably  due  to  biliary  cirrhosis. 

Progressive  and  black  jaundice  suggest  mahgnant  disease,  while 
chronic  jaundice  which  varies  from  time  to  time  is  more  compatible  with 
a  stone  impacted  in  the  common  duct  or  biliary  cirrhosis. 

Degree  and  Intensity  of  Jaundice. — Slight  icterus  may  be  catarrhal, 
or,  if  associated  with  fever  and  constitutional  disturbance,  toxaemic. 


JAUXDICE.  553 

The  commonest  causes  of  deep  jaimdice  are  malignant  disease,  impac- 
tion of  a  gall-stone  in  the  common  duct,  and  biliary  cirrhosis.  Extremely 
deep  jaundice  almost  postulates  malignant  disease;  that  accompany- 
ing gall-stone  impaction  is  deeper  than  that  of  cirrhosis,  but  never 
equals  that  seen  in  compression  of  the  common  bile-duct  b}^  tumors, 
such  as  carcinoma  of  the  head  of  the  pancreas,  or  in  malignant  disease 
of  the  duct. 

Outbreaks  of  jaundice  in  epidemics  suggest  some  form  of  toxsemic 
or  infectious  jaundice,  such  as  Weil's  disease. 

Fever  suggests  toxsemic  jaundice  or,  when  associated  with  considera- 
ble splenic  enlargement,  biliary  cirrhosis;  pyrexia,  of  course,  occurs  in 
calculous  cholangitis,  in  hepatic  suppuration,  such  as  abscess  or  pyle- 
phlebitis, and  occasionally  in  malignant  disease. 

The  condition  of  the  gall-bladder  is  of  great  importance  in  the 
diagnosis  of  the  cause  of  jaundice.  It  is  not  enlarged  or  palpable  in 
cases  of  toxsemic  or  intra-hepatic  jaundice,  in  biliarj^  cirrhosis,  or  in  cases 
where  there  is  pressure  on  the  hepatic  ducts.  Obstruction  of  the  cystic 
duct  usually  leads  to  distension  of  the  gall-bladder  -v\dth  mucous  fluid. 
In  obstruction  of  the  common  bile-duct  by  tumors  pressing  on  it  from 
without,  such  as  carcinoma  of  the  head  of  the  pancreas,  or  arising  in 
its  walls,  the  gaU-bladder  is  distended;  on  the  other  hand,  in  obstruc- 
tion by  gaU-stones  the  gall-bladder,  contrary  to  what  might  naturally 
be  expected,  is  not  enlarged.     This  is  known  as  Courvoisier's  law. 

In  100  cases  of  obstruction  of  the  common  duct  by  causes  other  than  calculi 
the  gall-bladder  was  enlarged  in  92,  while  of  87  cases  of  calculous  obstruction  the 
gall-bladder  was  shrivelled  up  and  small  in  70,  or  80  per  cent.  (Cour\^oisier  *). 
Slayo  Robson,t  Tuffier,J  Tessier,§  and,  quite  recently,  R.  C.  Cabot  ||  have  supported 
Courvoisier's  dictum.  Cabot's  figures  are  more  striking  than  Courvoisier's,  and 
show  that  the  law  is  true  in  95  per  cent,  of  the  cases. 

The  explanation  of  the  shrivelled  condition  of  the  gall-bladder  in 
gall-stone  obstruction  of  the  common  duct  is  past  cholec^^stitis. 

Condition  of  the  Liver. — Great  enlargement  occurs  in  malignant 
disease,  h^qsertrophic  biliary  cirrhosis,  and  in  abscess.  But  in  abscess 
jaundice  is  slight  or  absent.  In  malignant  disease  the  surface  is  gener- 
ally nodular  and  the  enlargement  is  progressive;  in  hypertrophic  biliary 
cirrhosis  the  liver  is  smooth  and  the  spleen  is  much  enlarged. 

The  association  of  ascites  points  to  malignant  disease  or  cirrhosis, 
but  in  cirrhosis  jaundice  is  usually  less  marked  than  in  malignant  dis- 
ease. 

The  existence  of  disease  elsewhere  in  the  body  has  already  been  in- 
sisted on  as  of  supreme  importance  in  arriving  at  a  diagnosis  of  the  cause 
and,  therefore  of  the  prognosis  and  treatment,  of  jaimdice. 

*  Courvoisier:  Path.  u.  Chirurg.  d.  Gallenwegen,  1890. 

t  Mayo  Robson:  Gall-stones  and  Their  Treatment,  1892 

X  Tuffier:  La  Semaine  Medicale,  1893,  p.  .55. 

§  Tessier:  La  Semaine  Medicale,  1893,  p.  7. 

II  Cabot,  R.  C:  St.  Paul  Med.  Journ.,  Dec,  1901. 


554  DISEASES    OF   THE   LIVER. 


PROGNOSIS. 


The  occurrence  of  jaundice  in  certain  diseases  is  of  importance  as 
showing  that  liepatic  comphcations  have  supei^^ened;  thus  when,  as 
very  rarely  happens,  jaundice  is  met  with  in  the  course  of  typhoid  fever, 
inflammation  of  the  gall-bladder  or  ducts  should  be  thought  of.  In 
puerjoeral  eclampsia  jaundice  is  of  extremely  bad  omen;  death  usually 
follows  in  a  few  hours  or  days.  The  onset  of  jaundice  after  phosphorus 
poisoning  is  a  sign  that  the  liver  is  affected  and  must  be  regarded  as  of 
the  most  grave  significance,  since  very  few  cases  recover  when  this  stage 
is  reached.  The  onset  of  jaundice  in  a  patient  w^ho  has  had  malaria 
causes  some  anxiety  at  first,  as  it  may  be  due  to  the  severe  hseixdc  in- 
fection of  hemoglobinuria  or  "backwater"  fever.  Jaundice  in  relapsing 
fever  makes  the  prognosis  grave.      (Sandvdth.*) 

The  ultimate  prognosis  in  any  given  case  of  jaundice  depends  not 
so  much  on  the  degree  of  jaundice  as  on  the  underlying  cause.  Thus 
the  comparatively  slight  icteric  tint  (toxsemic  jaundice)  in  some  cases 
of  pyaemia  and  the  ''black"  jaundice  of  complete  obstruction  of  the 
ducts  in  malignant  disease  do  not  differ  very  materially  in  their  ulti- 
mate prognosis. 

Prognosis  in  Chronic  Jaundice.— ^\Tien  gall-stones  in  the  conmion 
duct  set  up  chronic  jaundice  there  is  a  chance,  though  rather  a  slender 
one,  that  the  calculus  or  calculi  may  pass  and  that  a  spontaneous  cure 
may  result.  ]\Iore  commonly  jaundice  may  disappear  for  a  time  as  a 
result  of  bile  escaping  by  the  side  of  the  gall-stone.  Subsequently  jaun- 
dice may  return  and  may  be  accompanied  by  periodic  attacks  of  pain, 
fever,  and  increase  in  jaundice  or  intermittent  hepatic  fever.  In  such 
cases  the  prognosis  is  good  if  operation  for  removal  of  the  calculus  is 
undertaken  before  the  patient  becomes  weak  or  deeply  jaundiced.  But 
when  continued  fever  has  developed  and  there  is  reason  to  fear  that 
suppurative  cholangitis  has  supervened,  the  prognosis  is  vei}^  grave. 

In  chronic  jaundice  of  hypertrophic  biliary  cirrhosis,  though  the 
chances  of  ultimate  recovery  are  practically  nil,  hfe  is  often  prolonged 
for  years.  In  such  cases  the  general  state  of  nutrition  and  the  length 
of  the  intervals  between  the  exacerbations  are  points  of  importance  in 
estimating  the  probable  expectancy  of  life.  Emaciation,  weakness,  and 
attacks  repeated  at  short  inten^als  point  to  death  in  the  near  future. 
In  the  rare  but  interesting  conditions  where  jaundice  is  associated  with 
splenic  enlargement  (splenomegalic  jaundice,  vide  p.  308;  and.  meta- 
icteric  splenomegaly,  vide  p.  672)  the  prognosis  is  good,  as  the  condition 
may  go  on  for  very  many  years.  In  the  extremely  rare  condition  of 
chronic  hereditary  jaundice  {vide  p.  562)  the  prognosis  is  good  after  the 
first  few  years  of  life,  but  should  always  be  verv^  guarded  in  an  infant. 

In  very  pronounced  chronic  jaundice,  due  to  whatever  cause,  the 
prognosis  is  unfavourable,  since  if  operation  is  undertaken,  there  is  con- 
siderable danger  from  heemorrhage,  even  though  heroic  doses  of  chloride 
of  calcium  are  given  before  the  operation.  A-VTiile  if  the  patient  is  not 
*  Practitioner,  vol.  Ixxii,  p.  660. 


JAUNDICE.  500 

operated  upon,  cholsemia  ^\dll  develop  sooner  or  later.  In  such  cases 
good  effects  from  iodide  of  potassium  point  to  gummatous  obstruction 
and  make  the  prognosis  good. 

In  chronic  jaundice  due  to  malignant  disease  the  prognosis  is  neces- 
sarily fatal,  but  it  is  not  quite  so  desperate  in  cases  presumed  to  be  malig- 
nant disease  of  the  pancreas  as  in  cases  where  new-gro\\i:h  is  palpable 
elsewhere.  The  explanation  of  this  statement  is  that  some  cases 
formerty  regarded  as  slow-growing  ("scirrhus")  carcinoma  of  the  head 
of  the  pancreas  are  in  reality  chronic  intei-stitial  pancreatitis.  (Mayo 
Robson.*) 

In  chronic  jaundice  much  depends  on  the  functional  activity  of  the 
kidneys  being  weU  maintained ;  if  the  amount  of  urine  falls  and  waste- 
products  are  less  freely  excreted,  bihary  toxaemia  is  likely  to  result. 
The  presence  of  albuminuria  points  to  the  kidneys  being  damaged  by  the 
toxaemia  accompanying  the  jaundice,  and  is,  therefore,  an  index  of  a 
severe  condition.  The  detection  of  leucin  and  tyrosin  in  the  urine  of  a 
case  of  jaundice  makes  the  prognosis  very  grave. 

'\^^len  jaundice  is  accompanied  by  hepatic  insufficiency,  so  that 
poisons  which  should  have  been  destroyed  by  the  liver  escape  into  the 
general  circulation  and  give  rise  to  a  general  toxaemia,  as  shown  by 
nerv^ous  symptoms,  such  as  dehrium,  drowsiness,  and  coma,  and  b}^ 
haemorrhages,  the  prognosis  is  very  grave  indeed,  since  life  cannot  be 
long  maintained  after  the  development  of  cholaemia.  The  occurrence, 
therefore,  of  nervous  symptoms  in  cases  of  jaundice  should  always  arouse 
anxiety. 

There  are  cases  at  first  quite  indistinguishable  from  simple  catarrhal 
jaundice  in  which  nervous  symptoms  somewhat  rapidly  develop,  and 
the  cases  then  run  the  course  of  acute  yellow  atrophy  of  the  liver.  Again, 
in  other  instances  the  jaundice  associated  with  malignant  disease  of  the 
liver  may  begin  exactly  Hke  catarrhal  jaundice.  Caution  is,  therefore, 
necessary  in  fonning  a  prognosis  in  the  early  stages  of  what  appears  to 
be  simple  catarrhal  jaundice,  especially  in  patients  past  middle  life. 

When  chronic  jaundice  is  accompanied  by  xanthelasma  or  by  the 
bulbous  or  "hippocratic  fingers,"  it  may  be  assumed  that  the  cause  of 
the  jaundice  is  not  malignant  disease,  inasmuch  as  this  would  have  killed 
the  patient  before  these  changes  would  have  had  sufficient  time  to  develop. 


TREATMENT. 

The  radical  and,  of  course,  the  only  satisfactory  course  is  the  removal 
or  cure  of  the  underlying  condition  of  which  jaundice  is  a  result;  for 
this  an  accurate  diagnosis  in  each  case  is  essential.  The  methods  of  treat- 
ment in  the  various  conditions  giving  rise  to  jaundice  are  dealt  with 
elsewhere,  and  will  not  be  repeated  here.  The  necessity  for  a  diagnosis 
of  the  cause  in  order  to  make  successful  treatment  possible  is  shown  by 
the  cure  of  jaundice  in  the  early  stage  of  syphilis  l)y  mercury,  or  when 
due  to  the  pressure  of  a  gumma  on  the  ducts  by  iodides,  or  surgically  by 
*  Mayo  Robson :  Lancet,  1900,  vol.  ii. 


556  DISEASES    OF   THE    LIVER. 

the  removal  of  calculi  from  the  common  bile-duct  in  intermittent  hepatic 
fever. 

In  a  large  number  of  cases  jaundice  depends  on  catarrhal  inflamma- 
tion of  the  ducts,  and  the  removal  of  this  condition  can  often  be  effected 
by  medical  measures  which  increase  the  flow  of  bile  and  so  flush  the  bile- 
ducts,  e.  g.,  draughts  of  water  containing  salts  in  solution,  drinking  the 
water  at  a  spa,  such  as  Carlsbad,  Vichy,  etc.,  and  the  administration  of 
saHcylates.  In  some  cases  medical  measures  fail  to  remove  catarrhal 
inflammation  of  the  ducts  and  surgical  interference  in  the  form  of  free 
drainage  may  be  necessary. 

Symptomatic  or  Palliative  Treatment  of  Jaundice. — Constipation 
should  be  prevented  by  exercises,  plenty  of  water,  salines,  such  as  phos- 
phate and  sulphate  of  soda,  sulphate  of  magnesia,  or  the  natural  Carls- 
bad or  other  purgative  waters,  taken  on  an  empty  stomach  before  break- 
fast. If  necessary,  a  few  grains  of  calomel  or  of  blue  pill  may  be  taken 
the  night  before.  Vigourous  purgatives  should  be  avoided,  as  intestinal 
catarrh  may  be  thus  set  up,  or,  if  present,  increased.  For  gastric 
catarrh  careful  dieting,  bicarbonate  of  soda,  and  for  vomiting  bismuth, 
dilute  hydrocyanic  acid,  and  warm  applications  to  the  abdomen  should 
be  ordered.  For  flatulence  minute  doses  {^  grain)  of  calomel  or  of 
liquor  hydrargyri  perchloridi,  salicylate  of  bismuth,  creasote,  turpen- 
tine in  capsules,  or  salol  may  be  given. 

Fresh  ox  bile  contained  in  capsules  or  keratin-coated  pills,  so  as  to 
pass  unaltered  through  the  stomach,  are  sometimes  given  to  replace  the 
absent  bile  in  the  bowel,  and  may  be  taken  three  times  a  day  before 
food. 

For  pruritus,  which  is  often  extremely  troublesome,  and,  if  unrelieved, 
may  lead  to  great  disturbance  of  the  night's  rest  and  sleeplessness,  the 
skin  may  be  sjDonged  "sviih  carbolic  acid  lotion  1  :  40,  or  the  patient  may 
take  an  alkaline  or  an  acid  bath.  An  acid  bath  containing  nitrohydro- 
chloric  acid  is  gii^en  in  a  wooden  bath,  the  patient  remaining  in  it  for 
about  twenty  minutes.*  Hypodermic  injection  of  pilocar]Dine,  ^  to  ^ 
grain,  is  often  employed  "udth  relief.  Thyroid  extract  has  been  found  to 
give  relief  by  Gilbert  and  Herscher.f  Antipyrin  is  recommended  by 
R.  CrockerJ  on  account  of  its  sedative  action  on  the  nervous  system. 
For  itching  of  the  skin  and  haemorrhages  the  administration  of  chloride 
of  calcium  in  15  or  20-grain  doses  may  be  tried  three  times  a  day  for  two 
or  three  days,  but  not  longer  at  a  stretch,  as  its  effect  in  promoting  coagu- 
lation of  the  blood  is  lost  after  a  comparatively  short  time. 

Before  an  operation,  such  as  a  cholecystotomy,  on  a  jaundiced  patient 
it  is  well  to  give  chloride  of  calcium  so  as  to  diminish  the  risk  of  bleeding 
from  the  jaundiced  tissues. 

Milk  is  the  most  satisfactory  food  in  the  early  stages,  and  as  long  as 
jaundice  is  progressive,  since  it  is  easily  digested,  minimises  intestinal 
putrefaction  and  fermentation  and  acts  as  a  diuretic.     The  patient's 

*  Tanner's  Index  of  Diseases,  4th  ed. 

t  Gilbert  and  Herscher :  Le  Bulletin  Medical,  July  30,  1902. 

X  Crocker :  Diseases  of  the  Skin,  2d  ed. 


JAUXDICE   IN   THE    NEWLY   BORN.  557 

inclination  should  be  consulted,  and  when  appetite  returns,  boiled  rice, 
chicken,  fish,  and  a  little  meat  may  be  given.  Fatty  food,  for  which 
jaundiced  patients  often  have  a  marked  distaste,  should  be  avoided. 
Alcoholic  drinks  are  also  contraindicated. 

Even  in  cases  of  inoperable  maUgnant  disease,  such  as  carcinoma  of 
the  head  of  the  pancreas,  surgical  measures  may  still  give  some  rehef  by 
removing  the  extreme  jaundice.  Cholecystenterostomy,  or  uniting  the 
gall-bladder  to  the  small  intestine,  allows  the  bile  to  enter  the  intestine 
and  thus  removes  the  jaundice,  prevents  the  occurrence  of  biliary  tox- 
aemia or  cholsemia,  and  greatly  improves  the  patient's  condition  for  a  time. 
The  operation  must  be  performed  early;  if  "black  jaundice"  has  already 
developed,  the  patient  is  in  a  very  unfavourable  state  for  this  procedure. 


JAUNDICE  IN  THE  NEWLY  BORN. 

Jaundice  occurring  within  a  few  days  or  weeks  of  birth  has  such 
special  bearings  that  it  requires  separate  consideration.  The  term 
icterus  neonatomm  has  been  specially  employed  for  the  simple  jaundice 
so  commonly  seen  ^^'ithin  a  few  days  of  birth,  but  it  is  better  to  use  it  as 
a  general  description  for  jaundice  at  or  shortly  after  birth. 

A  number  of  different  forms  of  jaundice  may  attack  newly  born 
infants. 

As  many  as  nine  varieties  have  been  tabulated  by  Skormin :  (i)  Benign  jaundice; 
(ii)  septic,  due  to  umbilical  infection ;  (iii)  infective  jaundice;  (iv)  Winckel's  dis- 
ease; (v)  catarrhal  jaundice;  (vi)  toxic  jaundice,  due  to  drugs,  such  as  carbohc 
acid,  resorcin;  (vii)  jaundice  following  hsemorrhages  into  the  skin;  (viii)  jaundice 
of  acute  yellow  atrophy;    (ix)  various  forms  of  obstructive  jaundice. 

Some  of  the  forms  are  extremely  rare;  thus  Skormin*  could  only 
refer  to  seven  examples  of  acute  yellow  atrophy  in  infants.  From  a 
practical  point  of  view  jaundice  in  infants  may  be  conveniently  divided 
into  two  main  groups:  (i)  Those  which  are  mild  and  tend  to  recover; 
(ii)  the  severe  forms  in  which  the  prognosis  is   grave. 


MILD  FORMS  OF  JAUNDICE  IN  THE  NEWLY  BORN. 

The  mild  or  innocent  forms  of  jaundice  in  the  newly  born  are:  (a) 
Idiopathic,  simple,  or  physiological  jaundice,  (h)  The  mild  infective  or 
catarrhal. 

IDIOPATHIC,  SIMPLE,  OR  PHYSIOLOGICAL  JAUNDICE. 

Etiology. — It  is,  like  many  diseases,  commoner  among  the  poor,  and 
is  known  under  the  name  of  the  "yellow  ginn."  It  is  thought  to  be  more 
frequent  in  premature  and  feeble  infants  with  deficient  resistance,  and 
has  been  said  to  be  commoner  in  males  than  in  females  (J.  L.  Steven), 
but  it  is  doubtful  whether  this  is  so.     It  has  been  suggested  that  if  the 

*  Skormin:  Jahrb.  f.  Kindcrhoilk.,  Aug.,  1902.  Epitome,  Brit.  Med.  Joum., 
1902,  vol.  ii,  No.  308. 


558  DISEASES    OF   THE    LIVER. 

cord  is  ligatured  late,  so  that  the  infant  obtains  a  niaxiniuni  of  the  placen- 
tal blood,  icterus,  presumably  depending  on  increased  haemolysis,  is  more 
likely  to  result. 

Bauzon,*  hcn^ever,  from  a  consideration  of  240  cases,  came  to  the  conclusion 
that,  far  from  favourmg  the  occurrence  of  jaundice,  delayed  ligation  of  the  um- 
bilical cord  unproved  the  resistance  of  the  infant  and  thus  tended  to  prevent  the 
onset  of  icterus. 

There  is  no  proof  that  delayed  birth  or  abnormal  presentations, 
such  as  a  breech,  are  important  factors. 

The  occurrence  of  jaundice  so  soon  after  birth  has  naturally  been 
thought  to  depend  on  events  special  to  birth  and  the  first  fe^v  days  of 
independent  existence.  Birch-Hirschfeld  thought  it  might  depend  on 
vascular  engorgement  of  the  liver  leading  to  oedema  of  the  portal  spaces, 
and  thus  to  pressure  on  the  bile-ducts.  The  postmortem  observe ations  of 
Cohnheim  failed  to  lend  any  support  to  this  view.  Moreover,  oedema  of 
the  portal  spaces,  though  it  may  be  associated  with  jaundice,  for  example, 
when  there  is  a  tumor  pressing  on  the  bile-ducts  and  lymphatic  vessels, 
does  not  of  itself  induce  jaundice. 

Quinckef  suggested  that,  owing  to  patency  of  the  ductus  venosus,  bile 
absorbed  from  the  intestine  and  on  its  way  to  the  liver  passed  from  the 
portal  vein  directly  into  the  inferior  vena  cava  and  so  into  the  general 
circulation. 

It  is  tempting  to  associate  the  microbic  invasion  of  the  previously 
sterile  intestine  with  the  appearance  of  jaundice,  especially  as  the  bile 
is  often  very  viscid.  There  is  another  factor  which,  when  taken  in  con- 
junction ^dth  microbic  infection  of  the  ahmentary  canal,  may  help  to 
account  for  icterus  neonatorum.  In  the  newly  born  there  is  an  increased 
number  of  red  blood-corpuscles  (hyperglobinaemia)  and  a  correspondingly 
increased  haemolysis.  This  would  normaUy  lead  to  an  increased  pro- 
duction of  bile,  and  if,  from  microbic  activity,  there  was  even  slight 
inflanmiation  of  the  ducts,  diffusion  of  bile  into  the  lymphatics  and 
jaundice  would  readily  result. 

Morbid  Anatomy. — "\A^ien  such  a  jaundiced  child  dies  from  accident 
or  from  other  disease,  there  is  widespread  staining  of  the  organs  and 
tissues  of  the  body  with,  the  exception  of  the  liver,  kidneys,  and  spleen. 
It  is  remarkable  that  the  brain,  spinal  cord,  and  cartilages  which  are  not 
stained  by  bile-pigment  in  the  jaundice  of  adults  are  distinctty  coloured 
by  the  bile  in  this  unimportant  condition.  The  liver  cells  contain  a  good 
deal  of  bile-pigment,  but  there  are  no  other  changes ;  the  ducts  are  nor- 
mal, and  bile  can  be  squeezed  from  the  gall-bladder  into  the  duodenum. 
The  bile  is  sometimes  found  to  be  peculiarly  viscid.  (Still. J)  The 
pericardial  fluid  contains  bile  acids  and  bile-pigment,  showing  that  there 
is  true  jaundice.  The  kidneys,  as  is  so  commonly  the  case  in  the  newly 
born,  show  masses  (''infarcts")  of  uric  acid   in  the   collecting  tubules. 

Incidence. — It  occurs  in  from  30  to  80  per  cent,  of  infants.     It  is 

*  Bauzon :  Le  progres  Medical,  April  14,  1899. 

t  Quincke:  Archiv  f.  exper.  Path.  u.  Pharmak.,  1885,  Bd.  xix. 

t  Still,  G.  F. :  Clmical  Journal,  vol.  xvii,  p.  323,  March  13,  1901. 


JAUNDICE   IN   THE    NEWLY   BORN.  559 

said  to  be  more  frequent  in  lying-in  hospitals  than  in  private  Ufe.  But 
Holt's  *  figures  from  the  Sloane  Maternity  Hospital  of  900  births  with 
300  cases  of  jaundice  (intense  in  88,  mild  in  212)  give  about  the  lowest 
incidence.  Steven, f  by  adding  up  various  statistics,  found  that  it 
occurred  1212  times  in  2086  children,  or  in  58.1  per  cent.  In  248  newly 
bom  infants  examined  by  PorakJ  it  occurred  in  80  per  cent. 

Clinical  Characters. — It  comes  on  within  the  first  four  days  of  life, 
most  commonly  on  the  second  or  third  day,  and  lasts  from  one  to  two 
weeks.  In  some  instances  it  persists  longer,  and  after  arousing  a  sus- 
picion that  there  is  some  more  serious  factor  at  work,  eventually  passes 
away.  After  its  appearance  it  increases  both  in  extent  and  in  intensity 
for  about  a  couple  of  days  and  then  gradually  diminishes.  There  are 
no  symptoms  whatever  connected  with  the  presence  of  the  jaundice — 
the  temperature,  pulse,  appetite,  and  fajces  are  normal.  The  urine  is 
free  from  bile  except  in  exceptionally  marked  cases,  and  there  is  no  albu- 
minuria. The  jaundice  begins  on  the  face,  chest,  back,  and  extends  to  the 
abdomen,  limbs,  and  lastly  to  the  hands  and  feet.  The  jaundice  shows 
up  more  prominently  because  of  the  general  cutaneous  engorgement 
of  the  newly  born  infant.  The  staining  is  perhaps  best  seen  on  the  back, 
and  can  be  distinguished  from  the  normal  redness  of  the  infant  by  press- 
ing the  blood  out  of  the  cutaneous  vessels  when  the  skin  remains  jaun- 
diced. The  gums  may  be  seen  to  be  yellow.  The  sclerotics  are  not 
always  yellow.  A  division  has  been  made  into  the  slightest  cases,  where 
the  whites  of  the  eyes  are  unaffected,  and  those  where  the  conjunctivae 
show  an  icteric  tint. 

Porak  described  three  classes — (a)  The  staining  is  slight  and  passes  away  in 
four  days,  and  involves  the  face,  back,  and  chest,  but  the  conjunctivaj  are  not 
affected,  (b)  The  jaundice  extends  to  the  abdomen,  arms,  and  thighs,  while  the 
conjunctivge  may  or  may  not  be  affected,  (c)  There  is  universal  jaundice  and  the 
conjunctivae  are  always  involved. 

It  is  difficult  to  give  a  satisfactory  explanation  of  the  curious  facts 
that  the  sclerotics  are  affected  later  and  in  a  less  degree  than  the  skin; 
exactly  the  reverse  of  what  occurs  in  ordinary  jaundice.  It  is  possible 
that  it  may  depend  upon  the  hypereemic  state  of  the  skin  and  the  cor- 
respondingly large  amount  of  blood,  containing  bile,  that  passes  through 
the  vessels  of  the  surface  of  the  body. 

Diagnosis. — It  is  distinguished  from  the  normal  reddish-brown  tint 
of  the  young  infant  by  pressing  on  the  skin  and  finding  that  the  yellow 
discolouration  remains  after  the  vessels  have  been  obliterated.  Its  short 
duration  prevents  any  confusion  with  congenital  obliteration  of  the 
ducts;  in  the  rare  instances  of  more  prolonged  simple  jaundice  there  is 
an  absence  of  the  enlarged  and  firm  liver  and  spleen  seen  in  the  former 
condition.  It  must  be  distinguished  from  the  grave  forms  of  jaundice, 
such  as  septic  infection  of  the  umbilical  vein,  syi^hilitic  disease  of  the 
liver,  and  Winckel's  disease,  by  the  healthy  condition  of  the  patient, 

='=  Holt,  E. :  Quoted  by  Osier,  Practice  of  Medicine,  ]k  r,'A,  4tli  cd. 
t  Steven,  .1.  L. :  (llasgow  Medical  .Jour.,  1897,  \()1.  \l\ii,  ]).  4. 
t  Porak:  Rev.  Mens,  de  Med.,  1878,  p.  342. 


560  DISEASES    OF  THE   LIVER. 

the  absence  of  fever,  and,  indeed,  of  every  sign  or  symptom  except 
jaundice. 

Prognosis. — In  this  condition,  for  it  cannot  be  called  a  disease,  the 
outlook  is  perfectly  cloudless.  But  in  cases  of  Jaundice  in  the  newly  born 
there  is  always  the  question  whether  the  jaundice  is  "physiological"  or 
whether  it  is  the  first  sign  of  some  grave  organic  or  septic  change.  The 
prognosis  of  jaundice  in  the  first  few  days  is,  therefore,  very  difficult  in 
the  absence  of  any  definite  diagnosis.  No  special  form  of  treatment  is 
required. 

CATARRHAL  OR  MILD  INFECTIOUS  JAUNDICE. 

In  the  first  few  days  of  life  the  alimentary  canal  normally  becomes 
invaded  by  micro-organisms,  and  sometimes  the  infection  is  more  or 
less  virulent.  The  grave  forms  of  infectious  jaundice  are  described  on 
page  561.  The  mild  forms  of  infectious  jaundice  are  much  the  same 
as  the  catarrhal  jaundice  of  adults,  and  clinically  I  do  not  think  that  any 
reliable  distinction  can  be  drawn  between  mild  infections  and  catarrhal 
jaundice.  Many  writers,  however,  consider  that  catarrhal  jaundice  is 
almost  unknown  in  infants.     Skormin*  refers  to  but  three  recorded  cases. 

The  disease  may  occur  in  epidemics  or  sporadically. 

Lesage  and  Demelin  f  have  described  a  small  epidemic  and  have  specially 
studied  the  characters  of  the  disease. 

It  may  occur  in  the  first  few  days  of  life  and  in  breast-fed  infants. 
There  is  loss  of  appetite;  vomiting  may  occur,  but  though  so  common 
in  infants,  it  is  not  specially  noticeable  in  this  form  of  jaundice;  there  is 
also  diarrhoea,  jaundice,  slight  fever,  and  drowsiness.  Lesage  and 
Demelin  lay  stress  on  the  appearance  of  cyanosis  and  on  the  fact  that 
the  stools,  which  may  contain  bile,  are  alkaline  or  neutral  instead  of 
being  acid.  The  jaundice  is  universal  and  the  urine  contains  bile-pig- 
ment, but  the  stools  need  not  be  devoid  of  bile.     The  prognosis  is  good. 

Treatment. — The  infants  should  be  kept  warm,  but  the  room  should 
be  well  ventilated.  Water  should  be  freely  given,  and  fractional  doses 
of  calomel  or  gray  powder  should  be  given  five  or  six  times  daily. 


SEVERE  FORMS  OF  JAUNDICE  IN  THE  NEW-BORN. 

The  severe  forms  of  jaundice  which  affect  the  newly  born  may  be 
divided  into — 

(1)  Those  due  to  very  definite  obstruction  or  organic  change,  such 
as  obliteration  of  the  ducts  (vide  p.  639),  syphilitic  disease  of  the  li^'er 
(vide  p.  373),  or,  in  very  rare  instances,  gall-stones. 

(2)  Virulent  infections,  either  of  a  local  nature,  as  in  umbilical 
vein  infection,  or  in  general  ha3mic  infections,  as  in  Winckel's  disease. 

*  Skormin:  Jahrb.  f.  Kinderheilk.,  Aug.,  1902. 

t  Lesage  and  Demelin:  Rev.  de  M&l.,  1898,  Jan.,  p.  14. 


JAUNDICE    IX   THE    NEWLY   BORN.  oGl 

JAUNDICE  DUE  TO  DEFJNITE  OBSTRUCTION  OR  ORGANIC  CHANGE. 

Congenital  obliteration  of  the  ducts  (p.  639)  and  jaundice  occurring 
in  hereditary'  s^^Dhilitic  disease  of  the  liver  {vide  p.  373)  are  dealt  '\\'ith 
elsewhere. 

Gall-stones. — In  very  rare  instances  gall-stones  are  found  in  the 
newly  born.  Still  *  has  collected  ten  cases  either  in  still-born  infants 
or  infants  dying  ^nthin  a  few  weeks  of  birth.  Seven  of  these  were  jaun- 
diced. It,  therefore,  appears  that  gall-stones  must  be  regarded  as  a  rare 
cause  of  se^^ere  jaundice  in  the  newly  born.  Thomsonf  puts  foiTvard 
the  suggestion  that  the  inflammation  of  the  biliar}^  tract  which  induces 
cholelithiasis  in  infants  is  probably  of  the  same  nature  as  that  responsi- 
ble for  congenital  obliteration  of  the  ducts.     {Vide  p.  639.) 

SEVERE  INFECTIVE  FORMS  OF  JAUNDICE. 

Umbilical  Infection. — A  very  fatal  form  of  jaundice  is  associated 
with  infection  of  the  navel  in  the  newly  born.  There  is  suppurative 
phlebitis  of  the  umbilical  vein.  This  form  of  pyaemia  formerly  gave  rise 
to  a  very  high  mortality  among  infants  born  in  lying-in  hospitals,  and 
has  been  prevented  by  cleanliness  and  antisepsis.  According  to  Cantlie,| 
it  is  very  common  in  Hong-Kong.  Haemorrhage  may  occur  from  the 
umbilical  wound. 

The  infection  may  be  conveyed  from  the  mother  and  is  streptococcal. 
At  the  postmortem  examination  there  is  suppurative  phlebitis  of  the 
umbihcal  vein,  and  the  liver  is  pale  and  shows  areas  of  small-cell  infiltra- 
tion in  the  portal  spaces.  There  may  be  other  pysemic  manifestations, 
such  as  peritonitis,  pleurisy,  meningitis. 

There  is  jaundice,  accompanied  by  fever  and  evidence  of  local  sup- 
puration at  the  umbilicus,  which  is  red  and  swollen. 

There  are  vomiting  and  diarrhoea;  the  respiration  and  pulse  are 
rapid.  The  child  is  first  restless,  and  then  becomes  comatose.  Death 
may  be  due  to  haemorrhage  from  the  umbilicus  or  from  the  gastro- 
intestinal tract. 

Grave  Forms  of  Jaundice  due  to  General  Infections. — Septicaemia 
may  give  rise  to  toxa?mic  jaundice  in  the  newly  born  at  the  same  time 
that  the  severity  of  the  general  hcemic  infection  produces  haemorrhages 
and  haematuria.  It  may  be  sporadic,  as  in  pyaemia  secondary  to  sup- 
])urative  arthritis  or  to  infected  epi])hyseal  disease  in  congenital  syphilis. 

Epidemic  Forms  of  Grave  Infective  Jaundice. — Epidemics  of  jaun- 
dice in  infants  accompanied  l)y  diarrhoea,  hiematuria,  and  attended  with 
great  mortality  were  described  l)y  Pollak,^  Laroyenne,  ||  Parrot,**  and 
Winckel.ft     Winckel  descrilied  an  epidemic,  wliich  i)r()\c(l  fatal  to  23 

=^  Still,  G.  F. :  Trans.  Path.  Sop.,  vol.  1,  p.  151. 

t  Thoiiison,  J.:  Ediiiburgli  Hospital  Reports,  vol.  v,  p.  1. 

X  Cantlie:  Encvclopa'dia  .Medica,  vol.  vii,  p.  41. 

§  Pollak:  \Vici;('r  ined.  Pmsso,  1871. 

II  Laroyenne:  Congres  ))our  ravaneenient  des  Sciences,  Lyon,  1S73. 
**  Parrot:  Arcliiv  Phvsiolofr.  norm,  et  path.,  1.S73,  p.  .512. 
tt  Winckel:  Deutsche  nied.  Woclien.,  Bd.  v,  S.  303,  1S79. 

36 


562  DISEASES    OF   THE    LIVER. 

out  of  the  24  infants  attacked,  under  the  name  of  pernicious  icteric 
cyanosis. 

This  disease  in  the  newly  born  has  been  called  Winckel's  disease.  It 
is  regarded  by  Lesage  and  Demelin  as  a  very  severe  form  of  infection 
of  intestinal  origin,  corresjD ending  to  the  mild  form  of  infectious  or  catar- 
rhal jaundice.  It  is  probably  a  severe  form  of  septicaemia,  and  closel}' 
resembles  Buhl's  disease,  in  which  there  are  jaundice,  gastro-intestinal 
haemorrhages,  with,  infarcts  and  acute  fatty  degeneration  of  the  organs 
of  newly  born  infants. 

The  clinical  features  are  mainly  those  of  a  severe  septicaemia  occur- 
ring in  epidemics  among  newly  born  infants  and  accompanied  by  hsema- 
turia  and  jaundice.  The  skin  has  a  bronzed  appearance,  probabty  due 
to  a  combination  of  jaundice  and  the  cyanotic  condition  of  the  skin. 
An  important  feature  is  hsematuria;  Winckel,  however,  described  haemo- 
globinuria.  The  condition  is  extremely  fatal,  and  treatment  is  prac- 
tically useless.  Treatment  should  be  directed  to  removing  the  contents 
of  the  bowels  by  jDurgatives  and  enemata.  IMinute  closes  of  calomel 
should  be  given  every  two  or  three  hours  until  eight  or  ten  doses  have 
beeii  given,  so  as  to  disinfect,  as  far  as  possible,  the  intestinal  tract.  The 
disease  differs  from  umbilical  phlebitis  in  the  absence  of  any  signs  of 
local  inflammation  about  the  navel,  and  in  the  slighter  degree  of  fever. 

'  HEREDITARY   JAUNDICE. 

Jaundice  may  occur  in  parents  and  children  and  be  an  acquired  con- 
dition, probably  due  to  some  factor  which  attacks  both  generations  at 
the  same  time.  Examples  of  hy]3ertrophic  biliary  cirrhosis  in  parents 
and  children  have  been  recorded  by  Boinet,*  and  by  Boixf  {vide  p.  309), 
but  are  more  probably  dependent  on  environment  than  on  heredit}'. 
Cases  in  which  periodic  attacks  of  jaundice  associated  with  splenic  en- 
largement have  appeared  to  be  hereditary  have  been  described  hy  C. 
Wilson,!  who  gave  an  account  of  a  family  in  which  members  in  three 
successive  generations  were  affected,  and  by  Barlow  and  Shaw.§  These 
cases,  wliich  are  rather  obscure  in  their  etiology,  appear  to  form  a  kind 
of  connecting  link  l^etween  biliary  cirrhosis  and  chronic  splenic  anaemia. 

A  few  isolated  observations,  such  as  those  of  Cocking,  ||  ArkAvright,** 
and  A.  Pick,tt  have  l^een  made,  which  raise  the  cpestion  whether  hered- 
itary jaundice  may  depend  on  shght  congenital  abnormalities  in  the  bile- 
ducts;  Pick,  however,  opposes  this  view,  and  suggests  a  congenital 
communication  between  the  bile-ducts  and  the  lymphatics.  Parkes 
WeberJJ  puts  forward  the  view  that  there  is  obliterative  cholangitis  of 
one  or  more  of  the  smaller  intra-hepatic  ducts. 

*  Boinet:  Archiv.  general,  de  Med.,  t.  clxxxi,  p.  38-5,  A]-)ril,  1S9S. 

t  Boix:  La  Presse  Medicale,  March  16,  1898. 

t  AVilson,  C:  Trans.  Clinical  Soc,  vol.  xxiii,  p.  162. 

§  T.  Barlow  and  Battv  Shaw:  Trans.  Clinic.  Soc,  vol.  xxxv,  jx  15.5. 

It  Cocking:  Qiuvrterly'Med.  .Journ.  (Sheffield),  vol.  xi,  p.  104.  1903. 
**  Arkwright :  Edinljurgh  Med.  Journ.,  Aug.,  1902. 
tt  Pick,  A. :  Wien.  klin.'  Wochens.,  1903,  S.  493. 
tt  F.  Parkes  Weber:  Edinburgh  Med.  Journ.,  vol.  xiv,  p.  111.  Ausz;.,  1903. 


ICTERUS   GRAVIS.  563 

In  Arkwriglit's  report  a  woman  who,  when  four  years  old,  had  jaundice  herself, 
had  15  children,  14  of  whom  had  jaundice,  4  surviving.  Cocking  described  a  woman 
aged  fifty  years  who  had  been  jaundiced  since  she  was  three  weeks  old  and  had 
lost  one  child  with  jaundice  at  the  age  of  fifteen  weeks.  Pick  recorded  a  family  in 
which  the  mother  and  three  children,  between  the  ages  of  thirty-five  and  twenty- 
six  years,  had  been  jaundiced  since  birth;  in  these  cases  the  urine  did  not  contain 
bile-pigment  and  the  faeces  did,  so  the  condition  may  have  been  different  from  that 
in  Arkwright's  and  Cocking's  cases,  and  more  allied  to  family  cholaemia. 

In  some  of  these  hereditary  cases  jaundice  persists  throughout  hfe 
and  is  compatible  with  fair  health. 

The  condition  of  subicterus,  described  as  simple  family  cholsemia  and 
as  a  diathesis  rather  than  as  a  fully  developed  disease,  should  be  men- 
tioned in  connexion  with  hereditary  jaundice.*  The  subjects  of  this 
diathesis  are  specially  prone  to  jaundice,  biliary  cirrhosis,  cholelithiasis, 
and  may  be  compared  to  persons  specially  liable  to  bronchitis,  pharyn- 
gitis, or  diarrhoea. 

ICTERUS  GRAVIS. 

Icterus  gravis,  or  malignant  jaundice,  is  a  term  which  is  somewhat 
loosely  used  for  cases  of  toxsemic  jaundice  of  a  severe  type  which*  tend 
to  end  fatally  and  show  extensive  degeneration  of  the  liver  cells.  It 
thus  includes  a  number  of  different  conditions,  such  as  the  most  severe 
cases  of  febrile  jaundice  or  Weil's  disease,  acute  yellow  atrophy  of  the 
liver,  phosphorus  and  other  forms  of  mineral  poisoning,  and  other  cases 
where  an  acute  toxsemic  or  infective  condition  of  the  body  falls  on  the 
liver  and  gives  rise  to  widespread  acute  degenerative  and  necrotic  changes 
in  the  liver  cells;  for  example,  in  yellow  fever  and  in  streptococcal  and 
staphylococcal  hsemic  infections.  The  term  icterus  gravis  may  also  ap- 
propriately be  applied  to  cases  where  acute  degenerative  changes  are 
superimposed  on  some  pre-existing  disease  of  the  liver,  such  as  cirrhosis 
or  nutmeg  liver. 

Icterus  gravis  should,  therefore,  be  regarded  not  as  a  specific  disease, 
but  as  a  group  of  symptoms,  due  to  the  rapid  development  of  hepatic 
insufficiency,  eventually  becoming  absolute,  which  may  be  due  to  many 
different  causes. 

Icterus  gravis  may  be  divided  into — (a)  Those  cases  where  the  liver 
was  previously  healthy — e.  g.,  in  phosphorus  poisoning,  acute  yellow 
atrophy,  and  yellow  fever.  (6)  Those  cases  where  it  supervenes  as  a 
terminal  lesion  on  pre-existing  hepatic  disease — e.  g.,  in  cirrhosis  or  chronic 
venous  engorgement. 

The  following  classification,  though  based  on  different  grounds,  is 
given  by  Boix|  and  is  much  the  same: 

,,       .„  ,       .  fin  phosphorus  poisoning, 

bpeciric  and  lonmarv       '  t         n        r 
.  ,..-,.      "'  ^^^  yellow  fever. 

'    ^       '■  ( Essential  (acute  yellow  atroi)hy). 

TVT  -r-         IT  (  In   staphylococcal  and  streptococcal 

JNon-specmc  and  always  t      .   „    ,.  •  ' 

■i      r.  1       mtcctions. 

(.  lu  infection  with  the  colon  bacillus. 

*  Gilbert  and  Lereboullot:  C'.az.  ilclHldin.  de  Mdd.  et  deChirurg.,  1902,  p.  SS9. 
t  Boix:  Manuel  de  Medecine,  edited  l)y  Debove  and  Acliard   vol.  vi,  p.  342, 


564  DISEASES   OF   THE   LIVER. 

Acute  yellow  atrophy  is  a  special  form  of  icterus  gravis  and  may  be 
regarded  as  a  typical  variety,  since  it  is  uncomplicated  by  the  presence 
of  any  other  disease.  The  terms  icterus  gravis  and  acute  yellow  atrophy 
are  not  absolutely  synonymous,  for  all  cases  of  icterus  gravis  do  not  show 
the  naked-eye  appearance  of  acute  yellow  atrophy,  though  the  change — 
acute  degeneration  in  the  liver  cells — is  essentially  the  same  in  both. 
Under  the  microscope  the  appearances  are  so  closely  allied  that  from 
a  pathological  point  of  view  they  may  be  said  to  pass  into  each  other. 
Cases  of  acute  yellow  atrophy  are  often  described  as  icterus  gravis,  and, 
conversely,  cases  of  icterus  gravis  are  sometimes  reported  under  the 
heading  of  acute  yellow  atrophy. 

Since  some  of  the  various  conditions,  such  as  acute  yellow  atrophy, 
phosphorus  poisoning,  and  Weil's  disease,  which  are  or  may  be  included 
under  the  generic  term  icterus  gravis,  will  be  separately  described,  the 
clinical  features  of  icterus  gravis  will  not  require  any  further  description 
than  that  found  under  the  heading  of  acute  yellow  atrophy.  Generally 
speaking,  the  liver  is  somewhat  enlarged  in  icterus  gravis  and  the  de- 
generative changes  are  not  so  uniform  or  so  markedly  necrotic  as  in 
acute  yellow  atrophy.  The  morbid  changes  described  under  the  head- 
ing of  Acute  Hepatitis  may  be  present  in  cases  of  icterus  gravis,  or  in 
some  instances  very  extensive  fatty  change.  (Vide  p.  425.)  In  icterus 
gravis  due  to  staphylococcal  and  streptococcal  infection  the  tempera- 
ture is  raised,  while  in  other  instances,  where  the  infective  agent  has 
been  thought  to  be  the  colon  bacillus,  the  temperature  is,  as  in  phos- 
phorus poisoning,  depressed.     (Hanot,*  Boix.t) 


ACUTE  YELLOW  ATROPHY. 

Synonym:  Acute  Atrophy  of  the  Liver. 

Definition. — An  acute  degeneration  of  the  liver  cells  with  diminu- 
tion in  size  of  the  liver,  accompanied  by  jaundice,  fever,  nervous  symp- 
toms, and  usually  a  fatal  termination. 

The  history  of  acute  yellow  atrophy  has  been  most  carefully  in- 
vestigated by  Dr.  J.  Wickham  Legg|  in  his  elaborate  account  of  the  dis- 
ease, to  which  every  subsequent  writer  on  the  subject  must  refer.  The 
earliest  case  that  he  has  unearthed  is  one  by  Ballonius,  who  died  in  1616. 
Bright,  §  in  1836,  described  the  condition  as  due  to  acute  inflamma- 
tion, and  gave  a  good  coloured  drawing  of  the  liver. 

INCIDENCE  AND  ETIOLOGY. 

That  the  disease  is  rare  is  shown  by  the  fact  that  no  case  occurred 
in  the  first  eleven  years'  work  of  the  Johns  Hopkins  Hospital,  Baltimore, 
and  that  Osier,  ||  in  the  third  edition  of  his  Practice  of  ]Medicine,  saj^s 

*  Hanot:  Archives  general,  de  Med.,  t.  clxxvii,  p.  77,  1896. 
t  Boix:  Archives  general,  de  Med.,  t.  clxxviii,  p.  217,  July,  1896. 
t  Wickham  Legg:  Bile-Jaundice  and  Bilious  Diseases,  p.  416. 
§  Bright,  R.:  Guy's  Hospital  Reports,  vol.  i,  p.  613,  1836. 
!|  Osier:  Practice  of  Medicine,  3d  and  4th  ed. 


ICTERUS   GRAVIS.  565 

that  he  had  never  seen  a  case.  Curiously  enough,  some  observers  have 
met  with  a  succession  of  cases  in  quite  a  short  time.  Reiss  saw  five  cases 
in  three  months  and  Arnold  four  in  a  similar  period. 

In  twenty  years  I  have  seen  in  the  postmortem  room  or  examined  the  livers  of 
seven  cases. 

Up  to  1S94  ^y.  Hunter*  was  only  able  to  refer  to  250  pubHshed 
cases,  and  in  the  succeeding  four  years  McPhedran  f  collected  29  more. 
In  twenty-five  years  7  cases  occurred  at  St.  Bartholomew's  Hospital, 
which,  according  to  Brunton  and  Tumiicliffe,t  is  1  in  every  500,000 
appHcations  for  treatment  at  that  charity.  In  twenty-seven  years  there 
were  11  cases  brought  to  autopsy  at  Guy's  (Hilton  Fagge  |).  ■ 

Age. — It  is  commonest  bet^v^een  the  ages  of  twenty  and  tliirty. 
According  to  Hunter's  figures,  half  the  cases  occur  in  this  decade,  and 
four-fifths  between  the  ages  of  ten  and  forty.  A  certain  proportion— 
I  have  collected  22  such  cases — occur  within  the  first  ten  years  of  fife; 
while  in  rare  instances  it  has  been  seen  within  the  first  year  or  even 
shortly  after  birth. 

Skormin  ||  refers  to  7  pubHshed  instances  of  acute  yeUow  atrophy  in  newly 
bom  infants. 

In  connexion  with  the  occurrence  of  cases  in  very  early  hfe  the 
resemblance  between  some  cases  of  icterus  gravis  and  rather  rapid  peri- 
cellular cirrhosis  of  hereditary  syiDhihs  must  be  borne  in  mind. 

The  yoimgest  case  in  which  I  have  had  the  opportimity  of  cutting  sections  of 
the  liver  was  in  a  child  aged  two  years;  the  liver  weighed  11  ounces,  and  showed 
the  naked-eye  and  microscopic  apfjearances  of  acute  yellow  atrophy.  I  am  in- 
debted to  Dr.  Schorstein  and  Dr.  O.  Griinbaum  for  the  liver  of  this  case. 

Sex. — Females  are  more  often  attacked  than  males,  the  proportion 
between  the  two  being  nearly  2  to  1.  This  greater  incidence  of  the  dis- 
ease in  women  seems  to  depend  on  a  special  association  between  preg- 
nancy and  this  disease.  The  influence  of  pregnancy  is  borne  out  by  the 
fact  that  a  large  proportion  of  the  cases  occur  in  connexion  with  this 
event.  The  liver  appears  to  be  peculiarly  susceptible  to  morbid  changes 
during  pregnancy,  and  there  is  reason  to  believe  that  degenerative  changes 
in  the  liver  play  a  very  important  part  in  the  production  of  puerjDeral 
eclampsia.  It  is  not  impro]3able  that  the  discrete  focal  necrosis  in  the 
liver  seen  in  eclam])sia  represents  in  a  lesser  degree  or  in  an  earlier  stage 
the  changes  of  acute  yellow  atrophy.  Statistics  show  that  acute  yellow 
atrophy  occurs  most  often  between  the  fourth  and  seventh  months  of 
pregnancy. 

Mental  disturbance,  shock,  or  fright  has  preceded  the  onset  of  the 
disease  in  a  certain  numl)er  of  cases.  The  mental  worry  in  j^ersons  with 
s}q)hilis  or  in  women  that  are  pregnant,  especially  if  unmarried,  may 

*  Hunter,  W. :  Allbutt's  System  of  Medicine,  vol.  iv. 

t  McPhedran,  A. :  Sajous'  Annual,  1899,  vol.  iv,  p.  393. 

i  Brunton  and  Tuiinicliffe:  St.  Bartholomew's  Hosp.  Reports,  vol.  xxxii. 

§  A  Text-book  of  INIedicine,  edited  by  Pye  Smith,  vol.  ii,  p.  544,  4th  ed.,  1902. 

II  Skormin:  Jahr.  f.  Kiiulerheilk.,  Aug.,  1902. 


566  DISEASES   OF   THE   LIVER. 

tend  further  to  depress  the  resistance  of  the  body  and  to  dispose  to  the 
disease. 

In  six  fatal  cases,  recorded  by  Hardie,*  of  acute  yellow  atrophy  of  the  liver  in 
Australia,  importance  was  attached  to  the  anxiety  and  fear  with  which  women 
look  forward  to  parturition  in  hot  climates. 

Syphilis. — The  secondary  stage  of  syphiHs  is  sometimes  accom- 
panied by  jaundice,  which  is  usually  harmless  and  yields  to  specific 
treatment.  In  rare  instances  acute  yellow  atrophy  supervenes.  This 
is  said  to  be  more  often  seen  in  women  than  in  men.  The  syphilitic 
toxine  would  appear  to  attack  the  liver  acutely,  just  as  it  sometimes 
attacks  the  spinal  cord,  giving  rise  to  acute  myelitis. 

In  72  cases  of  acute  yellow  atrophy  syphilis  was  noted  as  a  causal 
factor  in  7  (Lebertt).  In  9  cases  of  acute  atrophy  following  syphiHs 
collected  by  Chauffard,  J  7  were  in  women.  I  have  references  to  28  cases 
of  post-syphilitic  acute  atrophy  of  the  liver. 

In  some  of  the  cases  the  jaundice  has  run  a  long  course,  and  although 
the  morbid  appearances  are  like  those  of  acute  yellow  atrophy,  it  is 
probable  that  for  a  considerable  time  the  jaundice  is  due  to  pericellular 
cirrhosis  and  that  a  terminal  and  acute  degeneration  of  the  liver  ceUs 
develops.     This  would  place  the  cases  in  the  category  of  icterus  gravis. 

In  a  case  reported  years  ago  Hilton  Fagge  §  drew  particular  attention  to  the 
resemblance  between  the  appearances  of  pericellular  cirrhosis  and  those  in  a  case 
of  acute  atrophy  supervening  on  the  secondary  stage  of  syphilis. 

As  already  mentioned,  the  mental  anxiety  experienced  by  persons 
who  are  aware  that  they  have  contracted  syphilis  has  been  thought  to 
play  a  part  in  the  production  of  acute  atrophy. 

Talamon  ||  has  described  an  interesting  case  in  which  a  severe  fright  in  a  girl 
aged  seventeen,  who  had  secondary  roseola,  enlarged  glands,  and  condylomata  at 
the  time,  was  followed  within  eighteen  hours  by  "emotional  jaundice";  this  lasted 
three  weeks  and  symptoms  of  acute  yellow  atrophy,  hsemorrhages,  delirium,  and 
convulsions  carried  her  off  on  the  twenty-ninth  day.  The  liver  was  in  a  state  of 
acute  parenchymatous  and  interstitial  inflammation.  In  this  case  the  emotional 
jaundice  seems  to  have  rendered  the  liver  more  susceptible  to  the  effects  of  the 
syphilitic  toxine. 

The  following  case,  for  which  I  am  indebted  to  Dr.  A.  H.  Wilson,  illustrates 
some  of  the  features  of  acute  yellow  atrophy  due  to  syphilis.  A  girl  aged  seventeen, 
with  a  sore  on  the  right  labium  and  a  roseolous  rash,  became  jaimdiced  six  weeks 
before  death.  Three  days  later  she  began  to  vomit  and  continued  to  do  so  until  her 
death;  at  no  time  was  there  blood  in  the  vomit.  Three  weeks  before  death  jaundice 
increased,  her  mental  condition  was  affected,  delirium  supervened,  and  the  urine 
and  faeces  were  passed  involuntarily.  She  became  extremely  hungry  and  suffered 
from  thirst.  She  was  admitted  to  the  South  Devon  and  East  Cornwall  Hospital 
in  a  state  of  collapse  twenty-four  hours  before  her  death.  There  were  bile-pigment, 
leucin,  and  tyrosin  in  the  urine.  She  died  comatose.  The  liver,  which  I  exam- 
ined microscopically,  showed  great  destruction  of  the  liver  cells  and  haemorrhages, 
with  some  pre-existing  fibrosis  often  passing  between  tlie  cells.  These  appearances 
suggested  a  combination  of  pericellular  cirrhosis  and  acute  necrosis  of  the  cells. 

*  Hardie,  D. :  Australian  Med.  Gaz.,  Mav,  1890. 

t  Lebert:  Virchow's  Archiv,  Bd.  vii,  S.  383. 

t  Chauffard:  La  presse  Med.,  Aug.  11,  1897. 

§  Hilton  Fagge:  Trans.  Path.  Soc,  vol.  xviii,  p.  136. 

II  Talamon :  La  Medecine  Moderne,  Feb.  13,  1897. 


ICTERUS   GRAVIS.  567 

Alcoholic  excess  in  a  few  instances  has  apparently  stood  in  a  causal 
relation  to  acute  3"ellow  atrophy ,  since  the  disease  has  been  noted  to 
come  on  after  recent  and  undoubted  excessive  indulgence. 

Thierfelder  *  refers  to  six  such  cases  among  his  143  cases  of  acute  atroph)-, 
and  cases  have  been  described  by  Moxon,t  Cayley,t  Carrington,§  Musser.  1| 

Acute  yellow  atrophy  may  occur  in  chronic  drunkards,  and  acute 
atrophy  has  been  described  as  supervening  on  existing  cirrhosis.  Thier- 
felder quotes  eight  cases  of  this  kind.  It  must,-  however,  be  borne  in 
mind  that  cases  of  protracted  acute  atrophy  may  show  some  recent 
fibrosis.  Inasmuch  as  alcohol  is  a  protoplasinic  poison,  it  is  not  im- 
probable that  the  resistance  of  the  liver  being  diminished  by  alcoholic 
excess,  other  causes  making  for  acute  yellow  atrophy  are  thus  enabled 
to  become  effective. 

Chloroform  narcosis  has  in  most  exceptional  instances  been  followed 
by  acute  yellow  atrophy.  Chloroform  has  a  toxic  effect  on  the  liver 
cells,  but  is  so  rarely  seen  in  practice  that  additional  factors,  such  as 
sepsis  and  diminished  resistance  of  the  liver,  must  be  necessary  to  ex- 
plain the  occurrence  of  acute  yellow  atrophy  after  the  administration  of 
chloroform.     (Compare  p.  425.) 

Max  BaUin  **  has  collected  nine  fatal  cases  of  acute  yellow  atrophy  after  opera- 
tions. 

The  Influence  of  Pre-existing  Hepatic  Disease. — The  lesions  of 
acute  yellow  atrophy  may  supervene  in  the  course  of  diseases  of  the 
liver,  such  as  cirrhosis,  catarrhal  jaundice,  chronic  venous  engorgement, 
or  gall-stone  obstruction.  The  onset  is,  no  doubt,  disposed  to  by  the 
morbid  condition  of  the  organ.  In  these  cases  it  is  more  convenient  to 
describe  the  condition  as  icterus  gravis  rather  than  as  acute  yellow 
atrophy.  Impaired  vitality  and  resistance  on  the  part^  of  the  hver  must 
render  it  more  susceptible  to  acute  infectious  or  toxic  influences,  and  so 
to  acute  atrophy.  This  very  probably  accounts  for  the  influence  of  preg- 
nancy in  disposing  to  acute  yeUow  atrophy.  The  occurrence  of  such  a 
rare  disease  in  two  sisters  (Graves  ff),  and  in  a  brother  and  sister 
(GriffinfJ),  suggests  the  possibility  that  congenital  want  of  resistance 
may  be  a  factor  of  importance. 

Relation  to  Phosphorus  Poisoning. — Inasmuch  as  there  is  a  marked 
resemblance  between  the  clinical  features  of  acute  yellow  atrophy  and 
phosphorus  poisoning,  and  since  the  nature  of  the  change  in  the  liver 
cells  is  essentially  the  same,  viz.,  one  of  acute  degeneration,  it  has  been 
thought  that  all  cases  of  acute  yellow  atrophy  are  due  to  phosphonis 
poisoning.     In  support  of  this  it  might  be  urged  that  examples  of  what 

*  Thierfelder :  v.  Zicmssen's  Cyclopajdia  of  the  Practice  of  Medicine,  vol.  ix, 
p.  245.  t  Moxon:  Trans.  Path.  Soc,  vol.  xxiii,  p.  138. 

t  Cayley:  Trans.  Path.  Soc,  vol.  xxxiv,  p.  127. 

§  Carrington:  Trans.  Path.  Soc,  vol.  xxxvi,  p.  221. 

II  Musser:  American  Journ.  Med.  Sciences,  vol.  Ixxxvii,  July,  LSS4. 
**  Max  Ballin :  Annals  of  Surgery,  March,  1903,  p.  3G2. 
tt  Graves:  Clinical  Medicine,  p.  459. 
XX  Griffin:  Dublin  Journal  of  Medical  and  Chemical  Science,  1S31. 


568  DISEASES    OF   THE    LIVER. 

were  for  a  time  considered  undoubted  instances  of  acute  yellow  atrophy 
have  on  further  enquiry  turned  out  to  be  due  to  phosphorus  poisoning. 
Poore,*  who  quotes  cases  of  this  kind;  unhesitatingly  believes  that 
chnically  and  pathologically  the  two  conditions  are  incUstinguishable. 

Generally  speaking,  however,  the  differences  between  the  two  con- 
ditions are  sufhcientty  definite  to  separate  them,  and  we  are  certainly 
not  justified  in  assuming  that  all  cases  of  acute  yellow  atrophy  are  due 
to  phosphorus  poisoning.  These  differences  between  the  liver  in  phos- 
phorus poisoning  and  acute  yeUow  atrophy  are — 

(1)  In  acute  yellow  atrophy  the  diminution  in  size  is  practically 
constant,  whereas  in  phosphorus  poisoning  enlargement  is  the  rule. 
(2)  In  acute  yeUow  atrophy  the  changes  in  the  liver  cells  lead  to  rapid 
disintegration  vith  but  slight  increase  in  the  amount  of  fat;  while  in 
phosphorus  poisoning  there  is  very  extensive  fatty  metamorphosis  of  the 
liver  cells,  the  amount  of  fat  in  the  organ  reaching  30  per  cent,  as  against 
5  per  cent,  in  acute  yellow  atrophy. 

SchmauSjt  however,  believes  that  these  differences  are  merely  a  matter  of  time 
and  that  as  death  occurs  more  rapidly  in  phosphorus  poisoning,  there  is  not  time 
for  the  absorption  and  removal  of  fatty  and  degenerative  products.  "^Mien  life 
is  prolonged,  the  condition  resembles  that  of  acute  yellow  atrophy. 

It  mSLj  be  safely  stated  that  they  are  closeh^  alhed  forms  of  icterus 
gravis,  but  at  present,  for  purposes  of  chnical  practice,  it  is  convenient 
to  regard  them  as  distinct  entities. 

MORBID  ANATOMY. 

Weight  and  Size. — The  liver  is  always  greatly  diminished  in  size; 
in  fact,  cases  otherwise  resembhng  acute  atrophy,  in  which  the  organ  is 
large,  belong  to  the  aUied  condition  of  icterus  gramas,  for  diminution  in 
size  is  an  essential  part  of  acute  yellow  atrophy.  It  may  weigh  half  or 
a  third  of  its  normal  weight.  Twenty-eight  ounces  is  not  uncommonly 
found  instead  of  the  normal  (53  ounces  in  males,  45  ounces  in  females). 
The  atrophied  condition  is  usually  fairly  universal,  but  the  left  lobe  is 
often  in  a  more  advanced  state  than  the  remainder,  and  the.  change  is 
often  thought  to  begin  there.  In  acute  cases  the  surface  is  smooth  and 
flaccid.  In  cases  wiiich  have  had  a  prolonged  illness — several  weeks  or 
months — adenomatous  nodules  resembhng  new-growths  may  be  seen  on 
the  surface. 

They  have  been  described  in  cases  which  died  one  and  a  half  to  two  years  after 
the  onset  of  acute  sjTnptoms.  In  Steinhaus'J  case  the  total  duration  was  twenty- 
one  months  and  m  Stroebe's  §  two  years. 

They  are  due  to  compensatory  hyperj^lasia  of  the  liver  cells,  and  are 
therefore  analogous  to  the  multiple  adenomata  in  cirrhosis.     These  pro- 

*  Poore,  G.  Y. :  Nervous  Affections  of  the  Hand  and  Other  Clinical  Studies, 
p.  166,  1897. 

t  Schmaus :  A  Text-book  of  Pathology  and  Pathological  Anatomy,  p.  396 
American  translation,  190-3. 

t  Steinhaus:  Prag.  med.  Wochen.,  1903,  S.  323. 

§  Stroebe:  Ziegler's  Beitriige,  Pd.  xxi,  S.  379,  1897. 


ICTERUS   GRAVIS.  569 

tracted  cases  merge  into  a  condition  of  nodular  parenchymatous  hepa- 
titis.* 

Cayley  f  described  and  figured  a  good  example  of  acute  attophj*  in  wliicli  there 
were  definite  tumor-like  projections  from  the  surface  of  both  lobes  of  the  liver. 
In  the  figure  accompanying  the  account  the  projections  seem  to  correspond  with 
the  yeUow  atrophy  and  the  depressed  areas  with  red  atrophy.  There  is  a  somewhat 
similar  specimen  from  a  child  in  the  museum  of  Charing  Cross  Hospital.  In  Mac- 
Callum's  t  case  these  h5'perplastic  nodules  were  green  in  colour. 

The  capsule  is  wrinkled  and  loose,  so  that  it  can  be  picked  up  by 
the  fingers,  like  the  walls  of  a  half-filled  bladder.  If  a  stream  of  water 
is  turned  on  to  the  organ,  the  capsule  is  thrown  into  folds  and  wrinkles. 
It  can  be  peeled  off  quite  easily  in  many  cases.  Externally  the  organ 
has  a  greenish-yellow  colour,  often  relieved  by  red  splashes.  There 
may  be  small  haemorrhages  under  the  capsule.  The  liver  is  flabby  and 
limp,  and  collapses  and  bends  under  its  own  weight;  thus  it  readily 
doubles  over  on  itself  and  is  without  the  rigidity  of  a  normal  liver.  This 
flabbiness  of  the  organ  during  fife  allows  it  to  drop  back  from  the  ab- 
dominal waU,  its  place  being  taken  by  the  colon.  As  a  result,  the  liver 
dulness  may  be  entirely  absent.  The  liver  cuts  with  the  same  kind  of 
resistance  that  collapsed  lung  does,  and  though  very  flabby,  is  not 
softer  or  more  easily  broken  down  by  the  finger  than  in  health.  Many 
writers,  however,  state  that  the  liver  is  softened.  Possibly  this  is  more 
true  in  icterus  gravis.  If  kept  for  some  time,  the  surface  of  the  liver 
becomes  covered  with  a  white  efflorescence  which  is  composed  of  crys- 
tals of  leucin  and  tyrosin. 

On  section  of  the  organ  the  surface  is  seen  to  be  of  a  bright  yellow 
colour.  Usually  in  addition  to  the  more  general  yellow  atrophy  there 
are  areas  of  red  atrophy.  As  a  nde,  there  is  more  of  the  yellow  change, 
but  in  some  rare  examples  of  what  have  been  caUed  acute  red  atrophy, 
diffuse  red  atrophy  greatly  predominates  or  is  universal. 

In  the  red  areas  the  degenerative  change  is  of  oldest  duration,  while 
in  the  yeflow  areas  it  is  more  recent.  The  longer,  therefore,  the  patient 
lives,  the  greater  will  be  the  extent  of  the  red  change  found  after  death. 
The  only  exception  to  this  general  statement  is  that  in  prolonged  cases, 
where  compensator}'-  hypei-plasia  has  taken  place,  there  may  be  nodular 
masses  composed  of  proliferating  liver  cehs  which  may  be  yellow  or  green 
and  contrast  with  the  surrounding  red  atrophy. 

In  the  areas  of  red  atrophy  al)sor|3tion  of  the  necrotic  and  degenerated 
cells  and  of  fat  has  taken  place,  and  the  only  tissue  left  is  the  fibrous 
matrix  and  the  capillaries  which  account  for  the  red  colour.  Red  atrophy 
is  thus  a  further  stage  of  the  yellow  atrophy  and  not  an  independent 
change.  The  areas  of  red  atrophy  are  sunken  and  depressed  below  the 
level  of  the  yellow  areas.  It  is  often  more  marked  in  the  left  than  in  the 
right  lobe. 

The  outlines  of  the  lobules  are  lost  in  the  red  areas  and  with  difficulty, 
if  at  all,  discernible  in  the  yellow  areas;  if  visible,  they  are  much  smaller 

*  Compare  Trans.  Path.  Soc,  vol.  xliii,  p.  83. 

t  Cayley,  W. :  Path.  Trans.,  vol.  xxxiv,  p.  127. 

t  MacCalluni;  W.  (i.:  Johns  Hopkins  Hosp.  Reports,  vol.  x,  ]i.  375,  1902. 


570  DISEASES   OF  THE   LIVER. 

than  in  health.  The  gall-bladder  contains  bile,  often  thick  from  mucus, 
but  the  larger  bile-ducts  often  show  only  mucus.  Budcl*  describes  a 
case  in  which  the  bile  was  markedty  acid. 

The  amount  of  fat  which  can  be  extracted  from  the  liver  is  increased 
by  about  5  per  cent,  above  the  normal,  but  this  is  far  below  the  amount 
of  fat  which  can  be  obtained  from  the  liver  in  acute  phosphorus  poison- 
ing. Possibly  the  fat  is  absorbed  in  acute  atrophy,  while  in  phosphorus 
poisoning  this  does  not  occur.  But  however  this  may  be,  the  difference 
in  the  amount  of  fat  is  a  point  of  distinction  between  the  two  conditions. 

Alonzo  Taylor  f  found  no  more  fat  in  the  liver  of  a  case  of  acute  atrophy  than 
in  a  normal  liver,  but  he  found  excess  of  a  free  fatty  acid,  and  albumose,  leucin,  and 
asparaginic  acid. 

A  scraping  of  the  fresh  section  shows  under  the  microscope  blood- 
corpuscles,  degenerated  liver  cells,  and  crystals  of  leucin,  tyrosin,  and 
xanthin.  lycucin  and  tyrosin  may  be  found  in  the  blood  of  the  veins 
of  the  liver,  in  the  kidne.ys,  and  in  the  spirit  in  which  portions  of  the  liver 
have  been  preserved.  In  the  alcoholic  extract  of  the  liver  of  acute 
yellow  atrophy  that  had  been  kept  for  two  years  Delepinet  found 
Charcot-Leyden  crystals. 

Crystals  of  leucin  and  tyrosin  may  be  seen  in  fresh  sections,  but  for 
any  satisfactory  examination  of  the  histological  condition  of  the  liver 
properly  hardened  sections  are  necessary.  Little  reliable  information 
can  be  obtained  from  fresh  sections  made  by  the  freezing  method.  It 
is,  indeed,  a  matter  of  ordinary  experience  that  fresh  sections  exaggerate 
existing  disorganization  of  the  liver.  The  liver,  especially  from  a  septic 
case,  if  allowed  to  decompose  a  little  and  then  examined  by  means  of 
fresh  sections,  shows  much  more  apparent  change  in  destruction  of  liver 
cells  than  a  hardened  section  of  the  same  specimen. 

Histologically,  the  appearances  vary  very  greatly,  not  only  in  dif- 
ferent parts  of  the  organ,  such  as  the  areas  attacked  by  the  yellow  and 
by  the  red  atrophic  change  respectively,  but  in  different  microscopic 
fields  of  the  same  section.  It  mil  be  weU  to  describe  the  slighter  changes 
first  and  then  to  pass  to  the  more  advanced  stages.  The  liver  cells  ma}' 
show  considerable  fatty  change,  and  in  some  parts  of  the  liver  this  may 
be  the  chief  alteration.  In  other  parts  the  liver  cells  are  granular,  bile- 
stained,  and  show  fragmentary  degeneration  of  the  nuclei,  which  stain 
badly.  Haemorrhages  occur  between  the  degenerated  liver  cells,  and 
as  the  cells  begin  to  undergo  a  further  stage  of  necrosis,  they  cease  to 
stain.  These  changes  begin  and  are  most  marked  at  the  periphery  of 
the  lobules,  and  pass  in  towards  the  intralobular  vein.  The  small  bile- 
ducts  are  in  a  condition  of  cholangitis;  there  is  proliferation  of  the  epi- 
thehal  cells,  which  are  discharged  into  the  lumen  of  the  duct  and  by 
obstruction  cause  jaundice.  Tater,  necrosis  of  the  cells  lining  the  small 
ducts  occurs.  Proliferative  changes  in  the  interlobular  bile-ducts  lead 
to  the  production  of  colunms  of  cells  which  pass  into  the  lobules  and  may 

*  Budd:  Diseases  of  the  Liver,  p.  264,  1857. 

t  Alonzo  Taylor:  Joum.  Med.  Research,  vol.  viii,  p.  -424. 

X  Del^pme,  S. :  Trans.  Path.  Soc,  vol.  xlii,  p.  45S. 


ICTERUS   GRAVIS. 


571 


be  regarded  as  an  attempt  at  compensatory  hj-peiplasia.  In  some  sec- 
tions the  process  of  regeneration  can  be  seen  to  be  commencing  in  the 
liver  cells,  which  are  collected  into  solid  columns,  so  as  to  imitate  a 
primitive  tubular  liver.  These  cellular  strands  are  separated  from  each 
other  by  fibrillar  tissue,  capillaries,  or  the  debris  of  the  degenerated 
lobule.  The  liver  cells  may  be  much  larger  than  natural,  contain  several 
nuclei,  and  may  give  the  impression  of  being  made  up  of  several  liver 
cells  which  have  iim  together.     {Vide  Fig.  72.) 

In  the  more  advanced  stages — ^that  is,  in  the  areas  of  red  atrophy — 
the  cells  of  the  lobules  have  completely  disappeared  as  the  result  of  very 
acute  necrotic  changes,  and  nothing  can  be  seen  except  the  skeleton  of 
the  lobules,  formed  of  the  fibrillar  vascular  connective  tissue,  enclosing 
a  few  nuclei  and  red 
blood-corpuscles.  Some- 
times the  necrosis  is  so 
complete  and  widespread 
that  it  is  difficult  to  rec- 
ognise the  tissue  as  hver 
or  to  make  out  the  to- 
pography of  the  section. 
There  is  often,  but  not 
always,  evidence  of  in- 
flammatory reaction  in 
the  connective  tissue  of 
the  hver  and  signs  of 
compensatory  changes  in 
the  remaining  liver  ceUs. 

Thus  there  may  be 
a  small-cell  infiltration 
starting  from  the  portal 
spaces  and  spreading 
into  the  peripheral  parts 
of  the  lobules;  a  similar 
small  -  cell  infiltration 
may  also  be  seen  around 
the  central  venula  of  the 
lobules. 

In  chronic  cases  where  there  has  been  prolongation  of  life  and  an 
approach  towards  recovery,  fibrosis,  often  intimate  and  resembling  peri- 
cellular cirrhosis,  may  be  found.  It  is,  indeed,  impossible  to  draw  a 
reliable  distinction  between  prolonged  cases  of  acute  yellow  atrophy  of 
the  liver  and  acute  cirrhosis.  The  proliferative  changes  in  the  inter- 
lobular bile-ducts  will  be  described  in  the  next  paragraph  on  the  re- 
generative changes. 

Regenerative  Changes. — Cases  of  acute  yellow  atrophy    which  do 

not  run  a  very  acute  course   show  changes  in  the  small  bile-ducts  and 

liver  cells  which  may  be  regarded  as  regenerative  and  compensatory 

in  character.    These  changes  have  been  specially  studied  by  Marchand  * 

*  Marchand:  Zicgler's  Bcitriige,  Bd.  xvii,  S.  200,  1S95. 


Fig.  72. — Drawing  of  Microscopic  Section  of  the  Liver 
IN  Acute  Yellow  Atrophy,  Showing  Acute  Degen- 
erative Changes  in  the  Liver  Cells. 
Many  of  the   cells  are   destroyed,  the  nuclei   of  some 

only  remaining  in  the  debris.  There  are,  in  addition,  groups 

of  liver  cells  and   some  with  two  or  more  nuclei — evidence 

of  regeneration.      X.  140. 


572 


DISEASES   OF  THE   LIVER. 


Meder,*  Stroebe.f  Barbacci,^  Ibrahim,^  and  W.  G.  MacCallum.  1|  The 
liver  cells  in  the  early  stages  of  regeneration  show  mitotic  figures  and 
later  hyperplasia,  so  that  columns  of  liver  cells  are  formed  resembhng 
a  tubular  formation;  the  liver  cells  may  become  much  enlarged,  espe- 
cially around  the  intralobular  vein,  and  may  contain  several  nuclei. 
Sometimes  this  compensatory  h3q3erplasia  occurs  only  in  one-half  of  a 
lobule,  the  liver  cells  in  the  remainder  having  been  too  much  necrosed 
to  undergo  any  compensatory  hyperplasia;  in  this  event  the  intralobular 
"S'ein  may  appear  at  the  margin  of  the  fresh  mass  of  liver  cells.  This 
method  of  regeneration  of  the  liver  cells  leads  to  the  production  of  hyper- 
plastic or  "adenomatous"  nodules  in  the  liver,  which  project  above  the 
surface  of  the  surrounding  parts.     In  cases  where  the  liver  cells  have 


Fig.  73. — Dhawing  of  a  Microscopic    Section  of  Acute  Yellow  Atrophy  of  the   Liver, 

Showing   Extensive  Necrosis  of  the  Liver  Cells. 
Around  the  periphery  of  the  lobules  there  are  small-cell  infiltration  and  groups  of  liver  cells. 

X  30. 


been  completely  destroyed,  regeneration  is  brought  about  in  another  way. 
As  a  result  of  proliferation  of  the  interlobular  bile-ducts  blind  bile-ducts 
work  their  way  into  the  degenerated  lobule.  The  cells  forming  these 
projections  increase  in  size  and  become  like  liver  cells.  The  terminal 
cells  in  the  invading  masses  of  cells  show  karyokinetic  figures  and  are 
evidently  proliferating.  Stroebe  and  MacCallum  have  specially  insisted 
on  these  points  and  are  opposed  to  ]\Iarchand's  earlier  view  that  these 
colunms  of  cells  are  derived  from  apposition  of  degenerating  liver  cells. 

*  Meder:  Ziegler's  Beitrage,  Bd.  xvii,  S.  143. 

t  Stroebe:  Ziegler's  Beitrage,  Bd.  xxi,  S.  379,  1897. 

j  Barbacci:  Ziegler's  Beitrage,  Bd.  xxx,  S.  49,  1901. 

§  Ibrahim:  Miinchen.  med.  Wochen.,  1901. 

II  MacCallum,  W.  G. :  Johns  Hopkins  Hosp.  Reports,  vol.  x,  p   379,  1902. 


ICTERUS   GRAVIS.  573 

To  sum  up,  regeneration  occurs  in  two  ways:  (i)  From  hyi^erplasia  of 
pre-existing  liver  cells,  and  (ii)  from  hj^perplasia  of  the  interlobular  bile- 
ducts  by  means  of  which  cells  approaching  Hver  cells  are  produced. 

Micro-organisms  have  been  found  in  some  cases,  but  not  in  others, 
and  no  definite  causal  connexion  can  be  said  to  exist  between  any  micro- 
organism and  the  changes  found. 

The  colon  bacillus,  though  often  found  after  death,  can  hardly  be  regarded  as 
the  causal  agent,  as  there  may  easily  be  postmortem  invasion  of  the  organ.  Strep- 
tococci, staphylococci,  pneumococci,  have  also  been  reported  in  some  cases. 

Probably  several  different  kinds  of  micro-organisms,  as  well  as 
several  poisons,  are  capable  of  producing  the  acute  inflanimator}^  and 
degenerative  changes  characteristic  of  acute  yellow  atrophy  of  the  liver. 

The  kidneys  are  swollen,  soft,  bile-stained,  and  show  small  hsemor- 
rhages.  Microscopically  the  epithelium  of  the  tubules  shows  degenera- 
tion. 

The  spleen  is  often  softened,  as  in  infective  disease,  and  often  en- 
larged. 

In  71  cases  Wickham  Legg  found  the  spleen  larger  than  natural  in  43.  He 
quotes  Liebermeister's  statistics  of  87  cases,  in  56  of  which  the  spleen  was  enlarged. 

The  heart  is  softened  and  swollen  and  shows  cloudy  swelling.  The 
blood,  as  in  other  toxic  and  septic  conditions,  stains  the  walls  of  the 
vessels  and  coagulates  imperfectly.  Haemorrhages  are  found  scattered 
through  the  body  on  the  cutaneous,  mucous,  and  serous  surfaces. 
Meningeal  and  cerebral  (Politzer,*  I;afitte  f)  haemorrhages  have  been 
known  to  occur.  Toxic  changes  in  the  vessel  walls  allow  extravasation 
to  take  place.  Brunton  and  Tunnichffe  point  out  that  viperine  poison 
has  the  same  effect  when  applied  locally  to  the  mesentery  of  a  frog. 

The  gastro-intestinal  tract  shows  evidences  of  catarrhal  inflamma- 
tion and  patchy  hemorrhage,  or  small  areas  of  necrosis  may  be  found. 
Altered  blood  may  be  found  in  the  stomach  and  intestines.  A  slight 
amount  of  ascitic  fluid  in  the  peritoneum  is  not  uncommon. 

Pancreas. — Degenerative  changes  in  the  acini  of  the  gland,  the  islands, of 
Langerhans  being  unaffected,  have  been  described  by  Sacquepec,t  who  lays  some 
stress  on  this  since  the  pancreatic  juice  has  been  found  to  have  the  power  of  de- 
stroying the  toxines  of  diphtheria,  tetanus,  etc. 

Changes  in  the  Central  Nervous  System. — In  addition  to  meningeal 
and  cerebral  haemorrhages  already  referred  to,  degenerative  changes, 
analogous  to  the  toxic  changes  seen  in  a  more  chronic  form  in  comloined 
sclerosis  and  in  grave  anaemia,  have  been  described  by  Goldscheider  and 
Moxter.  § 

PATHOGENY. 

The  essential  factor  is  a  very  acute  necrotic  degeneration  of  the  liver 
cells  resembling  that  produced  by  bacterial  toxines,  with  evidences  of 

*  Politzer:  Jahrb.  f.  Kinderlioilk.,  ISOO. 
t  Lafitte:  Bull.  Soc.  Anat.  Paris,  1S91. 

X  Sacquepec:  Archiv.  de  Mod.  ]']xi)i'riment.  ct  d'Aiiatoiuic  ]iath.,  t.  xiv,  p.  485. 
.Tulv,  1902. 

§  Goldscheider  and  Moxlcr:  Fortscliritl.  <l.'r  Med.,  lSi)7,  No.  14. 


574  DISEASES    OF   THE    LIVER. 

inflammation  in  the  supporting  fibrous  tissue  of  the  organ.  The  condi- 
tion is  a  very  acute  hepatitis ;  comparatively  chronic  or  protracted  cases 
have  been  regarded  as  acute  cirrhosis.  It  is  analogous  to,  but  more  ad- 
vanced than,  the  toxic  changes  seen  in  the  liver  in  phosphorus,  iodoform, 
or  arsenic  poisoning,  or  in  lupinosis. 

In  Germany  many  sheep  die  with  jaundice,  haemorrhages,  delirium,  and  acute 
yellow  atrophy  of  the  liver  as  a  result  of  eating  certain  lupins.  This  disease, — 
lupinosis, — which  is  not  met  with  in  man,  is  thought  to  be  due  to  a  poison — ictrogen 
or  lupinotoxin — produced  by  the  agency  of  fungi  in  the  husks  of  the  seeds.* 

In  the  vomit  of  a  fatal  case  of  acute  yellow  atrophy  Brunton  and 
Tunnicliffe  found  a  body  which  had  a  poisonous  effect  on  guinea-pigs 
and  was  thought  to  be  a  substitute,  in  all  probability  a  methylated 
diamine.  In  some  cases  the  poisons  may  be  produced  in  the  alimentary 
canal,  with  or  without  the  help  of  special  micro-organisms.  Brunton  and 
Tunnicliffe  compare  the  symptoms  in  acute  yellow  atrophy  with  those 
induced  by  some  viperine  venoms. 

Quincke  t  has  suggested  that  acute  yellow  atrophy  may  be  due  to  obstruction 
at  the  biliary  papilla,  allowing  the  pancreatic  juice  to  digest  the  liver.  There  is  as 
yet  no  proof  of  this  theory,  which  is  exactly  the  converse  of  Opie's  explanation  of 
haemorrhagic  pancreatitis  as  due  to  the  flow  of  bile  into  the  pancreatic  duct. 

Flexner  J  suggests  that  the  lesions  may  be  due  to  the  autolytic  action  of  intra- 
cellular ferments  produced  by  some  unknown  agency. 

As  already  pointed  out,  it  is  probable  that  a  number  of  poisons  or 
micro-organisms  may  give  rise  to  acute  yellow  atrophy.  At  present  it 
is  not  known  where  they  are  produced.  But  whether  taken  by  the 
mouth,  formed  in  the  alimentary  tract,  in  the  liver  itself,  or  elsewhere 
in  the  body,  the  liver  suffers  as  a  whole.  In  some  cases  the  liver  may 
be  primarily  involved,  the  changes  elsewhere  in  the  body  being  secondary, 
while  in  other  instances  the  hepatic  manifestations  may  be  merely  the 
local  result  of  a  general  hsemic  infection  or  intoxication. 


CLINICAL  PICTURE. 

Course. — The  disease  may  be  divided  into  two  stages.  The  first, 
which  usually  lasts  five  or  six  days,  but  may  be  prolonged  for  many 
weeks,  comes  on  either  like  catarrhal  jaundice  with  gastro-intestinal  dis- 
turbance followed  by  jaundice,  or,  more  gradually,  with  malaise.  During 
this  stage  there  is  nothing  to  distinguish  it  from  ordinary  jaundice  due 
to  gastro-intestinal  catarrh.  After  lasting  for  a  varying  time,  the  first 
stage  is  succeeded  by  the  second,  in  which  the  patient  passes' into  a 
"typhoid"  state  and  develops  nervous  symptoms  which  are  of  the  gravest 
significance  and  should  at  once  suggest  the  probability  of  acute  yellow 
atrophy.  This  stage  hardly  ever  lasts  more  than  a  week  and  is 
usually  limited  to  three  days. 

Duration. — More  than  half  the  cases,  as  shown  by  Thierf elder  and 

*  Vide  Brunton  and  Tunnicliffe:  St.  Bart.'s  Hosp.  Reports,  vol.  xxxii,  p.  425, 
1896. 

t  Quincke:  In  Nothnagel's  Encyclopspdia  of  Practical  Medicine,  Diseases  of  the 
Liver,  p.  642.     American  translation,  edited  by  F.  A.  Packard,  1903. 

I  American  Jour.  Med.  Sciences,  Aug.,  1903. 


ICTERUS   GRAVIS.  575 

Hunter's  statistics,  run  their  course  within  two  weeks.  Cases,  however, 
certainly  occur  in  which  the  disease  is  spread  over  many  weeks  or  even 
months.  The  disease  has  been  divided  into  acute,  subacute,  and  pro- 
tracted cases,  according  to  their  duration  and  severity.  The  prolonged 
cases  may  resemble  cases  of  obstinate  catarrhal  jaundice  until  the  nervous 
symptoms  develop,  the  long  course  of  the  disease  being  due  to  prolonga- 
tion of  the  earlier  or  first  stage.  But  in  rare  instances  partial  recovery 
may  occur  after  acute  symptoms  have  appeared,  the  patient  remaining 
jaundiced. 

Onset  and  First  Stage. — As  already  mentioned,  the  onset  may  be 
that  of  ordinary  catarrhal  jaundice;  in  a  minority,  about  one-tliird,  of 
the  cases  the  patient  suffers  from  indefinite  illness  and  malaise  for  some 
time  before  jaundice  makes  its  appearance.  As  a  rule,  during  the  first 
stage  there  is  little  or  nothing  to  distinguish  the  disease  from  ordinary 
catarrhal  jaundice.  It  is  true  there  is  generally  some  rise  of  temperature, 
but  this  is  often  seen  in  benignant  infectious  jaundice  and  is  not  enough 
to  justify  a  gloomy  prognosis.  Malaise,  vomiting,  constipation,  bilious 
urine,  and  not  uncommonly  muscular  pains  are  present. 

Jaundice  is  usually  the  first  objective  sign.  Its  intensity  varies  in 
different  cases:  it  may  gradually  become  more  marked,  or  it  may,  in 
cases  that  are  prolonged,  first  fade  and  then  become  more  intense  before 
death.  In  some  instances  it  may  be  less  marked  at  the  termination  than 
earlier  in  the  course  of  the  disease.  It  is  due  to  obstruction  in  the  smaller 
bile-ducts,  the  result  of  inflanmiatory  lesions  in  their  walls  produced  by 
the  same  poison  that  is  responsible  for  the  acute  degenerative  changes 
in  the  liver  cells.  In  some  exceptional  cases  of  acute  yellow  atrophy 
there  is  no  jaundice. 

This  was  so  in  a  case,  subsequently  published  by  Sir  T.  L.  Brunton  and  Dr. 
TunnicUffe,*  which  was  under  my  care  when  I  Avas  House  Physician  at  St.  Bartholo- 
mew's Hospital  in  1889.  A  case  of  acute  atrophy  without  jaundice  was  also  de- 
scribed by  Le  Roy.f 

In  the  following  case,  where  there  Avas  no  jaundice,  the  liver  had  the  micro- 
scopic appearances  of  acute  yelloAv  atrophy:  A  AA-oman  aged  thirty  years,  never 
strong,  had  shght  ha?matemesis  tAvo  j^ears  before,  from  AA'hich  she  recovered.  On 
Dec.  9,  1897,  she  suddenly  felt  pain  and  subsequently  vomited  a  little  blood;  next 
day  the  liver  duhiess  Avas  found  to  be  diminislied;  slight  hpematemesis  recurred 
on' December  10th  and  lltli,  and  melsena  on  December  12th,  13th,  14th;  after 
this  date  the  motions,  ahvays  offensive,  became  clay  coloured.  The  patient  got 
weaker,  droAvsy,  and  died  on  December  28tli.  There  Avas  never  any  jaundice. 
The  urine  Avas  not  tested  for  leucin  and  tyrosin.  The  temperature  Avas  generally 
between  99°  and  100°,  going  up  on  tAvo  occasions  to  101°,  and  Avas  often  beioAV 
normal.  At  the  postmortem  tlie  liver  Avas  very  small,  pale,  firm  to  the  touch  and 
to  the  knife.  The  surface  Avas  smooth  and  of  lightish  yclloAv  Avith  patches  of  slate 
colour;  the  edges  Avere  remarkably  thin.  Gall-liladder  Avas  fviU  of  dark  bile.  Kid- 
neys firm  and  pale.  Stomach  shoAvcd  nmncrous  sulinuicf)us  huMuorrhages,  espe- 
cially at  the  cardiac  end. 

Dr.  E.  T.  Wilson,  of  Cheltenham,  kindly  sent  me  tlie  liver  and  notes  of  the 
case.     Microscopic  examination  showed  the  lesions  of  acute  yellow  atroph3^ 

The  Second  Stage. — The  onset  of  the  second  stage  is  very  definite, 
and  is  marked  by  a  ])r()nnunced  change  for  the  worse  in  the  general 
condition  and  cs])ociall,\-  by  th(>  ap]ioarance  of  nervous  sym]-)toms.     Head- 

*  Biu-iitou  and  'i'liiuiicIinV:  St.  liartholomew's  Hosp.  Reports,  vol.  xxxii,  i^.  436, 
1890.  t  l>e  Roy:  Lancet,  lS8.o,  vol.  ii,  !>.  155. 


576  DISEASES    OF   THE    LIVER. 

ache  appears,  or  if  present  before,  becomes  intense.  Intolerance  of  light 
is  often  complained  of;  the  mental  processes  are  affected;  there  are  rest- 
lessness, delirium,  and  the  patient  may  scream  and  become  very  violent. 
T\Adtching  of  the  muscles  often  occurs,  and  general  convulsions  may 
supervene.  Transient  paralyses,  such  as  squint,  are  sometimes  noted. 
Apart  from  the  presence  of  jaundice,  the  clinical  manifestations  may  very 
closely  resemble  those  of  meningitis.  The  nervous  manifestations  tend 
to  pass  into  coma,  in  which  the  patient  finally  dies. 

With  the  onset  of  the  grave  nervous  symptoms  vomiting  becomes 
urgent,  and  the  vomited  matters  often  contain  altered  blood.  The  tongue 
is  usually  dry,  brown,  and  tremulous,  and  the  teeth  become  coated  with 
sordes.  Dilatation  of  the  pupils  has  been  regarded  as  an  important  sign, 
and  has  been  so  extreme  as  to  suggest  belladonna  poisoning.  The  pulse 
quickens  and  becomes  feeble  and  of  low  tension.  The  respiratory  rate 
tends  to  be  increased  or  to  become  irregidar  and  finally  stertorous.  The 
temperature  varies,  but  is  more  often  depressed  than  raised,  but  it  may 
rise  just  before  death.  The  presence  or  absence  of  fever  has  theoretically 
been  correlated  by  Hanot  *  with  different  microbic  poisons,  infection 
with  the  colon  bacillus  leading,  like  phosphorus  poisoning,  to  a  depressed 
temperature,  while  streptococcal  and  staphylococcal  infections  are  asso- 
ciated with  pyrexia.  Occasionally  a  red  rash  appears  on  the  skin. 
Petechise  and  haemorrhages  occur  under  the  skin,  and  blood  may  be 
passed  in  the  motions;  occasionally  epistaxis  and  haematuria  are  ob- 
served, and  in  women  metrorrhagia.  Pregnant  women  abort.  The 
faeces  may  be  darkened  by  blood  so  as  to  resemble  bile ;  in  the  later  stage 
it  is  improbable  that  bile  passes  into  the  duodenum,  inasmuch  as  after 
death  the  bile-ducts  contain  nothing  but  mucus.  But  as  constipation 
exists  throughout  the  disease,  some  of  the  faeces  may  contain  bile  ex- 
creted into  the  bowel  at  a  very  early  stage  of  the  disease.  The  dejecta 
are  often  extremely  offensive.     Diarrhoea  is  exceptional. 

Liver  Dulness. — At  the  onset  of  grave  symptoms  the  liver  may  or 
may  not  be  found  to  be  enlarged.  Temporary  enlargement  very  probably 
occurs,  though  it  is  not  made  out  in  all  cases.  The  increased  size  in  the 
early  stages  may,  of  course,  be  due  to  some  old-standing  change,  but 
this  is  not  the  case  in  most  instances.  Whether  preliminary  hepatic 
enlargement  is  made  out  or  not,  percussion  soon  shows  diminution  of 
the  liver  dulness,  which  may  progress  until  it  completely  disappears. 
Entire  absence  of  the  liver  dulness  is  due  to  the  atrophied  and  flabb}^ 
organ  falling  away  from  the  abdominal  walls  and  allowing  intestinal 
coils  to  take  its  place. 

In  a  very  exceptional  case  recorded  by  Gerhardt  f  the  hepatic  dubiess  did  not 
diminish,  although  the  liver  was  markedly  atrophied,  weighing  only  twenty-nine 
oiuices.  This  was  explained  by  the  fact  that  the  liver  was  firmly  adherent  to  the 
anterior  abdominal  Avail. 

Flatulent  distension  of  the  intestines  occurs  and  gives  rise  to  difficidty 
in  estimating  the  size  of  the  liver.     As  mentioned  aliove,  coils  of  intestine 

*  Hanot,  v.:  Arcliiv.  grneral.  de  Med.,  1896,  tome  clxxvii,  p.  77. 
t  Gerhardt:  Zeitschrift  f.  klin.  Med.,  Bd.  xxi,  1892. 


ICTERUS   GRAVIS.  0// 

may  pass  between  the  abdominal  wall  and  the  liver  and  entirely  obliterate 
the  hepatic  dulness.  The  liver  is  often  tender.  In  100  cases  collected 
by  Legg  *  this  was  definitely  noted  in  35. 

Enlargement  of  the  spleen  has  been  occasionally  noted.  Ascites, 
though  present  in  some  cases  after  death,  is  masked  by  flatulence  and 
is  hardly  ever  detected  during  life. 

There  is  no  very  special  feature  about  the  blood.  The  number  of  red 
blood-corpuscles  has  been  found  to  be  normal  or  to  be  somewhat  in- 
creased in  number,  and  a  very  moderate  leucocytosis  has  been  observed 
(Cabot  Ewing  t).  Bacteriological  examination  of  the  blood  has  been 
negative  in  some  instances,  while  in  others  the  colon  bacillus  has  been 
found  (Vincent  |). 

Urine. — The  amount  is  somewhat  diminished;  it  is  high-coloured 
from  the  presence  of  bile-pigment,  and  possibly  in  some  instances  from 
excess  of  urobilin.  From  degeneration  of  the  renal  cells  albumin  and 
casts  are  frec{uently  present  in  the  urine.  Albumosuria  is  sometimes  ob- 
served, and  it  is  not  improbable  that  the  albumose  is  directly  provided 
by  destruction  of  the  liver  cells. 

There  is  no  glycosuria.  This  is  a  remarkable  fact,  and  clearly  shows 
that  glycosuria  is  not  of  any  value  as  a  sign  of  hepatic  inadequacy. 
Patients  with  acute  atrophy  are  not  likely  to  take  much  sugar,  but  it  is 
very  striking  that  sugar  is  practically  never  found  in  the  urine.  The 
question  of  glycosuria  in  liver  disease  is  referred  to  on  p.  232  (Cirrhosis 
of  Liver) . 

The  amount  of  urea  is  very  greatly  diminished,  and  may  only  be 
present  in  fractional  amounts.  Corresponding  to  the  diminution  in  urea 
there  is  an  increase  in  the  percentage  of  nitrogen  present  as  ammonia 
in  the  urine.  It  may  increase  from  the  normal  2  to  5  per  cent,  up  to 
17  per  cent.  (Herter  g).  The  diminution  in  the  urea  is  probably  partly 
due  to  the  liver  cells  failing  to  manufacture  urea  from  ammonia,  but  it 
may  also  be  in  part  due  to  organic  acids  seizing  on  the  ammonia  and 
thus  preventing  the  formation  of  urea  out  of  the  basic  ammonia. 

Leucin  and  tyrosin,  to  which  great  importance  has  been  attached  as 
replacing  urea,  are  sometimes  present  in  such  quantities  that  they  are 
.spontaneously  precipitated  from  the  urine.  In  many  cases,  however, 
the  urine  must  be  concentrated  by  evaporation  in  order  to  demonstrate 
them.  Leucin  appears  in  the  form  of  rounded  discs,  while  the  crystals 
of  tyrosin  are  needle-shaped.  Leucin  and  tyrosin  are  not  invariably 
present  in  the  urine;  they  may  be  absent  in  cases  where  the  liver  is  foimd 
to  contain  them,  and  one  may  be  found  in  the  urine  without  the  other. 
Further  than  this  they  have  been  known  to  occur  in  the  urine  in  condi- 
tions other  than  acute  yellow  atrophy ;  thus  they  have  been  observed  in 
some  cases  of  erysipelas,  typhoid,  variola,  in  some  obscure  febrile  con- 
ditions, and  leukaemia.     Their  presence  in  the  urine,  therefore,  is  not 

*  Legg,  W. :   IVilc,  .launilicc,  and  Bilious  Diseases,  j).  46.5. 
t  Ewing:  Clinical  I'atliolfjgv  of  tlie  Blood,  ]).  841. 
t  Vincent:  La  Seniaine  Medical,  LS93,  p.  22S. 
§  Herter,  C.  A.:  Lecture.s  on  Chemical  Pathology,  p.  344. 
37 


578  DISEASES    OF   THE    LIVER. 

pathognomonic  of  acute  yellow  atrophy,  and  their  absence  does  not 
exclude  that  disease. 

It  was  formerly  assumed  that  the  presence  of  leucin  and  tyrosin  was 
due  to  the  degenerated  liver  cells  failing  to  transform  these  bodies  into 
urea.  This  explanation  is  probably  incorrect,  for  in  cases  where  the  Hver 
has  been  excluded  from  the  circulation  by  ligature  of  the  portal  vein 
and  the  hepatic  artery,  leucin  and  tyrosin  do  not  appear  in  the  urine. 
(Minkowski.)  It  appears  more  probable  that  the  leucin  and  tyrosin  are 
derived  from  the  liver  cells  themselves  as  a  result  of  their  extensive 
destruction.  This  view  is  supported  by  the  fact  that  leucin  and  tyrosin 
are  found  to  result  from  autolysis,  or  the  spontaneous  digestion  by 
intra-cellular  ferments  of  other  organs,  e.  g.,  a  pneumonic  lung  or  pus. 

Uric  acid  may  be  present  in  normal  or  even  in  increased  quantities; 
the  destructive  metabolism  in  acute  yellow  atrophy  explains  this  curious 
fact. 

Termination. — The  ''typhoid"  state  deepens  into  coma  and  absolute 
unconsciousness,  with  stertorous  breathing  and  incontinence  of  urine 
and  faeces. 

DIAGNOSIS. 

Jaundice  with  severe  constitutional  and  cerebral  symptoms  and 
diminution  in  the  liver  dulness  are  the  main  data  on  which  the  diagnosis 
is  made. 

Differential  Diagnosis. — From  Phosphorus  and  Allied  Forms  of 
Poisoning. — The  absence  of  any  evidence  that  phosphorus  or  other  poison 
has  been  taken  or  vomited  is,  of  course,  important.  The  progressive 
diminution  in  the  hepatic  dulness  and  the  diminution  in  the  amount  of 
urea  in  the  urine  are  strongly  in  favour  of  acute  yellow  atrophy.  The 
presence  of  leucin  and  tyrosin  is  not  conclusive,  as  they  may  be  absent, 
on  the  one  hand,  in  acute  atrophy,  and,  on  the  other  hand,  be  present 
in  phosphorus  poisoning  and  in  other  conditions,  such  as  typhoid  fever, 
erysipelas,  and  even  occasionally  in  leukaemia.  In  phosphorus  poisoning 
there  is  an  interval  between  the  severe  symptoms,  due  to  its  irritant 
action  and  the  onset  of  jaundice  with  severe  constitutional  symptoms; 
while  there  is  no  such  interval  between  the  first  and  second  stages  of 
acute  yellow  atrophy.  There  is  more  gastric  irritation  in  phosphorus 
poisoning. 

From  cases  of  icterus  gravis  the  chief  distinction  is  the  size  of  the 
liver — diminished  in  acute  yellow  atrophy  and  not  in  icterus  gravis. 
From  severe  cases  of  acute  infectious  jaundice  the  diagnosis  is  very  diffi- 
cult; in  fact,  the  two  conditions  run  into  each  other;  those  that  recover 
are  likely  to  be  spoken  of  as  infectious  jaundice,  and  those  that  prove 
fatal  as  acute  yellow  atrophy.  According  to  Osier,*  cases  of  infective 
endocarditis  have  been  mistaken  for  acute  yellow  atrophy.  Hypertrophic 
biliary  cirrhosis  is  not  likely  to  be  confused  with  acute  atrophy,  as  the 
course  of  the  disease  is  very  chronic  and  the  liver  is  greatly  enlarged. 

*0.sler,  W. :  Principles  and  Practice  of  Medicine,  p.  704,  3d  ed. 


ICTERUS   GRAVIS.  579 


PROGNOSIS. 

When  the  disease  has  fully  declared  itself,  the  prognosis  is  most 
gloomy;  in  fact,  doubt  will  always  arise  as  to  the  nature  of  cases  that 
recover,  and  where  an  opportunity  for  examining  the  liver  is  not  provided, 
by  death  later.  Some  of  the  cases,  of  which  a  good  number  are  on 
record,  may  have  been  examples  of  infective  jaundice  or  Weil's  disease 
of  a  severe  character,  or  of  some  other  form  of  acute  hepatitis. 

I  have  had  such  a  case  under  my  own  care  where  the  diagnosis  of  acute  atrophy 
and  death,  the  patient  being  in  a  condition  of  coma,  seemed  equally  certain,  but 
where  recovery  followed.  Fagge  *  refers  to  a  case  where  a  subsequent  postmortena 
showed  the  changes  of  acute  yellow  atrophy  in  a  patient  who  recovered  from  the 
acute  symptoms. 

Although  doubt'  may  arise  as  to  the  real  nature  of  the  lesion  in  the 
cases  that  recover  after  manifesting  the  characteristic  symptoms,  there 
are  ample  grounds  for  the  statement  that  this  does  occur. 

In  1897  Wickham  Legg  t  gave  a  list  of  28  cases  of  reputed  recoveries  from 
acute  yellow  atrophy.  In  1892  Wirsing  |  could  only  collect  15  cases,  not  asso- 
ciated with  syphilis,  of  recovery. 

Recovery  must  depend  on  the  compensatory  power  of  the  body  and 
especially  of  the  liver  cells.  Nodular  hyperplasia  of  the  hver  has  been 
described  in  cases  surviving  for  six  months  (Marchand  §),  a  year  and  a 
half  (Barbaccill),  a  year  and  three-quarters  (Steinhaus  **■),  and  two 
years  (Stroebeff).  But  the  symptoms  may  recur  and  prove  fatal  from 
degenerative  changes  attacking  the  areas  of  compensatory  hyperplasia. 
This  occurred  in  a  case  investigated  by  Professor  Delepine,  wliich,  by  his 
kindness,  is  referred  to  (p.  115)  under  the  heading  of  Acute  Hepatitis. 

As  in  all  forms  of  liver  disease,  the  state  of  the  kidneys  is  of  impor- 
tance. If  they  were  previously  healthy,  the  excretion  of  poisons  due  to 
the  acute  hepatic  inadequacy  will  diminish  the  intensity  of  the  toxaemia; 
but  even  with  kidneys  previously  intact  the  outlook  is  very  dismal,  since 
the  renal  epithelium  is  affected  by  the  poisons  reaching  them  by  the 
circulation  and  undergoes  acute  degeneration. 

TREATMENT. 

There  is  no  means  known  of  curing  the  disease;  theoretically,  free 
purgation  in  the  early  stages  of  the  disease,  to  eliminate  the  toxines 
before  their  degenerative  effects  have  been  produced,  might  be  recom- 
mended. Intravenous  or  subcutaneous  transfusion  with  saline  solution 
should  be  employed,  as  in  other  toxaemic  states. 

*  Fagge,  Hilton:  Principles  and  Practice  of  Medicine,  edited  by  Pye  Smith, 
3d  ed.,  vol.  ii,  p.  377. 

t  J.  Wickham  Legg:  Bile,  Jaundice,  and  Bilious  Diseases,  p.  676. 
j  Wirsing:    Inaug.    Disser.,  Wiirzburg.      Quoted    by    Albu,  Deutsche   med. 
Wochen.,  1901,  S.  216. 

§  Marchand:  Ziegler's  Beitriige,  Bd.  xvii,  S.  206. 
II  Barbacci :  Ziegler'.s  Beitriige,  Bd.  xxx,  S.  49. 
**  Steinhaus:  Prag.  mod.  Wochen.,  1903,  S.  323. 
tt  Stroebe:  Ziegler's  Beitriige,  Bd.  xxi,  S.  379. 


580  DISEASES    OF   THE    LIVER. 

Lenez  and  Schneider  *  have  reported  cases  where  recover j-  followed  repeated 
transfusions. 

Intestinal  antiseptics,  such  as  minute  doses  of  calomel,  salicylate 
of  bismuth,  salol,  and  /?-naphthol,  to  reduce  auto-intoxication  as  far  as 
possible,  may  be  given.  The  excretion  of  the  kidneys  should  be  increased 
by  the  administration  of  citrate  of  caffeine  and  free  draughts  of  water. 
Milk  diet  only  should  be  given,  '^''omiting  may  be  met  by  bismuth, 
dilute  hydrocyanic  acid,  bimeconate  of  morphine,  and  effervescing 
mixtures. 

JAUNDICE  OF  PHOSPHORUS  POISONING. 

Incidence. — Acute  phosphorus  poisoning  is  rare  in  this  country;  in 
the  ten  years  ending  1892  there  were  147  fatal  cases  in  England  and 
Wales.  (W.  Blythe.f)  It  is  commoner  in  Vienna,  and  is  said  to  be  a 
means  of  committing  suicide  in  prostitutes  and  unmarried  girls  who  are 
pregnant,  its  use  being  perhaps  associated  with  its  reputation  as  an 
aphrodisiac.  When  taken  with  suicidal  intent,  an  emulsion  of  the  heads 
of  lucifer  matches  or  of  rat  paste  has  been  employed.  When  accidental 
poisoning  occurs,  rat  paste  taken  under  the  impression  that  it  w^as  some- 
thing else  may  be  the  cause,  but  it  may  be  due  to  eating  the  flesh  of 
animals,  especially  poultry,  which  have  died  from  eating  vermin  poisoned 
by  phosphorus  (Poore  t),  or  even  from  the  application  of  phosphorescent 
paste  to  the  skin.  In  some  instances  it  has  followed  the  medicinal  use 
of  phosphorus.  It  has  been  thought  that  some  cases  of  acute  yellow- 
atrophy  are  in  reality  the  results  of  undetected  poisoning.  Results  re- 
sembling phosphorus  poisoning  may  be  due  to  iodoform,  arsenic,  and 
antimony. 

Morbid  Anatomy.- — The  liver  is,  as  a  rule,  much  larger  than  natural, 
firm  but  friable,  and  of  a  pale  yellow  colour.  In  a  few  cases  the  liver 
has  presented  exactly  the  features  of  acute  yellow  atrophy,  but  this  is 
exceptional,  and  the  change  in  the  liver  is  essentially  one  of  increase  in 
size  due  to  acute  fatty  metamorphosis,  and  resembles  that  of  iodoform 
poisoning.  It  is  said  that  if  life  is  sufficiently  prolonged,  the  liver  dimin- 
ishes in  size  from  absorption  of  the  fat  and  so  comes  to  be  in  the  same 
condition  as  in  acute  yellow  atrophy.  Under  the  capsule  and  on  section 
the  yellow,  buff  aspect  of  the  liver  substance  shows  here  and  there  reddish 
spots  due  to  hsemorrhage,  which  stand  up  against  the  bile-stained  liver 
substance. 

In  dogs  poisoned  by  phosphorus  there  is  a  large  quantity  of  fat  in-  the  liver, 
and  the  nuclei  of  the  liver  cells  show  fragmentation.  There  is,  however,  no  fat, 
or  almost  none,  in  the  myocardium,  none  in  the  voluntary  muscles,  and  only  a 
little  in  the  kidneys.     (Ray,  McDermott,  and  Lusk.§) 

Microscopically  the  liver  cells  show  cloudy  swelling  and  very  advanced 
fatty  metamorphosis.     The  cells  in  parts  of  the  lobules  may  contain  gran- 

*  Lenez  et  Schneider:  Arch,  de  Med.  et  Pharm.  mil.,  Paris,  1900,  tome  xxxv 
p.  66.     Schneider,  ibid.,  1903,  tome  xli,  p.  329. 

t  Blythe,  W. :  Poisons,  p.  213,  189.5. 

%  Poore,  G.  V. :  Nervous  Affections  of  the  Hand  and  Other  Studies,  p.  15.5. 

§  Rav,  McDermott,  and  Lusk:  American  Journ.  of  Physiology,  vol.  iii,  p.  139, 
Oct.,  1899. 


ICTERUS    GRAVIS.  581- 

iiles  of  bile-pigment.  Leucin  and  tyrosin  may  also  be  found  in  the  liver. 
There  is  sometimes  slight  proliferation  of  the  connective-tissue  elements 
of  the  portal  spaces,  and  in  cases  that  recover  some  cirrhosis  probably 
develops.  The  small  bile-capillaries  are  blocked  and  obstructed  (Eppin- 
ger  *),  and  thus  account  for  the  jaundice. 

The  heart  and  kidneys  usually,  but  not  ahva}^s,  show  advanced  fatty 
change;  the  heart  may  be  so  soft  as  to  be  readily  perforated  by  the 
fingers  during  its  examination.  The  voluntar}^  muscles  also  undergo 
fatty  change.  The  spleen  may  be  much  enlarged.  Haemorrhages 
are  found  scattered  throughout  the  body. 

Pathogeny. — The  destruction  of  the  liver  substance  leads  to  hepatic 
inadequacy  and  so  to  a  general  toxaemia,  poisons  which  should  have 
been  arrested  in  the  liver  passing  into  the  general  circulation.  It  is 
thought  that  there  is  an  acid  intoxication  due  to  the  presence  of  sarco- 
lactic  acid  in  the  blood. 

Clinical  Manifestations. — The  symptoms  due  to  the  irritating  effect 
of  phosphorus  on  the  gastric  mucous  membrane  come  on  in  from  a  few 
minutes  to  three  hours  after  taking  the  poison.  With  phosphorated  oil 
or  phosphorus  in  a  soluble  state  the  ill  effects  are  soon  manifest,  while 
if  the  poison  was  taken  in  a  solid  form,  the  onset  is  delayed. 

There  is  gastric  pain,  followed  by  vomiting,  which  greatly  interferes 
with  antidotal  treatment  and  feeding  and  may  be  so  constant  as  to  lead 
to  dangerous  collapse.  The  vomited  matters  and  eructations  may  be 
luminous  in  the  dark,  and  from  the  presence  of  blood,  dark  and  grumous. 
There  are  usually  intense  thirst  and  tenderness  over  the  stomach  and 
liver,  but  no  hepatic  enlargement  at  this  stage.  The  patient  may  die 
from  collapse;  if  this  does  not  occur  and  efficient  treatment  is  carried 
out,  permanent  recovery  may  follow,  but  in  a  considerable  number  of 
cases  there  is  a  temporary  improvement  succeeded  by  the  return  of  grave 
symptoms  due  to  the  toxic  effects  of  the  absorbed  poison  on  the  liver 
and  other  internal  organs.  These  severe  symptonxs  usually  begin  about 
four  days  after  the  poison  was  taken;  they  may  arise  sooner,  or,  on  the 
other  hand,  be  delayed  for  two,  three,  or  even  six  weeks,  as  in  S.  West's  f 
case. 

The  scene  reopens  with  jaundice  and  recurrence  of  ^'omiting  of  dark, 
grumous  matters,  followed  by  great  prostration,  ending  in  coma  and 
death,  usually  on  the  fifth  or  sixth  day  from  the  time  the  phosjihorus 
was  taken,  and  after  a  day  or  two  of  grave  constitutional  symptoms. 
Haemorrhages  into  the  skin  and  from  mucous  surfaces  are  a  constant 
feature  of  the  disease,  but  are  not  so  marked  as  in  deep  jaundice  due 
to  other  causes.  Jaundice  is  by  no  means  a  constant  symptom,  and 
does  not,  when  present,  l^ear  any  relation  to  the  severity  of  the  changes 
taking  place  in  the  liver.  From  experiments  on  animals  and  from  ob- 
servations on  man  (E]5pinger|)  there  is  reason  to  believe  that,  as  in 
acute  yellow  atrophy,  the  jaimdice  is  obstructive  and  due  to  infiamma- 

*  Eppinger:  Ziegler's  Beitrage,  Bd.  xxxiii,  S.  123,  1903. 

t  We.st,.S.:  Lancet,  1893,  vol.  i,  p.  245. 

J  Eppinger:  Ziegler's  Beitrage,  Bd.  xxxiii,  S.  123,  1903. 


582  DISEASES   OF   THE   LIVER. 

tion  of  and  stagnation  of  viscid  bile  in  the  smaller  ducts.  The  tempera- 
ture is  usually  below  normal.  The  Uver  is  enlarged  and  tender;  the 
spleen  is  also  enlarged,  and  the  abdomen  may  become  distended.  The 
most  marked  difference  between  tliis  stage  of  phosphorus  poisoning  and 
acute  yellow  atroph}^  is  in  the  size  of  the  liver.  But  in  exceptional  cases 
of  phosphonis  poisoning  the  hver  is  not  enlarged,  and  in  the  early  stages 
of  some  examples  of  acute  yellow  atrophy  it  is  enlarged,  so  that  the 
clinical  resemblance  between  the  two  affections  may  sometimes  be  very 
close. 

There  is  an  increase  in  the  number  of  the  red  blood-corpuscles 
(v.  Jaksch  *),  and  occasionally  there  is  leucocytosis. 

The  urine  is  somewhat  diminished  in  quantity,  but  never  suppressed; 
it  is  high  coloured  and  of  rather  liigh  specific  gra^nty.  It  may  contain 
albumin,  blood,  and  casts.  Albumosuria  may  also  be  present,  the  albu- 
mose  being  probably  the  direct  product  of  destructive  changes  in  the 
liver  cells.  There  are  generally  bile-pigments  and  bile  acids,  while  sar- 
colactic  acid,  united  to  anunonia,  is  frequently  present;  it  is  not,  however, 
always  present,  as  sho^\Ti  by  Miinzer's  careful  observations.  It  was 
formerly  said  that  leucin  and  tj^rosin  were  not  present  in  the  urine,  and 
stress  was  laid  on  this  in  the  diagnosis  from  acute  yellow  atrophy;  it  is 
now  knoT\Ti  that  leucin  and  tyrosin  may  be  present  in  the  urine  in  phos- 
phorus poisoning,  but  are  far  from  being  constantly  foimd.  Leucin  is 
less  frequently  found  than  tyrosin. 

The  presence  of  leucin  and  tyrosin  in  the  urine  is  due,  Uke  the 
albumosuria,  to  destructive  changes  in  the  protoplasm  of  the  liver  cells. 
That  it  is  not,  as  has  often  been  thought,  due  to  failure  on  the  part  of 
the  Uver  to  transform  leucin  and  tyrosin  into  urea  is  shoT\ai  by  the  fact 
that  the  experimental  exclusion  from  the  circulation  of  the  liver  in  geese 
by  ligature  of  the  portal  vein  and  hepatic  artery  does  not  lead  to  the 
appearance  of  leucin  and  tyrosin  in  the  urine.  The  amount  of  urea  was 
formerly  thought  to  be  greatly  diminished;  it  now  appears  that  though, 
in  common  with  the  total  nitrogen  excretion,  it  is  diminished  in  the  early 
stages  when  all  food  is  refused  by  the  stomach,  it  is  absolutely  increased 
in  the  later  stages  as  a  result  of  increased  metabohsm.  Experimentally 
it  has  been  sho■s^^l  that  the  rise  in  the  proteid  metabohsm  in  phosphorus 
poisoning  is  only  equalled  by  that  in  phloridzin  diabetes. 

The  proportion  of  the  urinary  nitrogen  excreted  as  ammonia  is 
greatty  increased:  instead  of  the  normal  2  to  5  per  cent.,  it  rises  to  10 
to  20  per  cent,  of  the  total  nitrogen;  this  occurs  at  the  same  time  that 
the  amount  of  urea  is  increased.  The  increased  amount  of  ammonia 
in  the  urine  can  be  diminished  by  the  administration  of  sodium 
bicarbonate.  The  explanation  of  this  is  that,  owing  to  an  increase  in 
organic  acids  in  the  body,  ammonia  is  utihsed  as  a  base  and  appeare  in 
the  urine  in  combination  with  organic  acids;  when  sodium  bicarbonate 
is  given,  the  ammonia  is  no  longer  utihsed  in  this  way,  and  it  is  therefore 
free  to  be  converted  into  urea.f     In  other  words,  the  presence  of  am- 

*  V.  Jaksch:  Deutsch.  med.  Wochen.,  1893,  S.  10. 

t  Vide  Herter  Lectures  on  Chemical  Pathology,  p.  347. 


ICTERUS    GRAVIS.  583 

monia  in  the  urine,  though  associated  with  changes  in  the  hver,  is  not 
due  to  any  faihire  in  the  hepatic  cells  to  form  urea  out  of  ammonia,  but 
is  evidence  of  incipient  intoxication  or  acidosis.  Sugar  is  not  present 
in  the  urine,  though  in  Poore's  case  it  was  found  in  the  urine  passed 
shortly  before  death.     Hunter  ssljs  there  are  only  three  cases  on  record. 

In  19  cases  of  phosphorus  poisoning  Frerichs  *  gave  large  quantities  (200 
grams)  of  sugar,  but  only  obtained  alimentary  glycosuria  in  two. 

Diagnosis. — The  history  that  phosphorus  has  been  swallowed  or  that 
symptoms  justifying  this  conclusion  have  recenth"  occurred  is  a  most 
important,  if  not  an  essential,  point.  The  presence  of  phosphorus  in 
the  vomit  or  the  fact  that  the  vomited  matters  are  luminous  in  the  dark 
of  course  settles  the  question.  In  the  differential  diagnosis  from  acute 
yellow  atrophy  the  following  points  should  also  be  borne  in  inind:  (i) 
The  large  size  of  the  liver,  (ii)  The  amount  of  urea  is  not  diminished 
except  in  the  earhest  stage,  (iii)  The  greater  prominence  of  gastro- 
intestinal symptoms. 

In  the  absence  of  a  reliable  historj^  great  difficulty  may  arise  in  the 
differential  diagnosis;  in  fact,  Poore  t  tliinks  that  there  can  be  no  doubt 
that  chnically  and  pathologically  the  two  conditions  are  indistinguishable. 

Prognosis. — In  cases  where  jaundice  and  enlargement  of  the  liver 
come  on  the  outlook  is  very  grave;  most  cases  die. 

Treatment. — When  the  poison  has  been  recently  taken,  the  stomach 
should  be  emptied  and  washed  out.  As  an  antidote,  French  or  old  or 
oxidised  oil  of  turpentine  should  be  given  every  quarter  of  an  hour  for 
the  first  hour,  40  minims  in  an  emulsion,  and  afterwards  three  or  four 
times  daily.  Permanganate  of  potash  and  sanitas  have  also  been  recom- 
mended. Mucilaginous  drinks  should  be  given,  but  oils  or  fats  should 
be  avoided,  as  they  render  the  phosphorus  more  soluble.  Purgatives 
are  advisable.  AATien  the  grave  constitutional  symptoms  have  developed, 
no  special  treatment  can  be  relied  on.  But  it  would  be  reasonable  to 
give  large  doses  of  sodium  bicarbonate  by  tlie  mouth  or  by  subcutan- 
eous transfusion  to  counteract  acidosis. 


INFECTIOUS  JAUNDICE. 

Among  the  various  forms  of  toxsemic  or  hsemohepatogenous  jaundice 
there  is  a  group  which,  in  contradistinction  to  the  malignant  forms  of 
toxaemic  jaundice  or  icterus  gravis,  such  as  acute  atrophy  and  pliosphorus 
poisoning,  is  spoken  of  as  benign  infectious  jaundice  or  merely  infectious 
jaundice.  Of  this  group,  Weil's  disease  is  a  well-marked  example.  The 
general  characters  of  toxaemic  jaundice  have  already  been  sketched  (vide 
p.  530),  and  it  was  there  pointed  out  that  the  jaundice  is  sul^ordinate 
both  in  degree  and  in  importance  to  the  constitutional  symptoms  of 
a  general  hsemic  infection  or  intoxication.  In  many  instances  the  pri- 
mary infection  constitutes  a  definite  disease,  as  in  the  specific  fevers, 

*  F.T  .  Frerichs:  Ueber  den  Diabetes,  1884.  Quoted  by  Williamson,  Diabetes, 
p.  116. 

t  Poore,  G.  V. :  Nervous  Affections  of  the  Hand  and  Other  Studies,  p.  155,  1897. 


584  DISEASES    OF   THE    LIVER. 

yellow  fever,  pyaemia,  septicseniia,  etc.,  but  in  this  group  of  infectious 
jaundice,  although  there  is  a  general  infection,  its  characters  are  not 
sufficiently  typical  to  allow  of  its.  recognition  as  a  definite  disease  apart 
from  the  febrile  condition  and  jaundice. 

There  are  thus  many  examples  of  toxgemic  jaundice  of  undetermined 
nature  grouped  under  the  heading  of  infectious  jaundice.  The  more 
severe  cases  are  considered  in  a  special  category  under  the  name  of  Weil's 
disease.  Among  the  slight  forms  are  some  cases  often  termed  catarrhal 
jaundice,  but  presenting  fever  and  enlargement  of  the  liver  and  spleen; 
the  onset  of  these  cases  is  the  same  as  that  of  catarrhal  jaundice,  but 
there  are  the  above-mentioned  additional  features,  which  tend  to  show 
that  there  is  not  a  mere  local  obstruction  at  the  lower  end  of  the  bile- 
duct,  but  a  more  widespread  infection.  No  doubt  transitional  cases 
between  a  local  infection  and  obstruction  at  the  lower  end  of  the  bile- 
duct  and  a  more  extensive  obstruction  of  the  ducts  exist,  and  it  is,  there- 
fore, convenient  to  speak  of  the  cases  as  infectious  catarrhal  jaundice. 
It  is  not  infrequent  for  epidemics  of  this  form  of  jaundice  to  occur,  and 
it  is  not  always  easy  to  be  certain  whether  it  is  a  mild  infectious  jaundice, 
the  infection  falling  chiefly  on  the  bile-ducts,  or  whether  there  is  an  epi- 
demic form  of  gastro-intestinal  catarrh  in  which  the  lower  end  of  the 
bile-duct  is  obstructed,  while  the  ducts  remain  free  from  more  exten- 
sive infection. 

The  epidemic  jaundice  whicli  occurred  in  our  troops  in  the  South  African  war 
(1899-1902)  Avas  regarded  by  some  as  infectious  and  by  otliers  as  due  to  epidemic 
gastro-intestinal  catarrh.* 

WEIL'S  DISEASE. 

Synonyms:  Infective  Jaundice;  "  Bilious  Typhoid." 

In  1886  Weil  t  described  a  condition  of  febrile  jaundice  associated 
with  nephritis  and  enlargement  of  the  spleen.  It  occurs  in  epidemics, 
one  of  which  had  previously  been  described  by  Weiss  in  1866  as  infectious 
jaundice.  The  disease  was  called  after  Weil,  of  Heidelberg,  by  his  com- 
patriots, but  the  French  school  did  not  consider  it  was  different  from 
icterus  gravis  or  infectious  jaundice.  This  unwillingness  to  acknowledge 
it  as  a  new  disease  distinct  from  other  forms  of  toxgemic  or  infectious 
jaundice  is  shared  by  Hunter  |  in  his  article  in  AUbutt's  "System  of 
Medicine." 

Weil's  disease  is  an  excellent  example  of  acute  infective  jaundice 
secondary  to  a  haemic  infection  by  a  proteus  bacillus.  The  jaundice  is 
toxgemic,  and  has  close  analogies  with  that  induced  experimentally  by 
means  of  toluylendiamin.  It  is  allied  to,  but  less  acute  than,  acute 
yellow  atrophy  of  the  liver;  thus  cases  formerly  recorded  as  examples 
of  recovery  from  acute  yellow  attophy  would  probably  be  regarded  now 
by  many  as  Weil's  disease.  Conversely,  fatal  cases  of  Weil's  disease  are 
sometimes  described  as  acute  yellow  atrophy  or  icterus  gravis. 

*  Vide  Report  of  the  Imperial  Yeomanrj'  Hospitals  in  Soutli  Africa,  vol.  iii, 
p.  195.  t  Weil:  Deutsches  Archiv  f.  klin.  Med.,  Rd.  xxxix,  1886. 

X  Hunter,  W. :  Allbutt's  System,  vol.  iv,  p.  100. 


ICTERUS    GRAVIS.  585 

Etiology.— It  usually  attacks  young  adults,  and  is  more  frequent  in 
males  between  the  ages  of  twenty  and  forty  years,  but  children  are  some- 
times attacked.  The  infection  is  probably  conveyed  into  the  system 
by  eating  decomposed  meat  or  drinking  water  which  has  l^een  infected 
by  tainted  meat  or  by  the  bodies  of  animals  dying  from  a  similar  disease. 
Its  frequency  in  the  German  army  has  been  referred  to  the  consumption 
of  rancid  and  improperly  cooked  sausages.  (H.  Brooks.*)  Semmola 
and  Geoffredi  t  quote  cases  where  the  disease  appeared  to  be  due  to 
inhalation  of  sewer-gas.  It  is,  therefore,  more  likely  to  occur  in  those 
classes  of  the  population  who  are  exposed  to  the  sources  of  infection, 
such  as  butchers,  sewermen,  soldiers,  etc. 

Most  of  the  cases  occur  in  the  summer  months,  and  are  met  with  in 
epidemics.  It  may  arise  repeatedly  in  the  same  place,  but  does  not 
appear  to  be  contagious. 

The  disease  is  rare  in  England,  though  some  epidemics  of  catarrhal 
jaimdice  have  been  erroneously  described  as  Weil's  disease,  and  is  usually 
seen  in  Germany,  Russia,  and  France.  Very  few  cases  have  been  re- 
corded in  America  (Raymond,^  Lamphear,  H.  Brooks, §  libman,  || 
Satterlee  **) . 

Bacteriology. — Jaeger,tt  Banti,JJ  and  others  have  described  a  pro- 
teus  bacillus  as  the  essential  cause  of  the  disease.  Jaeger  found  the  same 
organism  (Bacillus  proteus  fluorescens)  in  ducks  dying  with  jaundice, 
which  frequented  the  water  in  which  his  patients  had  bathed  and  pre- 
sumably become  infected.  Satterlee  has  given  a  useful  table  showing 
the  characters  of  the  bacilli  found  by  Weil,  Jaeger,  Brooks,  Libman,  and 
himself. 

This  bacillus  is  found  in  the  viscera  in  large  numbers,  and  when  cul- 
tivated and  injected  into  animals,  leads  to  acute  degenerative  changes 
in  the  hver  and  kidneys.  It  appears  that  bacilli  are  rarely  present  in 
the  blood,  and  that  dissemination  occurs  chiefly  by  the  lymphatics.  (H. 
Brooks.) 

Morbid  Anatomy. — The  tissues  of  the  body  are  bile-stained  and 
show  the  effects  of  a  general  toxic  process.  The  liver  is  either  somewhat 
increased  in  size,  or  of  the  normal  volume,  and  thus  differs  from  the 
condition  in  acute  yellow  atrophy. 

Haemorrhages  may  be  present  in  the  skin  and  in  the  mucous  and 
serous  membranes.  The  spleen  is  swollen,  enlarged,  and  has  been  seen 
to  contain  haemorrhages.     The  kidneys  show  tubal  nephritis. 

There  is  cloudy  swelling  of  the  cells  of  the  kidney,  liver,  and  heart- 
muscle,  going  on  to  the  further  degenerative  change  of  fatt}'  metamor- 
phosis.    The  changes  in  the  liver  may  progress  further  and  reseml.ile 

*  Brooks,  H. :  Archives  of  Neurology  and  Psych opathology,  ]i)00,  p.  34-i. 

t  Semmola  and  Cieoffredi:  Twentieth  Century  Practice,  vol.  ix. 

t  Raymond:  Medical  Age,  Detroit,  Oct.  10,  1S92. 

I  Brooks,  H. :  Arcliives  of  Neurology  and  Psych opathology,  vol.  iii,  i).  343. 

■||  Libman:  Pliiladolpliia  Mod.  Journ'.,  1S99,  i").  (i20. 
**  Satterlee:  Medical  News  (N.  Y.),  June  G,  19U3,  p.  1069. 
tt  Jaeger:  Zeitschrift  f.  Hygiene,  lid.  xii,  S.  525. 
U  Banti:  Deutsche  nied.  Wochen.,  1895,  S.  493. 


586  DISEASES   OF  THE   LIVER. 

those  in  acute  yellow  atrophy;  the  mucous  membrane  of  the  bile-ducts 
becomes  swollen  and  degenerated. 

Symptoms. — The  onset  is  sudden  and,  generally  speaking,  resembles 
that  of  influenza.  The  chief  symptoms  are  malaise,  headache,  fever, 
severe  muscular  pains,  especially  in  the  calves,  and  often  more  or  less 
marked  gastro-intestinal  disturbance.  The  pulse-rate  is  about  120  at 
first,  but  becomes  slower  after  the  appearance  of  jaundice.  Jaundice 
begins  on  the  second  or  third  day,  is  generally  slight,  and  lasts  about 
two  weeks;  the  motions  may  be  clay-coloured,  but  usually  contain  bile 
and  are  often  loose.  The  liver  becomes  enlarged  and  tender,  and  a 
marked  feature  of  the  disease  is  the  splenic  enlargement.  Fever  reaching 
103°  to  104°  F.  lasts  for  about  a  week;  the  temperature  then  falls  and 
becomes  normal  at  about  the  tenth  day. 

Nervous  symptoms  are  prominent;  the  muscular  pains  in  the  calves 
are  severe,  prostration  and  giddiness  may  be  marked,  and  delirium  is 
usually  present.  Epistaxis,  purpura,  and  various  cutaneous  rashes,  such 
as  herpes,  erythema,  and  urticaria,  may  be  met  with.  A  relapse  may 
occur  a  week  or  so  after  the  temperature  has  become  normal;  its  occur- 
rence may  be  suspected  if,  after  the  end  of  the  first  attack,  the  spleen 
remains  enlarged.  The  relapse  lasts  about  a  week.  Chauffard  *  de- 
scribes Weil's  disease  as  ''relapsing  infectious  jaundice,"  but  in  Germany 
relapses  are  comparatively  infrequently  described;  thus,  in  84  cases,  of 
which  73  were  collected  from  German  literature,  Tymowski  f  found  that 
relapses  were  mentioned  in  19.  Quincke  J  says  that  a  relapse  occurs  in 
40  per  cent,  of  the  cases. 

Bacteriological  examination  of  the  blood  shows  that  it  is  almost 
always  sterile,  and  that  the  proteus  bacillus,  described  by  Jager  and 
others,  in  the  viscera,  is  not  to  be  found  in  the  general  circulation.  The 
blood-serum  may  agglutinate  the  Bacillus  typhosus  even  when  diluted 
(Eckhardt  §). 

The  urine  is  albuminous,  contains  bile-pigment,  casts,  and  sometimes 
blood-corpuscles  and  bile  acids.  Bacteriological  examination  of  the  urine 
shows  that  the  same  proteus  bacillus  found  in  the  viscera  is  present. 
Bacteriuria  may  persist  for  a  considerable  time;  in  Satterlee's  case,  where 
it  was  still  present  and  rendered  the  urine  turbid  a  month  after  the  dis- 
ease, it  may  have  been  due  to  local  infection  of  the  prostate. 

Diagnosis. — Fever,  jaundice,  enlarged  spleen  and  liver,  pains  in  the 
calves,  and  albuminuria  occurring  in  epidemics,  running  an  acute  course, 
and  ending  in  recovery  are  the  characteristics  of  the  special  form  of 
infectious  jaundice  called  Weil's  disease.  Very  similar  forms  of  infectious 
jaundice  occur  and  differ  in  some  clinical  features,  such  as  the  absence  of 
albuminuria  or  constant  association  with  gastro-intestinal  symptoms. 
It  is,  indeed,  hardly  worth  while  separating  Weil's  disease  from  these 
forms  of  infectious  jaundice. 

*  Chauffard:  Traits  de  M6decine  (Bouchard,  Brissaud),  tome  v,  p.  98. 
t  Quoted  by  Chauffard,  loc.  cit. 

X  Quincke :  Diseases  of  Liver  in  Nothnagel's  Encyclopaedia  of  Practical  Medi- 
cine, EngUsh  translation,  p.  504. 

§  Eckhardt:  Miinchen.  med.  AVochen.,  Bd.  xUx,  S.  1129,  1902. 


ICTERUS    GRAVIS.  587 

From  ordinary  catarrhal  jaundice  it  is  distinguished  by  its  greater 
severity  and  by  evidence  of  its  being  not  a  local  disease  limited  to  the 
bile-ducts,  but  a  general  infection,  as  shown  by  albuminuria. 

From  Typhoid  Fever. — Griesinger  originally  described  the  disease  as 
"bilious  typhoid."  Not  uncommon^  cases  of  Weil's  disease  occur  in 
association  with  typhoid  fever.  Further,  according  to  Eckhardt,*  the 
blood-serum  in  Weil's  disease  may  agglutinate  typhoid  bacilli  in  a  marked 
manner  even  when  diluted,  and  so  lead  to  difficulty  in  a  differential  diag- 
nosis. That  Weil's  disease  is  not  modified  typhoid  fever  seems  quite 
clear,  as  the  lesions  of  typhoid  are  not  found  in  fatal  cases  of  Weil's 
disease.  In  differentiating  the  two  diseases  clinically  the  onset  of  Weil's 
disease  is  sudden,  and  gradual  in  typhoid  fever.  The  duration  and  course 
of  Weil's  disease  are  shorter  than  those  of  typhoid  fever.  Jaundice  is 
extremely  rare  in  typhoid  fever. 

The  more  severe  examples  of  Weil's  disease  approach  icterus  gravis 
and  acute  yellow  atrophy.  The  difference  is  one  of  degree,  so  far  as  our 
present  knowledge  goes. 

Relapsing  fever  should  be  recognised  by  examination  of  the  blood 
and  the  presence  of  the  Spirillum  Obermeieri.  Mild  cases  of  yellow  fever, 
according  to  Brooks,  are  much  the  same  as  Weil's  disease,  and  it  is 
possible  that  not  only  are  they  both  examples  of  toxa^mic  jaundice,  but 
that  the  infection  is  the  same. 

The  prognosis  is  fairly  favourable,  but  convalescence  may  be  pro- 
tracted. 

In.  the  44  cases  obtained  by  adding  Weil's,  Jager's,  Haas's,  and  Wassilieff's 
figures  there  were  only  five  deaths.  It  must  be  borne  in  mind,  however,  that 
fatal  cases  are  very  likely  to  be  described  as  icterus  gravis  or  acute  yellow  atrophy 
simply  because  they  are  fatal. 

Treatment. — ^The  patient  should  remain  in  bed  until  after  the  tem- 
perature has  become  normal,  and  should  be  restricted  to  a  milk  diet. 
All  alcoholic  drinks  should  be  interdicted,  and  the  patient  should  be 
encouraged  to  drink  freely  of  water.  Intestinal  antiseptics,  such  as 
calomel  (4V  gr.)  in  minute  doses,  salol,  saHcylate  of  bismuth,  or  /5-naph- 
thol,  should  be  given. 

*  Eckhardt:  Miinchen.  med.  Wochen.,  Bd.  xlix,  S.  1129,  190?. 


DISEASES   OF   THE   GALL-BLADDER. 


ABNORMALITIES. 

Complete  Absence  of  the  Gall-bladder. — This  is  the  normal  condi- 
tion in  the  horse,  mule,  ass,  elephant,  and  other  animals.  It  is  sometimes 
seen  in  man,  but  som.e  of  the  older  observations,  such  as  those  of 
Cholmeley,*  Thomas,t  were  evidently  on  cases  of  obliteration  of  the 
gall-bladder  due  to  inflammation  during  foetal  life,  and  not  of  genuine 
absence  of  the  gall-bladder. 

I  have  seen  only  one  case  at  St.  George's  Hospital,  in  a  man  aged  forty-nine 
who  died  from  pulmonary  tuberculosis;  the  ducts  were  quite  normal,  and  there 
was  no  evidence  of  past  inflammation  or  of  any  dilatation.  This  case  was  dissected 
and  described  by  Dr.  A.  Latham. f  Thursfield  showed  an  undoubted  case  at  the 
Pathological  Society  on  April  7,  1903. 

In  genuine  cases  the  common  bile-duct  is  sometimes  dilated  in  some 
part  of  its  course.  This  change  has  also  been  said  to  occur  in  some  cases 
where  the  gall-bladder  has  been  removed  by  the  surgeon. 

Crucknell's  §  case,  in  which  the  common  hepatic  duct  was  described  as  opening 
into  the  gall-bladder  and  the  common  bile-duct  as  coming  off  separately  from  the 
gall-bladder,  so  that  all  the  bile  must  have  passed  through  the  "gall-bladder," 
was  probably  a  case  of  absence  of  gall-bladder  and  dilatation  and  pouching  of  the 
upper  end  of  the  common  bile-duct. 

Double  Gall-bladder. — In  exceptional  instances  there  have  been 
two  gall-bladders,  each  with  a  cystic  duct. 

Purser  II  described  an  example  in  1886  and  referred  to  a  case  recorded  in  the 
Philosophical  Transactions  of  1693-4  in  which  there  was  a  gall-bladder  on  the  left 
lobe  and  another  on  the  right  lobe  of  the  liver. 

Malposition  of  the  Gall-bladder. — In  rare  instances  the  gall-bladder 

is  found  to  the  left  of  the  longitudinal  fissure  and  on  the  under  surface  of 
the  left  lobe. 

There  is  a  specimen  showing  this  in  the  Anatomical  Museum,  Cambridge,  and 
D(^v6  **  figures  another  e.xample. 

In  cases  where  the  left  lobe  is  atrophied  the  gall-bladder  appears  to 

*  Cholmeley:  Med.  Trans.  Roy.  Coll.  Physicians,  London,  vol.  vi,  p.  50,  1820. 
t  Thomas:  Medical  Times,  vol.  xvii,  p.  171,  1848. 

X  Latham:  Proc.  Anat.  Soc,  Feb.,  1898.     Journ.  of  Anat.  and  Physiol.,   1898. 
§  Crucknell:  Trans.  Path.  Soc,  vol.  xxii,  p.  163. 

II  Purser:  Trans.  Acad.  Med.  Ireland,  vol.  v,  Brit.  Med.  Journ.,  1886,  vol.  ii, 
p.  1106. 

**  Deve:  Bull.  Soc.  Anat.  Paris,  1903,  p.  261. 

589 


590  DISEASES   OF  THE    GALL-BLADDER. 

be  attached  to  the  left  margin  of  the  hver  (tide  Fig.  3),  and  may  be- 
come so  situated  as  to  have  its  long  axis  at  right  angles  to  the  long 
axis  of  the  body. 

In  some  instances  the  fundus  of  the  gall-bladder  is  deeply  indented 
into  the  substance  of  the  liver,  and  may  show  through  on  the  anterior 
surface  of  the  right  lobe,  looking  like  a  cyst  embedded  in  the  substance 
of  the  organ.  The  notch  at  the  .anterior  margin  of  the  liver  is  absent 
in  these  cases.  In  exceptional  instances  the  posterior  surface  of  the 
gall-bladder  may  be  covered  over  for  some  distance  by  a  bridge  of  Hver 
substance  and  justifies  the  term  intra-hepatic  gall-bladder.     (Deve.) 

Abnormalities  in  Size  and  Shape  of  the  Gall-bladder.— Quite 
apart  from  inflammation  or  gall-stones  the  fundus  of  the  gall-bladder, 
just  where  it  projects  beyond  the  anterior  margin  of  the  hver,  may  show 
a  constriction  which  resembles  the  pathological  hour-glass  gall-bladder. 
The  projecting  portion  of  the  gall-bladder  may  be  twisted  like  a  fish- 
hook (Deve).  In  rare  instances  fat  is  found  under  the  peritoneal  coat 
of  the  gall-bladder;  it  is  of  no  pathological  importance.  Subserous 
oedema  is  sometimes  present  in  cases  of  ascites,  in  the  backward 
pressure  of  heart-disease,  and  occasionally  when  there  is  no  associated 
pathological  change  to  be  found. 


ACUTE  CHOLECYSTITIS. 

Acute  cholecystitis  has  various  degrees  of  intensity;  it  may,  hke 
appendicitis,  be  catarrhal,  suppurative,  ulcerative,  and  phlegmonous  or 
gangrenous,  according  to  the  virulence  of  the  infection  and  the  resistance 
of  the  organ.  It  is  possible  that  an  inflammation  which  at  first  is  charac- 
terized by  a  serofibrinous  exudation  may  subsequently  become  purulent, 
so  that  what  is  an  acute  serous  cholecystitis  at  the  outset  may  eventually 
present  itself  as  an  empyema  of  the  gall-bladder.  The  causes  of  acute 
cholecystitis  will  first  be  considered  generally,  and  then  a  separate  de- 
scription will  be  given  of  the  acute  catarrhal,  suppurative,  phlegmonous, 
and  gangrenous  forms. 


CAUSES  OF  ACUTE  CHOLECYSTITIS. 

Acute  inflammation  of  the  gall-bladder  is  very  closely  bound  up  with 
the  same  process  in  the  ducts,  and  from  the  point  of  view  of  causation 
it  is  rather  an  artificial  distinction  to  describe  these  two  conditions 
separately.  Acute  inflammation  may  begin  in  the  ducts,  as  in  suppura- 
tive cholangitis  due  to  the  rupture  of  an  hydatid  cyst  into  the  ducts,  and 
spread  to  the  gall-bladder.  In  some  instances  an  acute  cholangitis  may 
infect  the  gall-bladder,  which  eventually  goes  on  to  suppuration  while 
the  primary  lesion  resolves.  On  the  other  hand,  acute  inflammation 
may  begin  in  the  gall-bladder,  as  in  typhoidal  infection,  and  remain 
limited  to  it,  or  subsequently  spread  to  the  ducts. 

The  conditions  leading  to  acute  cholecystitis,  whether  suppurative 
or  not,  are:   (1)  Disposing;  (2)  exciting. 

I.  DISPOSING  CAUSES. 

The  factors  which  reduce  the  resistance  of  the  gall-bladder  and  render 
it  more  liable  to  infection  and  inflammation  are:  (a)  A  previous  attack 
of  inflammation  of  the  gall-bladder  naturally  renders  the  organ  more 
susceptible.  Possibly  the  micro-organisms  may  remain  in  a  latent  condi- 
tion and  a  relapse  may  be  induced.  Further,  an  attack  of  mild  chole- 
cystitis leads  to  the  formation  of  calculi  in  the  gall-bladder. 

(b)  Calculi  in  the  gall-bladder  may,  by  their  action,  render  a  secondary 
infection  more  easy. 

(c)  The  rare  occurrence  of  foreign  Ixxlies,  such  as  worms,  the  ova 
of  parasites,  in  the  gall-ljladdor  would  haA'e  a  similar  influence  to  calculi 
in  the  gall-bladder. 

(d)  Any  factors  leading  to  l)iliarv  o])struction  or  stagnation  of  bile 
in  the  gall-bladder  favour  the  multii)lication  of  any  micro-organisms 
which  have  gained  entrance  to  tlie  gall-bladder,  inasmucli  as  they  are 
not  fluslied  out,  l)ut  remain  in  lliat  viscus.     These  factors  are  discussed 

591 


592  DISEASES    OF   THE    GALL-BLADDER. 

under  the  heading  of  Gall-stones  (p.  703),  and  include  sedentary  habits, 
obesity,  abdominal  tumors,  pregnancy,  tight  lacing,  and  other  conditions 
which  interfere  with  the  descent  of  the  diaphragm. 

II.  DIRECT  OR  EXCITING  CAUSES. 

(a)  Microbic  infection  of  the  gall-bladder;  this  is  the  cause  of  almost 
all  the  cases. 

(6)  Toxines  reaching  the  gall-bladder  and,  in  the  absence  of  any 
micro-organisms,  setting  up  cholecystitis.  This  is  largely  a  theoretical 
consideration. 

(c)  Traumatism  of  the  gall-bladder. 

(A)  Microbic  Infection. — The  infectious  diseases  which  lead  to  local 
manifestations  in  the  gall-bladder,  by  means  of  microbic  infection,  may 
be  divided  into  two  classes,  which,  however,  to  a  certain  extent,  overlap : 
(1)  General  hsemic  infections.  (2)  Diseases  of  the  alimentary  canal  and 
the  direct  spread  of  acute  inflammation  from  the  larger  bile-ducts.  (Vide 
Cholangitis.) 

In  the  first  group  come  septicaemia,  pyaemia,  and  influenza,  while  in 
chronic  Bright's  disease,  where  terminal  infections  are  common,  the  gall- 
bladder might  be  picked  out.  The  diseases  of  the  alimentary  canal  in- 
clude typhoid  fever,  which  is  of  great  interest,  cholera  (Galliard  *),  and 
other  microbic  infections  of  the  bowel.  Appendicitis  is  a  probable  focus 
from  which  micro-organisms  may  travel  to  the  liver  and  the  gall-bladder  t 
and  it  is  far  from  uncommon  to  find  gall-stones  (or  the  evidence  of  past 
cholecystitis)  and  appendicitis  in  the  same  individual.  Influenza  may 
also,  in  virtue  of  its  gastro-intestinal  form,  be  included  under  this  heading. 

(1)  In  general  hcemic  infections  micro-organisms  may  reach  the  gall- 
bladder, being  excreted  into  its  cavity  and  into  the  bile-ducts  from  the 
branches  of  the  hepatic  artery.  Acute  cholecystitis  may  follow  pneu- 
monia and  be  due  to  infection  of  the  gall-bladder  with  the  Diplococcus 
pneumoniae. 

Acute  cholecystitis  apparently  following  influenza,  but  resolving,  so 
that  no  proof  of  its  nature  can  be  obtained,  is  probably  not  very  rare. 
Some  of  the  cases  of  jaundice  following  influenza  may  show  cholecystitis, 
as  well  as  inflammation  of  the  ducts. 

F.  A.  Packard  t  records  a  case  of  what  appeared  to  be  influenzal  cholecystitis. 
The  following  case  occurred  at  St.  George's :  A  man  aged  forty  was  admitted  luider 
my  care  with  the  pains  of  influenza  behind  the  eyes  and  in  the  limbs.  He  had  had 
a  sudden  onset  of  vomiting  and  intense  colic,  like  that  of  gall-stones.  There  was 
tenderness  oyer  the  gall-bladder,  which  could  not  be  felt,  and  the  vermiform  ap- 
pendix, but  there  was  no  jaundice  and  no  calculus  could  be  found  in  the  stools. 
He  made  a  rapid  recovery.  The  case  appeared  to  be  one  of  the  gastro-intestinal 
form  of  influenza  with  cholec3'stitis. 

In  diseases  of  the  alimentary  canal  the  infection  of  the  gall-bladder  is 
due  to  the  passage  of  micro-organisms,  especially  the  colon  and  typhoid 

*  Galliard :  La  Cholera.  Bibliotheque  Charcot-Debove,  1894. 
t  Vide  Ochsner:  Philadelphia  Med.  Journ.,  Oct.  6,  1900,  p.  652. 
t  Packard:  Philadelphia  Med.  Journ.,  Nov.  4,  1899,  p.  879. 


ACUTE    CHOLECYSTITIS.  593 

bacilli,  from  the  bowel  to  the  gall-bladder.  The  channel  by  which  this 
infection  takes  place  is  often  assumed  to  be  one  of  direct  extension  up 
the  common  bile-duct.  In  the  case  of  typhoidal  cholecj^stitis  there  are 
grounds  for  doubting  whether  this  is  necessarily  the  case.  (Vide  p.  595.) 
The  fact  that  under  normal  conditions  the  empty  duodenum  is  sterile, 
or  almost  so,  makes  it  probal^le  that  in  the  absence  of  duodenal  inflam- 
mation micro-organisms  reach  the  gall-bladder  by  the  blood  stream 
rather  than  by  direct  extension  up  the  common  bile  and  cystic  ducts. 
The  occurrence  of  influenzal  cholecystitis  has  already  been  referred  to. 
The  relation  of  appendicitis  and  cholecystitis  is  one  of  considerable 
interest.  The  two  conditions  may  coexist.  It  is  possible  that  in  some 
cases  both  organs  are  attached  by  a  simultaneous  infection;  that  in  others 
appendicitis  is  primary  and  provides  an  inlet  for  micro-organisms  which 
set  up  cholecystitis  (Ochsner  *),  or,  lastly,  that  the  cholecystitis  is  primary 
and  the  appendicitis  secondary  (Dieulafoy  f)-  Catarrhal  or  suppurative 
cholecystitis,  with  or  without  gall-stones,  may  be  found  associated  with 
appendicitis. 

Cholecystitis  Due  to  Infection  with  Bacillus  Coli. — This  subject  is  of 
great  importance  in  connexion  with  the  production  of  gall-stones,  and 
is  referred  to  under  that  heading.  The  channels  by  which  colon  bacilli 
pass  into  the  gall-bladder  are  probably  much  the  same  as  those  by  which 
typhoid  bacilli  reach  the  gall-bladder,  viz.,  by  the  blood  of  the  portal 
vein.  In  some  cases  an  ascending  infection  from  the  duodenum  may 
occur.  Infection  of  the  gall-baldder  may  follow^  intestinal  disorders  in 
which  the  colon  bacilli  become  virulent,  or  may  be  due  to  absorj3tion  of 
bacilli  from  an  intestinal  ulcer  or  possibly  from  an  inflamed  vermiform 
appendix. 

Cholecystitis  Due  to  Typhoidal  hifection. — The  clinical  fact  that  in- 
flammation of  the  gall-bladder  may  complicate  t3'phoid  fever  has  been 
known  since  Louis'  and  Andral's  time  (1826).  Budd,t  Ayres,§  Pepper,  || 
and  other  observers  recorded  early  cases.  A  good  resume  of  the  history 
of  typhoidal  cholecystitis  will  be  found  in  A.  L.  Mason's,**  and  Camac'sft 
articles. 

Gilbert  and  Girode,|J  in  1890,  were  the  first  to  prove  bacteriologically 
that  suppurative  cholecystitis  may  be  due  to  typhoid  bacilli.  Since  that 
time  numerous  cases  confirming  this  discovery  have  been  reported  by 
Chiari^^  and  others. 

Cholecystitis  during  or  after  typhoicHever  need  not,  however,  be  cUie  to  tj^phoidal 
infection.     Thus  Gushing  ]!  ||  has  met  with  five  cases  of  post-typhoidal  cholecystitis 

*  Ochsner:  Philadelphia  Med.  Journ.,  Oct.  6,  1900,  p.  652. 
t  Dieulafoy:  La  presse  Medicale,  June  17,  1903,  p.  445 
t  Budd:  Diseases  of  the  Liver,  2d  ed.,  1S57,  p.  195. 
§  Ayres:  New  York  .Tourn.  Med.,  1840,  vol.  vii,  p.  315. 
II  Pepper,  W.,  Sr. :  American  .louni.  Medical  Sciences,  Jan.,  1857. 
**  Mason,  A.  L. :  Trans.  Assoc.  American  Pliysicians,  vol.  xii,  p.  23. 
tt  Camac:  American  Journ.  Med.  Sciences,  1899,  vol.  cxvii,  ]).  275. 
it  Gilbert  and  Girode:  G.  R.  et  Mem.  de  la  Soc.  biol.  Paris,  1890,  p.  7.56,  1890; 
ibid.,  1893,  p.  956. 

f^§  Chiari:  Prag.  med.  \\'ochen.,  1893,  Xo.  22.  Zeitschrift  f.  Ilcilkunde,  Bd.  xv, 
S.  199. 

II II  Cashing :  Johns  Hopkins  Hosp.  Bulletin,  May,  1898. 
38 


594  DISEASES    OF   THE    GALL-BLADDER. 

in  which  a  pure  culture  of  Bacillus  coli  was  obtained.     There  may  be  a  mixed 
infection  of  BaciUus  coU  and  Bacillus  tj-phi,  as  in  ^larsden's  *  case. 

The  incidence  of  cholecystitis  in  typhoid  fever  is  difficult  to  estimate, 
inasmuch  as  the  shghter  cases  must  often  escape  detection.  Sometimes 
palpation  of  the  gall-bladder  gives  rise  to  pain  but  to  no  further  symp- 
toms, and  it  is  impossible  to  speak  -^dth  any  certainty  as  to  the  condition 
of  affairs.  Murcliisonf  and  Cliiari's  obsen-ations  are  in  favour  of  latent 
cholecystitis  in  enteric  not  being  uncommon.  Camac  has  collected  115 
cases. 

In  494  cases  of  enteric  at  Montreal  tabulated  by  Gillies  X  there  were  four  ex- 
amples of  cholecystitis,  of  which  one  (suppurative)  was  fatal. 

In  1016  cases  of  enteric  fever  admitted  into  the  Imperial  Yeomanry  Hospitals 
in  South  Africa  during  the  War  1900-1901  only  one  case  of  cholecystitis  was  suffi- 
ciently marked  to  require  operation  or  to  be  recognised  beyond  any  doubt. 

Typhoidal  cholecystitis  usually  occurs  in  young  adults,  but  cases  in 
girls  of  five  and  six  years  old  have  been  recorded  by  Alexief  §  and 
Mason.  ]| 

There  is  very  considerable  variation  in  the  inter^-al  between  the  pri- 
mary attack  of  typhoid  fever  and  the  attack  of  cholecystitis.  It  may  com- 
plicate the  attack  or  may  occur  as  long  as  fourteen  **  or  twent}^  jt  years 
after.  In  some  instances  there  is  no  history  of  any  attack  of  tj'phoid 
fever.  (Osler,±J  Cushing,tf  Richardson.  §§)  Cholecystitis  complicating 
typhoid  fever  is  ver>"  seldom  associated  with  cholelithiasis,  though  the 
presence  of  gall-stones  would  dispose  the  gaU-bladder  to  inflanunation 
should  enteric  fever  super\^ene.  Acute  cholecystitis  following  typhoid 
fever  after  an  interi^al  of  months  or  years  is  more  often  associated  "^dth 
cholehtliiasis. 

In  1898  Gushing  collected  6  cases  of  post-typhoid  cholecystitis  associated  with 
gall-stones  which  had  been  operated  upon  and  shown  to  contain  the  tj^phoid  bacilli. 
In  31  cases  of  cholecj'stitis  operated  upon  by  Halsted  10  gave  a  history  of  enteric 
fever,  the  inter\'al  being  from  a  few  months  to  twenty  years.  ||  || 

It  is  generally  assumed  that  the  bacilU  found  in  the  gaU-bladder  years 
after  an  attack  of  tj^Dhoid  are  the  descendants  of  those  that  gave  rise 
to  the  original  illness.  But  it  is  possible  that  thej^  have  been  subse- 
quently derived  from  the  alimentarj"  canal  of  a  person  who,  from  a 
previous  attack  of  enteric  fever,  is  immune. 

The  t}Tohoicl  bacilli  may  conceivably  reach  the  gall-bladder  by  several 
routes,  viz.,  by  the  portal  vein,  the  hepatic  artery,  the  common  bile-duct, 
or  possibly  even  through  the  walls  of  the  bowel. 

*  Marsden:  Medical  Ghronicle,  Jan.,  1901,  p.  269. 

t  Murchison:  Gontinued  Fevers,  3d  ed.,  p.  634. 

j  Gillies:  Montreal  Medical  Joum.,  June,  1900. 

§  Alexief:  Joum.  Lietskaya    Meditzina,   1896;  abstract    in  American    Journ. 
Med.  Sciences,  Oct.,  1897. 

II  Mason :  Trans.  Assoc.  American  Physicians,  vol.  xii,  p.  23. 
**  V.  Dungern:  Miinchen.  med.  Wochen.,  June  29,  1897. 
tt  Osier:  Trans.  Associat.  American  Physicians,  vol.  xii,  p.  384,  1897. 
tt  Gushing:  Bull.  Johns  Hopkms  Hosp.,  May,  1898. 

§§  Richardson,  M. :  American  Joum.  Med.  Sciences,  June,  1898,  vol.  cxv,  p.  648. 
nil  Quoted  by  Gushing:  Johns  Hopkins  Hosp.  Bull.,  May,  1898. 


ACUTE    CHOLECYSTITIS.  595 

By  the  Portal  Vein. — The  bacilli  have  but  a  short  way  to  travel  to  reach  the 
liver  by  the  portal  vein;  here  they  set  up  areas  of  focal  necrosis,  and,  having  thus 
injured  the  liver  tissue,  are  able  to  pass  into  the  bile-ducts. 

Sherrington  *  has  shown  that  bacilli  alone,  even  though  teeming  in  the  blood, 
cannot  pass  through  normal  hepatic  tissues,  but  that  some  previous  damage  by  the 
toxines  they  produce  is  first  necessary.  Carmichael  t  has  also  shown  that  after 
injections  of  typhoid  cultures  mto  the  portal  vein  the  bile  still  remains  sterile.  It 
is,  however,  not  improbable  that  during  the  course  of  typhoid  fever  the  walls  of 
the  ducts  or  of  the  gall-bladder  would  become  damaged  by  toxines  excreted  from 
the  blood-stream  and  so  permeable  to  micro-organisms,  and  that  typhoidal  infec- 
tion from  the  portal  vein  may  then  take  place. 

From  the  Hepatic  Artery. — Typhoid  bacilli  may  also  reach  the  liver  by  the 
hepatic  artery  and  so  be  excreted  into  the  bile-ducts  and  gall-bladder.  Though 
in  typhoid  fever  bacilli  are  not  ordinarily  present  in  the  general  circulation,  thej^ 
may  pass  out  of  the  portal  system  into  the  circulation  in  a  kind  of  wave,  and  then 
settle  down,  in  the  bone-marrow,  liver,  and  other  situations,  the  circulation  thus 
becoming  cleared  of  them.  This  is  shown  by  the  fact  that  typhoid  bacilli  may 
pass  into  the  urine.  In  cases  of  typhoidal  septicaemia  without  intestinal  ulceration 
the  baciUi  have  been  found  in  the  bile.  So  both  in  ordinary  typhoid  fever  and  in 
typhoid  septicaemia  typhoid  bacilli  may  travel  by  the  arterial  system  to  the  liver. 

By  Direct  Extension  up  the  Common  Bile-duct. — The  motile  typhoid  bacilli 
might  readily  travel  from  the  duodenum  up  the  common  bile-duct  and  reach  the 
gall-bladder.  The  belief  in  an  ascending  infection  of  the  gall-bladder  from  the 
duodenum  is  widely  received.  Carmichael,|  finding  that  experimental  injection 
of  various  micro-organisms  into  the  portal  vein  did  not  lead  to  infection  of  the  bile, 
argues  in  favour  of  a  direct  extension  up  the  common  bile-duct. 

Gushing  and  Livingood,§  however,  in  experiments  on  the  bacteriological  con- 
dition of  the  duodenum,  find  that  it  is  often  sterile  when  not  containing  food, 
while  the  lower  portion  of  the  small  intestine  contains  numerous  micro-organisms. 
This  would  in  some  degree  render  an  ascending  infection  of  the  ducts  improbable. 
Further,  if  typhoidal  cholecystitis  were  an  ascending  infection,  it  is  probable  that 
other  micro-organisms,  such  as  the  Bacillus  coli  or  streptococci,  would  be  present, 
and  that  the  culture  would  not  be  a  pure  one.  (Gushing.  ||)  On  these  grounds  it 
is  unlikely  that  the  infection  in  typhoidal  cholecystitis  is  an  ascending  one. 

It  has  been  suggested  that  micro-organisms  pass  directly  through  the  walls 
of  the  intestine  into  the  peritoneal  cavity  and  then  through  the  walls  of  the  gall- 
bladder. This  may  take  place  when  both  the  viscera  concerned  are  inflamed  and 
so  allow  of  the  passage  of  micro-organisms  through  their  walls;  in  this  way  a  sec- 
ondary infection  of  the  gall-bladder  when  already  inflamed  may  be  brought  about, 
but  it  is  highly  improbable  that  primary  gall-bladder  infection  is  started  in  this 
way. 

Typhoid  bacilli  are  almost  constantly  present  in  the  gall-bladder  in 
fatal  cases  of  typhoid  fever;  this  contrasts  with  the  comparative  infre- 
quency  of  cholecystitis.  Probably  some  additional  factor,  such  as  trau- 
matism, previous  disease,  gall-stones,  or  extreme  stagnation  of  bile,  is 
necessary  before  the  bacilli  are  able  to  set  up  cholecystitis. 

Bacteriology  of  Cholecystitis. — Besides  the  colon  and  t^'phoid  bacilli, 
streptococci,  staphylococci,  or  pneumococci  may  give  rise  to  cholec3'stitis. 
The  Diplococcus  pneumoniae  may  attack  the  gall-bladder  primarily,  there 
being  no  pulmonary  or  other  manifest  lesions.  According  to  Richard- 
son,** pneumococcal  cholecystitis  is  more  acute  and  severe  than  that 
due  to  colon  or  typhoidal  infection.  Mignot  tt  foimd  that  tliere  was 
no  remarkable  anatomical  difference  in  experimental  cholecystitis  due  to 

*  Sherrington:  Journ.  Path,  and  Bact.,  vol.  i,  p.  258,  1893. 

t  Carmichael:  Journ.  Path,  and  Bact.,  vol.  viii,  p.  276. 

j  Garmichael:  Journ.  Path,  and  Bact.,  vol.  viii,  p.  27G. 

§  Gushing  and  Livingood :  Johns  Hopkins  Hosp.  Reports,  vol.  ix. 

II  Gushing:  Johns  Hopkins  liuUetin,  Nos.  101,  102,  Aug.-Sept.,  1899. 
**  Richardson:  American  Journ.  Med.  Sciences,  June,  1898,  vol.  cxv,  p.  637. 
tt  Mignot:  Th^se  Paris,  1897. 


596  DISEASES    OF   THE    GALL-BLADDER. 

streptococci;  staphylococci,  or  the  colon  bacillus.  Secondary  infections 
may  occur,  so  that  typhoid  bacilli,  streptococci,  staphylococci,  etc.,  may 
be  found  together.  In  primary  typhoidal  cholecystitis  the  inflamed 
gall-bladder  may  become  adherent  to  adjacent  intestinal  coils,  and  the 
tissues  being  inflamed,  micro-organisms  may  pass  from  the  bowel  into 
the  gall-bladder. 

Wanchscheim  *  records  a  case  bearing  this  interpretation.  In  a  fatal  case  of 
typhoid  fever  the  gall-bladder  contained  pus  and  typhoid  bacilli  while  the  peritoneal 
lymph  on  the  surface  of  the  gall-bladder  showed  the  Staphylococcus  pyogenes  aureus, 
which  was  regarded  as  a -secondary  infection  from  the  walls  of  the  intestine. 

(B)  Toxic  Cholecystitis. — Although,  practically  speaking,  acute 
cholecystitis  is  always  due  to  bacterial  infection  of  the  gall-bladder,  it 
has  been  shown  by  Claude's  t  experiments  that  bacterial  poisons  are 
capable  of  inducing  changes  allied  to  inflammation  in  the  gall-bladder. 

In  82  animals  poisoned  with  abrin  or  with  the  toxines  of  diphtheria,  tetanus, 
streptococci,  staphylococci,  Bacillus  coli,  and  Bacillus  pyocyaneus  Claude  found 
haemorrhages  into  the  gall-bladder  in  seven. 

On  the  analogy  of  toluylendiamin,  which  sets  up  an  inflammation  of 
the  small  ducts  in  the  liver  which  may  spread  down  into  the  duodenum 
(Hunter  J),  it  is  reasonable  to  assume  that  toxic  inflammation  of  the 
small  bile-ducts  in  man  might  extend  into  the  gall-bladder  and  set  up 
acute  cholecystitis.  It  is,  however,  probable  that  if  a  toxic  cholecystitis 
occurred  it  would  soon  become  infected  with  micro-organisms  reaching 
the  gall-bladder  by  the  blood-stream.  As  the  matter  stands,  cholecystitis 
due  to  poisons,  as  apart  from  microbic  infection,  is  a  theoretical  possi- 
bility rather  than  an  established  occurrence  in  practice. 

Traumatism,  such  as  a  fall  or  blow  in  the  region  of  the  gall-bladder, 
may  so  reduce  its  resistance  that  any  micro-organisms  present,  which 
would  otherwise  be  removed  or  destroyed,  are  enabled  to  gain  a  footing 
and  set  up  inflammation.  It  is  known,  for  example,  that  in  typhoid 
fever  the  bacilli  are  practically  always  found  in  the  gall-bladder,  but  that 
cholecystitis  is  comparatively  infrequent.  Traumatism  in  such  cases 
would  be  a  directly  exciting  cause  of  cholecystitis.  A  blow  may  set  up 
acute  inflammation  in  cases  where  a  calculus  is  latent  in  the  gall-bladder. 

Kehr  §  reports  the  case  of  a  doctor,  who  after  being  knocked  down  by  a  bicyclist, 
rapidly  developed  acute  inflammation  in  a  contracted  gall-bladder  the  cystic  duct 
of  which  was  blocked  bj^  a  single  calculus. 

FORMS  OF  ACUTE  CHOLECYSTITIS. 

There  are  several  forms  of  acute  cholecj'stitis.  In  the  least  severe, 
serous  or  catarrhal  cholecystitis,  the  exudation  does  not  contain  pus. 
In  suppurative  cholecystitis  the  gall-bladder  is  the  site  of  an  acute  puru- 
lent inflammation.  Midway  between  these  two,  and  somewhat  difficult 
to  include  in  either,  is  chronic  empyema  of  the  gall-bladder.     In  this 

*  Wanchscheim :  Prag.  med.  Wochen.,  1898. 

t  Claude :  Bull.  Soc.  Anat.  Paris,  1896,  p.  502.     Medical  Week,  1897,  p.  309. 

t  Hunter,  AV. :  Trans.  Path.  Soc,  vol.  xli,  p.  105. 

§  Kehr:  Gail-Stone  Disease,  p.  223,  American  translation. 


ACUTE    CHOLECYSTITIS.  597 

condition  an  acute  attack  of  inflammation  is  succeeded  by  a  chronic 
infection  of  the  gall-bladder  which  gives  rise  to  the  gradual  formation 
of  pus.  This  chronic  suppurative  cholecj^stitis  is  clinically  more  alhed 
to  dropsy  of  the  gall-bladder,  and  is  referred  to  again  as  one  of  the  sequelae 
of  acute  catarrhal  cholecystitis.  The  most  severe  forms  of  acute  chole- 
cystitis are  the  phlegmonous  and  gangrenous. 

It  will  be  seen  that  these  three  forms,  catarrhal,  suppurative,  and 
phlegmonous,  constitute  an  ascending  series  in  the  severity  of  the  in- 
flammation, but  that  they  merge  into  each  other,  and  that  a  distinction 
between  anv  two  of  them  mav  be  difficult. 


ACUTE  CATARRHAL  INFECTIVE  CHOLECYSTITIS. 

Under  this  heading  are-  included  acute  inflammations  of  the  gall- 
bladder which  stop  short  of  the  production  of  pus.  A  number  of  different 
forms  of  inflammation  are  here  grouped  together.  In  some  instances 
there  is  only  a  serous  exudation;  in  others  it  is  serofibrinous  or  may  go 
on  to  ulceration.  Acute  catarrhal  cholecystitis  is  also  an  early  stage. of 
suppurative  inflammation. 

The  causes  of  cholecystitis  have  already  been  described,  and  need 
not  be  recapitulated,  but  it  may  be  pointed  out  that  the  less  severe 
form  (catarrhal)  of  acute  cholecystitis  may  be  produced  by  the  same 
micro-organisms  which,  under  more  favourable  conditions  or  when  more 
virulent,  set  up  suppurative  inflammation;  thus  typhoidal  infection  of 
the  gall-bladder  may  give  rise  to  a  simple  serous  cholecystitis  or  to  a 
severe  suppurative  inflammation. 

Morbid  Anatomy. — The  gall-bladder  is  distended  and  its  walls  are 
tense;  the  serous  coat  may  be  dulled  from  the  presence  of  fibrin, 
and  adherent  to  adjacent  parts.  In  severe  cases  the  coats  of  the  gall- 
bladder are  swollen  from  infiltration  and  softened.  The  mucous  mem- 
brane is  congested,  and  may  be  ulcerated  or  show  a  deposit  of  bile  on 
its  surface.  The  cystic  duct  is  often  closed  by  catarrhal  swelling  of  its 
mucous  membrane,  or,  as  the  result  of  past  inflammation  and  ulceration 
due  to  the  passage  of  a  calculus,  may  be  permanently  obliterated.  The 
cystic  duct,  hoM^ever,  is  not  necessarily  closed  in  catarrhal  cholecystitis. 
The  contents  of  the  gall-bladder  may  be  practically  clear  and  like  serum 
when  the  cystic  duct  has  been  blocked  for  some  time,  or  consist  of  sero- 
fibrinous or  bile-stained,  turbid  fluid.  There  may  be  gall-stones  or  in- 
spissated bile.  The  lymphatic  glands  in  relation  to  the  cystic  and  com- 
mon bile-ducts  are  enlarged.  In  cases  where  recurrent  attacks  of  acute 
cholecystitis  occur  the  glands  may  become  so  hard  as  to  imitate  infiltra- 
tion with  malignant  disease,  when  felt  during  an  operation. 

Microscopically  the  fibromuscular  coat  shows  small-cell  infiltration 
and  dilatation  of  the  bl()()d-\'cssels.  It  is  difficult  to  speak  with  any 
certainty  al)out  the  condition  of  the  mucous  membrane,  since  under 
normal  conditions  the  mucosa  is  macerated  and  destroyed  by  the  bile 
and  disappears  about  five  hours  after  death.     (Sudler.*)      In  the  less 

*  Stidlcr,  M.  '['.:  Proo.  .\ssoc.  American  Aiia((iini-.t  s,  1900,  ]).  177. 


598  DISEASES    OF   THE    GALL-BLADDER. 

severe  cases  one  would  expect  to  find  catarrhal  inflammation  of  the 
mucous  membrane. 

In  specimens  I  have  examined  the  inner  surface  of  the  gall-bladder 
has  been  lined  by  small  cells  resembling  granulation  tissue,  and  the 
culs-de-sac  of  the  tubular  glands  are  seen  to  be  inflamed. 

Clinical  Features. — Acute  catarrhal  cholecystitis  probably  varies 
a  good  deal  in  its  severity  in  different  cases  and  in  different  infections. 
Many  of  the  slighter  examples  never  come  under  obser\-ation,  while 
others  are  entirely  overlooked  or  are  regarded  as  dyspepsia,  cohc,  etc.; 
in  many  of  these  cases  the  symptoms  are  not  sufficiently  marked  to 
allow  of  accurate  diagnosis.  The  frequency  with  which  the  gall-bladder 
is  found  at  autopsies  to  be  adherent  to  the  stomach  or  colon  T\dthout 
any  evidence  of  chronic  inflammation  supports  the  behef  that  acute 
cholecystitis  is  by  no  means  uncommon.  Another  argument  is  that  gall- 
stones are  due  to  some  past  attack  of  cholecystitis  and  that  in  many,  if 
not  most,  cases  of  cholelithiasis  there  is  no  history  of  such  an  acute 
attack. 

The  signs  and  symptoms  of  acute  cholecystitis  are  b}^  no  means 
constant,  and  in  this  respect  the  chnical  picture  of  acute  cholecystitis 
resembles  that  of  appendicitis. 

Acute  cholecystitis  is  very  likely  to  escape  detection  when  it  occurs 
during  the  course  of  typhoid  fever.  The  abdominal  signs,  pain,  etc., 
may  be  thought  to  be  due  to  the  original  disease,  and  the  patient,  from 
mental  torpor,  may  not  complain  of  pain  in  the  region  of  the  gall-bladder. 

In  a  well-marked  case  the  earhest  and  most  prominent  symptoms  are 
local  pain  and  tenderness.  The  character  of  the  pain  may  vary:  in  most 
instances  it  is  paroxysmal  and  resembles  that  of  gall-stone  colic,  but 
is  less  excruciating.  It  must  be  remembered  that  more  or  less  acute 
cholecystitis  probably  always  accompanies  gall-stone  colic,  and  that  the 
inflammatory  process  is  probably  responsible  for  the  passage  of  the 
calculus  out  of  the  gall-bladder  {vide  p.  723).  The  pain  may  be  con- 
tinuous from  inflammation  of  the  serous  coat  and  dull. 

The  pain  may  shoot  down  into  the  right  iliac  fossa  and  be  so  definiteh" 
localised  there  as  to  suggest  appendicitis.  This  seems  to  be  due  to  the 
fact  that  in  these  cases  local  peritonitis  set  up  by  cholecystitis  involves 
the  serous  coat  of  the  appendix  and  therefore  naturally  produces  symp- 
toms of  appendicitis  (Tripier  and  Paviot  *).  It  is  not  surprising  that 
cases  of  cholecystitis  are  often  diagnosed  and  operated  upon  as  appen- 
dicitis. 

The  two  conditions,  cholec3^stitis  and  appendicitis,  may  occur  to- 
gether, and  it  is  not  improbable,  as  suggested  by  Ochsner,t  that  the 
infective  micro-organisms  responsible  for  cholecystitis  may,  in  some 
instances,  be  derived  from  an  inflamed  appendix. 

There  is  tenderness  over  the  upper  right  quadrant  of  the  abdomen, 
which  becomes  localised  and  more  intense  over  the  region  of  the  gall- 
bladder, at  a  spot  a  little  above  and  to  the  right  of  the  imibilicus,  or,  to 

*  Tripier  and  Paviot:  La  Semaine  Medicale,  1903,  p.  29. 
t  Ochsner:  Philadelphia  Med.  Journ.,  1900,  Oft.  6,  p.  652. 


ACUTE    CHOLECYSTITIS.  599 

be  more  exact,  at  the  junction  of  the  upper  two-thirds  with  the  lower 
third  of  a  Hne  drawn  from  the  ninth  rib  to  the  umbiUciis.  (Mayo 
Robson.)  The  gall-bladder  may  be  felt  and  sometimes  seen  as  a  pear- 
shaped  tumor,  either  fluctuating  or  rather  tense.  It  usualty  moves  with 
respiration  and  can  be  displaced  laterally  like  a  pendulum.  It  may, 
however,  be  quite  fixed  from  the  presence  of  old  adhesions.  The  dis- 
tension of  the  gall-bladder  is  due  to  the  inflammatory  exudation  being 
rmable  to  pass  through  the  cystic  duct,  the  mucous  membrane  of  which 
is  swollen.  When  the  acute  inflammation  subsides,  the  fluid  is  able  to 
discharge  through  the  cystic  duct  and  the  tumor  disappears.  There 
may  be  distinct  tenderness,  but  no  palpable  tumor,  in  the  position  of 
the  gall-bladder,  which  is  covered  by  intestines  in  a  condition  of  paral5i;ic 
distension  due  to  peritonitis  spreading  from  the  gall-bladder.  From  this 
tympanitic  distension  the  right  h}q30chondrium  and  epigastrium  may 
become  somewhat  prominent. 

Halsted  *  records  a  remarkable  case  where  sharpty  localised  paral3i;ic  dila- 
tation of  the  first  part  of  the  duodenum  and  pjdoric  end  of  the  stomach,  corre- 
sponding to  circumscribed  peritonitis,  was  foimd  at  an  operation  for  removal  of 
gall-stones  from  the  gall-bladder.  The  paralysed  bowel  was  glued  to  the  gall- 
bladder by  recent  exudation.  The  walls  of  the  gall-bladder  were  white  and  thiclv- 
ened,  and  its  cavity  contained  fluid  like  white  of  egg. 

Local  peritonitis  around  the  gall-bladder  often  sets  up  vomiting, 
just  in  the  same  way  as  in  appendicitis,  and  the  symptoms  of  acute 
intestinal  obstruction  may  arise. 

Richardson  f  refers  to  four  cases  of  acute  cholecystitis  (without  cholelithiasis) 
in  which  this  occurred.  Mayo  Robson  J  previouslj^  drew  attention  to  acute  ob- 
struction due  to  paralytic  distension  of  peritonitic  origin  in  cholelithiasis.  The 
hepatic  flexure  of  the  colon  is  probably  the  part  affected.  The  symptoms  usually 
pass  off  without  surgical  interference. 

The  liver  as  a  whole  is  not  enlarged  m  cholecystitis  imless  the  inflam- 
mation has  spread  to  the  ducts,  and  so  into  the  substance  of  the  organ. 
When  cholangitis  is  superadded  to  cholecystitis,  both  jaundice  and  hepatic 
enlargement  are  produced  and  the  condition  is  more  complicated  than 
in  cholecystitis,  which  is  a  local  affection  limited  to  the  gall-bladder. 

Elongation  of  the  lower  part  of  the  right  lobe  covering  the  gall-bladder 
is  met  ^\^th  as  the  result  of  gall-stones  and  past  or  chronic  cholec3'stitis, 
and  so  might  be  present  when  an  acute  attack  supervenes  in  these  con- 
ditions. This  elongation,  often  called  Riedel's  lobe,  is  described  else- 
w^here  (p.  12). 

Jaundice  is  very  far  from  being  a  necessary  accompaniment  of  chole- 
cystitis; it  may  depend  on  an  extension  of  inflammation  and  spasm  to 
the  ducts  or  on  the  presence  of  some  obstruction  in  the  ducts.  Kehr,g 
indeed,  emphasises  the  rarity  of  jaundice  in  cholecystitis. 

In  the  mild  degrees  of  serous  and  catarrhal  cholecystitis  the  tempera- 

*  Halsted:  Johns  Hopkins  Hospital  Bulletin,  .Jan.,  1900. 
t  Richardson:  Boston  Medical  and  Surgical  .louriial,  Dec.  28,  1899. 
X  Mayo  Robson:  Trans.  Royal  Medical  and  Chirurgical  Soc,  vol.  Lxxviii,  p.  117, 
1895. 

§  Kehr :  Diagnosis  of  Gall-stone  Disease,  p.  39,  American  translation. 


600  DISEASES    OF   THE    GALL-BLADDER, 

ture  usually  remains  normal.  But  if  the  inflammation  is  severe  or  ex- 
tends to  the  ducts  or  to  the  peritoneal  coat  of  the  gall-bladder,  there 
may  be  fever,  sometimes  of  such  a  degree  as  to  suggest  suppuration, 
which,  however,  as  shown  by  operation,  is  not  present. 

In  rare  instances  micro-organisms  absorbed  from  the  mucous  mem- 
brane of  the  gall-bladder  may  give  rise  to  infection  elsewhere,  such  as 
appendicitis  (Dieulafoy  *)  or  endocarditis  (Lorrain  f). 

Diagnosis. — "WTien  the  gall-bladder  is  felt  as  a  tumor  it  must  be 
distinguished  from  such  conditions  as  impacted  fgeces  in  the  colon, 
hydronephrosis  or  renal  tumor,  and  floating  kidney.  The  differential 
diagnosis  of  a  distended  gall-bladder  from  other  conditions  is  given  on 
page  737  (mechanical  results  of  gall-stones). 

The  diagnosis  from  supj^urative  cholecystitis  may  present  considerable 
difficulties;  no  hard-and-fast  line  separates  the  more  acute  cases  of 
cholecystitis  without  actual  pus  formation  from  the  slighter  cases  of 
suppurative  cholecystitis.  Acute  cholecystitis  may  possibly  be  the  earh^ 
stage  of  the  suppurative  form.  From  a  clinical  point  of  view  the  differ- 
ence between  acute  catarrhal  and  suppurative  cholecystitis  is  one  of 
degree,  the  pain,  tenderness,  and  constitutional  symptoms  being  much 
more  marked  in  the  latter. 

From  biliary  colic,  Avhich  is  probably  always  accompanied  by  some 
inflammation  of  the  gall-bladder,  the  diagnosis  of  acute  catarrhal  chole- 
c^'stitis  may  also  be  difficult.  The  pain  is  more  excruciating  in  gall- 
stone colic,  while  the  signs  of  local  mischief,  such  as  tenderness,  paralj^tic 
distension  of  the  intestines,  or  a  palpable  tumor  in  the  situation  of  the 
gall-bladder,  are  more  prominent  in  acute  cholecystitis. 

The  milder  cases  of  acute  cholecystitis  are  sometimes  a  secondary 
part  of  acute  cholangitis,  and  are  due  to  extension  of  the  inflammatory 
process;  in  such  cases  the  aspect  of  the  disease  is  that  of  catarrhal  jaun- 
dice, the  existence  of  cholecystitis  being  determined  only  by  tenderness 
over  the  gall-bladder,  which  may,  perhaps,  be  palpably  enlarged. 

A  mistake  which  is  very  easily  made  is  to  regard  as  appendicitis  a 
case  of  cholecystitis.  This  is  very  likely  to  occur  when  the  gall-bladder 
is  dilated  or  so  elongated  as  to  reach  into  the  right  ihac  fossa.  In  cases 
where  the  right  lobe  of  the  liver  is  prolonged  into  a  Riedel's  lobe,  the 
gall-bladder  ma}^  approach  the  anatomical  situation  of  the  vermiform 
appendix,  and  Avhen  inflamed,  will  imitate  perit\q3hlitis.  The  presence 
of  peritoneal  adhesions  between  the  two  organs  may,  to  some  extent, 
account  for  the  puzzling  fact  that  in  some  cases  of  cholecystitis  the  pain 
is  referred  to  the  position  of  the  vermiform  appendix.  Adenot  %  has 
discussed  the  differential  diagnosis  of  these  two  conditions  in  considerable 
detail.  It  is  much  less  often  that  the  converse  mistake  is  made,  and  a 
case  of  appendicitis  regarded  as  cholecystitis.  But  when  the  vermiform 
appendix  is  abnormally  situated  and  runs  up  so  as  to  come  into  close 
contact  with  the  right  lobe  of  the  liver  or  even  the  gall-bladder,  appendi- 

*  Dieulafoy:  La  Presse  Medioale,  June  17,  1903,  p.  -±45. 
t  Lorrain:  Bull.  Soo.  Anat.  Paris,  1903,  p.  527. 
j  Adenot:  Lyon  Medical,  t.  xcvi,  p.  227,  1901. 


ACUTE    CHOLECYSTITIS.  601 

citis  may  imitate  cholecystitis  very  closely,  as  the  pain  and  swelling  are 
in  the  hepatic  and  not  in  the  right  iliac  region.  It  may  be  pointed  out 
that  in  the  absence  of  any  localising  signs  or  of  a  history  of  gall-stone, 
the  pain  of  cholecystitis  is  followed  by  more  severe  constitutional  symp- 
toms, such  as  collapse,  than  is  the  case  in  appendicitis.  It  should  also 
be  remembered  that  acute  inflammation  of  the  appendix  and  of  the  gall- 
bladder may  be  present  at  the  same  time. 

Prognosis. — In  the  milder  cases  of  acute  cholecystitis,  which,  how- 
ever, are  just  those  which  are  likely  to  be  overlooked,  the  progno- 
sis is  good  and  the  inflammatory  process  tends  to  subside  rapidly. 
There  is,  however,  a  strong  probability  that  gall-stones  will  result  from 
the  acute  attack,  and  that  biliary  colic  may  possibly  occur  subsequently. 
In  the  more  severe  attacks  the  danger  to  life  from  ulceration  and  per- 
foration must  be  faced,  and  the  prognosis  is  much  the  same  as  in  acute 
suppurative  cholecystitis. 

Treatment. — The  patients  should  be  kept  in  bed  on  a  nourishing  and 
easity  digestible  diet,  and  local  pain  treated  by  hot  fomentations  or,  if 
severe,  by  the  application  of  leeches.  If  the  pain  is  very  severe,  morphine 
h\"]3odermically  may  be  required;  but  it  has  the  grave  disadvantage  of 
masking  the  symptoms  and  should,  therefore,  be  given  with  reluctance. 
Sickness  should  be  controlled  by  effervescing  draughts,  bismuth,  dilute 
hydrocyanic  acid,  or  by  fractional,  -g-^Q-grain,  hypodermic  injections  of 
morphine.  In  cases  where  the  temperature  is  high  and  there  are  signs 
of  constitutional  disturbance  and  the  area  of  local  peritonitis  is  increasing, 
surgical  interference  will  very  probably  be  required.  In  cases  of  a  milder 
type  salicylate  of  soda  should  be  given,  so  as  to  increase  the  flow  of  bile 
through  the  ducts  and  so  prevent  extension  of  inflammation  from  the 
gall-bladder  to  the  ducts.  Solis-Cohen*  recommends  succinate  of  soda, 
and  Reichmannt  methylene-blue  (^-1^  grains)  in  capsules.  A  mild 
laxative  should  be  given  to  keep  the  bowels  open  and  to  favour 
evacuation  of  the  infianunatory  contents  of  the  gall-bladder. 

Sequelae  of  Acute  Cholecystitis. — Some  cases  of  sei^ous  distension 
(hydrops)  of  the  gall-bladder  may  be  due  to  transient  infective  chole- 
cystitis of  very  slight  severity,  in  which  there  is  a  calculus  at  the  neck 
of  the  gall-bladder  preventing  the  exit  of  the  inflammatorv  exudation 
through  the  cystic  duct.     (Kehr.J) 

Chronic  or  Simple  Empyema  of  the  Gall-bladder. — Acute  cholec3'stitis 
may  develop  into  suppurative  cholecystitis  rapidly,  so  that  the  process 
is,  for  all  practical  purposes,  suppurative  inflammation  of  the  gall-bladder 
throughout,  or  the  symptoms  of  acute  inflammation  may  pass  off  and 
be  followed  by  a  chronic  infective  condition  of  the  gall-bladder  which 
leads  to  the  formation  of  pus  inside  the  gall-bladder— simple  or  chronic 
empyema  of  the  gall-bladder,  as  it  has  been  called. 

From  the  presence  of  ]5us  in  the  gall-bladder  these  cases  might  be 
regarded  as  suppurative  cholecystitis,  but  their  clinical  course  is  much 

*  S.  Solis-Coheu:  Proc.  Pliihulclpliia  Count v  Med.  Soc,  vol.  xxiii,  p.  36. 

tLa  Sem.  Med.,  1903,  p.  140. 

t  Kehr:  Diagnosis  of  Gall-stones,  p.  32,  .Vnierican  translation. 


602  DISEASES    OF   THE    GALL-BLADDER. 

more  like  Iwdrops  or  dropsy  of  the  gall-bladder.  They  bear  the  same 
relation  to  acute  suppurative  cholec3^stitis  that  a  chronic  abscess  does 
to  an  acute  one.  In  these  cases  there  should  be  a  history  of  acute  chole- 
C3'stitis  in  the  past.  Later  there  are  abdominal  pain,  a  tumor,  and 
absence  of  fever.  Cases  of  simple  emp3'ema  of  the  gall-bladder  may 
intermit,  the  swelhng  passing  awa}^  and  then  recurring.  In  the  follo-^\'ing 
case  cholecystitis  supervened  in  early  primary  carcinoma  of  the  gall- 
bladder and  was  followed  by  a  chronic  empyema : 

T.  G.,  fifty-six,  a  valet  admitted  Nov.  17,  1900,  under  my  care,  with  jaimdice 
and  abdominal  pain  radiating  to  botli  shoulders,  had  been  Avell  until  two  months 
ago,  when  his  appetite  began  to  fail  and  vomitmg  came  on.  He  then  experienced 
sharp  cutting  pain,  followed  by  vomiting.  The  pain  recurred  daily  since.  Jaundice 
was  first  noticed  three  weeks  before  admission.  He  has  lost  weight;  motions  are 
clay  coloured. 

There  was  a  tense,  tender  tumor  in  region  of  gall-bladder,  but  no  enlargement 
of  the  liver.  Rectum  normal.  Free  HCl  in  vomit.  Jaundice  became  more  marked. 
Much  bile  in  urine;  motions  clay  coloured.  As  pain  continued  and  as  it  was  desir- 
able to  prevent  cholsemia,  the  probable  diagnosis  bemg  carcinoma  of  the  head  of 
the  pancreas  compressing  the  common  duct,  Mr.  Sheild  operated,  with  a  view  of 
doing  cholecystenterostomy  on  December  1,  1900;  the  gall-bladder  was  found  to 
contain  6  oimces  of  offensive  pus;  there  was  a  white  gro\(-th  on  the  surface  near 
the  middle,  and  a  hard  growth  on  its  neck,  as  well  as  a  mass  near  the  pancreas. 
After  eA'acuation  of  the  gall-bladder  a  cholecystenterostomy  (transverse  colon) 
by  means  of  Murphy's  button  was  done.  Next  day  the  man  was  less  jaundiced 
and  bile  came  away  freely  from  the  wound.  It  is  noticeable  in  connexion  with 
the  existence  of  empyema  of  the  gall-bladder  that  during  the  patient's  first 
fortnight  in  the  hospital  the  temperature  never  went  above  99°.  He  sunk  in 
two  days'  time  after  the  operation,  apparentl}'  from  asthenia. 

At  the  autops}'  there  was  extensiA'e  haemorrhage  around  the  gall-bladder,  and 
the  commmiication  between  that  viscus  and  the  colon  leaked.  The  gall-bladder 
contained  two  small  calculi,  one  in  the  neck,  but  not  impacted.  The  growth  seen 
during  the  operation  was  foimd  microscopically  to  be  a  carcinoma  invading  the 
muscular  walls  of  the  gall-bladder.  It  was  a  columnar-celled  growth  undergoing 
transition  to  a  spheroidal-celled  type.  The  CA'stic,  hepatic,  and  conunon  bile- 
ducts  were  moderateh^  dilated.  There  was  a  hard  mass  close  to  the  head  of  the 
pancreas,  adherent  to  the  common  bile-duct,  and  probabh'  obstructing  it.  On 
section  this  mass,  which  Avas  about  the  size  of  a  pigeon's  egg,  was  firm,  white,  and 
mottled  with  haemorrhages.  Microscopically  it  was  a  carcinoma  showing  a  transi- 
tion from  a  columnar-  to  a  spheroidal-celled  type.  In  this  case  cholecystitis  super- 
vened in  early  primary  carcinoma  of  the  gall-bladder,  and  was  followed  by  a  chronic 
empyema. 

Ulceration  of  the  gall-bladder  may  occur  as  the  result  of  acute  chole- 
cystitis without  there  being  am'  suppuration.  Acute  cholecystitis  also 
may  pass  into  a  condition  of  chronic  cholecystitis,  which  may  take  one  of 
two  forms:  (1)  The  atrophic  sclerogenous,  with  great  thickening  of  the 
walls  of  the  gall-bladder,  which  ultimately  contracts  and  becomes  thick- 
walled  and  shrivelled  up  (vide  p.  615).  (2)  The  catarrhal  form,  in  which 
there  is  a  distended  gall-bladder  containing  thick,  ropy,  mucous  fluid. 
Calculi  are  \'er3^  prone  to  be  produced  by  this  process. 

Another  result  of  acute  inflammation  of  the  gall-bladder  is  that  al- 
though resolution  takes  place,  adhesions  form  around  the  gall-bladder 
and  connect  it  to  the  colon,  pylorus,  or  duodenum.  These  adhesions  may 
interfere  with  the  functional  activity  of  the  stomach  and  give  rise  to 
''adhesion  dyspepsia,"  pyloric  stenosis,  and  dilatation  of  the  stomach. 
These  results  are  described  under  the  morbid  results  of  cholelithiasis 
(p.  736). 


ACUTE    CHOLECYSTITIS. 


603 


An  attack  of  acute  cholecystitis  may  occur  and  pass  awa}^  to  be 
siibsecj[iiently  succedecl  by  a  series  of  relapses  or  I)}-  a  more  severe  form  of 
inflammation  of  the  gall-bladder. 


MEMBRANOUS  CHOLECYSTITIS. 

Synonyms:   Croupous  Cholecystitis;  Fibrinous  Cholecystitis. 

Inflammation  of  the  gall-bladder  may  give  rise  to  the  formation  of 
a  cast  of  its  cavity,  which  to  the  naked  eye,  at  an}^  rate,  exactly  resembles 
the  casts  of  the  bowel  in  mucous  colic  (mucous  colitis,  membranous 
colitis).  As  long  ago  as  1818  Dr.  Richard  Powell  *  read  a  paper  before 
the  Royal  College  of  Physicians  of  London  (published  two  years  later 
in  the  last  volume  of  the  Medical  Transactions  of  the  College)  in  which 
he  described  attacks  of  colic  followed  by  jaundice  in  patients  whose 
faeces  contained  membranes, 
but  no  calculi.  In  some  of 
his  cases  mucous  colic  must 
have  been  present  since 
"the  membrane  was  passed 
in  perfect  tubes,  some  of 
them  full  half  a  yard  in 
length  and  certainly  suffi- 
cient in  c{uantity  to  have 
lined  the  whole  intestinal 
canal,"  but  it  is  possible 
that  a  similar  condition  was 
present  in  the  bile-ducts  and 
gall-bladder. 

Cases  of  gall-stone  colic 
accompanied  by  membranes 
in  the  stools  have  been  de- 
scribed by  Mayo  Robson 
and  Macrae,t  and  by  P.  C. 
Fenwick.J  In  one  of  Mayo 
Robson's   cases    78    calculi 

were  aftenvards  removed  from  the  gall-bladder,  and  in  Fenwick's  case 
the  patient  had  almost  certainly  passed  gall-stones  previously.  In  a 
woman  whose  gall-bladder  Mr.  Allingham  opened  at  St.  George's  Hos- 
pital a  fibrinous  cast  of  the  gall-bladder  surrounding  a  single  large  cal- 
culus was  found  and  removed.  §  In  a  case  of  membranous  cholecystitis 
operated  upon  by  Moynihan||  368  calculi  were  removed.  It  is,  there- 
fore, probable  that  membranous  cholecystitis  is  usually  associated  with 
calculi  in  the  gall-bladder. 

*  Powell,  R. :  Medical  Trans.  College  of  Pliysicians,  vol.  vi,  p.  106,  1820. 
t  Robson  and  Macrae:  Diseasois  of  the  Call-bladder  and  Bile-ducts,  p.  32,  2d 
ed.,  1900. 

X  Fenwick,  P.  C. :  Brit.  Med.  Journ.,  1S98,  vol.  i,  p.  1072. 

§  Vide  Trans.  Path.  Soc,  vol.  liii,  p.  405. 

II  Moynihan:  Brit.  Med.  Journ.,  190.3,  vol.  i,  p.  187. 


Fig.  74. — Photomicrograi'h  Showing  FrBRiNous  Net- 
work Enclosing  Masses  of  Black  Bile-pigment  . 
(By  S.   G.   Penny,  Esq.) 


604  DISEASES    OF   THE    GALL-BLADDER. 

Microscopically  in  the  case  I  examined  there  was  a  fibrinous  network 
enclosing  bile-pigment  and  hexagonal  ciystals.  In  the  outer  layers  of 
the  cast  there  were  round-cells,  but  no  trace  of  the  mucous  membrane 
of  the  gall-bladder  was  found.  The  fibrinous  structure  differs  entirely 
from  the  microscopic  appearances  of  the  casts  of  the  intestine  passed  in 
mucous  colic. 

Clinically  the  symptoms  are  those  of  gall-stone  colic,  from  which 
it  can  be  distinguished  only  by  finding  membranous  casts  instead  of 
calculi  in  the  motions.  The  condition  may  be  found  only  when  the 
gall-bladder  is  open  in  the  course  of  an  operation,  as  in  the  folio ^^ang  case : 

A  woman  aged  fiftj'-two  who  had  never  had  jaundice  or  biliary  colic  was  seized 
with  pain  in  the  right  side  of  the  abdomen  and  vomiting  on  Nov.  14,  1900.  On 
admission  two  weeks  later  a  tumor  of  stony  harchaess  was  found  in  the  right  iliac 
fossa,  separated  by  a  zone  of  resonance  from  the  liver  duhiess.  It  was  thought  to 
be  probably  carcinoma  of  the  colon.  Laparotonw  was  performed  by  Mr.  Allmgham, 
and  revealed  a  greatly  enlarged  gall-bladder  with  adhesions  to  adjacent  parts. 
It  was  opened,  and  a  single  gall-stone,  rather  bigger  than  a  Avalnut,  was  fomid 
enclosed  in  a  thick  fibrinous  sac  about  -j  inch  thick.  The  calculus  and  the  cast 
were  removed,  but  the  gall-bladder  was  left.  This  envelope  was  quite  distinct  and 
easily  separable  from  the  lining  of  the  gaU-bladder.  Microscopic  sections  of  the 
walls  of  the  membranous  sac  showed  a  filarinous  network  enclosing  bile-pigment 
and  hexagonal  and  quadrilateral  crystals.     The  patient  made  a  good  recovery. 

The  treatment  of  an  attack  is  the  same  as  that  of  gall-stone  colic,  but 
if  attacks  recur,  the  gall-bladder  should  be  opened  and  calculi  removed. 
Moynihan  *  considers  that  the  gall-bladder  should  be  removed,  but  it 
appears  to  me  doubtful  whether  there  are  as  yet  sufficient  grounds  for 
this  dictum. 

SUPPURATIVE  CHOLECYSTITIS. 

In  this  condition  inflammation  of  the  walls  of  the  gall-bladder  gives 
rise  to  an  accumulation  of  pus  in  its  cavity  and  may  go  on  to  ulceration 
and  perforation.  There  are  two  conditions  which  have  in  common  the 
production  of  pus  inside  the  gall-bladder,  but  differ  in  their  clinical  course 
and  aspects.  In  one — chronic  empyema  of  the  gall-bladder — pus  is 
slowly  formed  within  the  gall-bladder,  and  its  features  are  much  the 
same  as  those  of  distension  of  the  gall-bladder  with  mucous  fluid  (drops}' 
of  the  gall-bladder).  In  the  other  there  is  an  acute  suppurative  inflam- 
mation. Except  where  specially  stated,  the  follo\\dng  description  refers 
to  the  latter  condition.  Chronic  empyema  is  referred  to  on  page  601. 
It  is  difficult  to  draw  a  hard-and-fast  line  between  the  less  severe  cases 
of  acute  suppurative  cholecystitis  and  chronic  empj'ema  of  the  gall- 
bladder. Acute  suppurative  cholecystitis,  when  very  acute,  is  described 
as  phlegmonous  cholecystitis. 

The  causes  of  suppurative  cholecystitis  are  nmch  the  same  as  those 
of  cholecystitis  in  general,  and  need  not  be  repeated  in  detail.  Acute 
suppurative  cholecystitis  is  frequently  associated  vnth.  the  presence  of 
gall-stones. 

Thus  in  55  cases  of  suppurative  cholecystitis  collected  by  Courvoisier  41  were 
associated  with  cholelithiasis. 

*  Moynihan:  Brit.  Med.  Journ.,  1903,  vol.  i,  p.  186. 


ACUTE    CHOLECYSTITIS.  605 

Impaction  of  a  calculus  in  the  cystic  duct  or  neck  of  the  gall-bladder 
favours  microbic  infection,  as  any  niicro-organisms  reaching  the  gall- 
bladder by  the  blood-stream  are  retained  and  able  to  multiply.  It  is 
possible  that  in  some  cases  of  suppurative  cholecystitis  a  calculus  may 
have  been  previously  expelled,  l^ut  the  presence  of  gall-stones  is  no  more 
necessar\^  than  are  enterohths  in  appendicitis.  Obstruction  of  the  cystic 
or  common  bile-duct  may  act  in  a  similar  manner.  Primary  carcinoma 
of  the  bile-ducts  may  thus  become  complicated  by  suppurative  chole- 
cystitis, as  shown  in  the  following  complicated  case: 

Carcinoma  of  Cystic  Duct;  Round  Worm  in  Common  Bile-duct;  Svftpvraiive 
Oiolecystitis. — A  woman  aged  forty-three,  after  long-continued  and  vague  pains 
suggesting  biliary  colic,  became  intensely  jaundiced,  developed  a  high  temperature, 
and  died.  There  were  gall-stones  in  the  gall-bladder  and  suppurative  cholecystitis 
due  to  a  member  of  the  colon  group,  primary  carcinoma  completely  obstructing 
the  cj^stic  duct,  and  a  dead  lumbricoid  worm  in  the  common  bile-duct  which,  it 
was  thought,  had  conveyed  the  infection.      (Etienne.*) 

Suppuration  may  spread  into  the  gall-bladder  from  suppurative 
cholangitis  due  to  various  causes,  such  as  the  rupture  of  a  hydatid  cyst 
into  the  ducts.  In  typhoid  fever  suppurative  cholecystitis  may  occur, 
but  it  is  fortunately  rare,  and  is  not  so  often  seen  as  catarrhal  chole- 
cystitis. 

In  494  cases  of  typhoid  fever  observed  during  sLx  years  at  Montreal  there  were 
25  deaths,  among  which  there  was  one  due  to  suppurative  cholecystitis. t  There 
were  also  3  cases  of  acute  cholecystitis  that  recovered.  In  2000  fatal  cases  at 
Mimich  tabulated  bv  Holscher  there  was  5  of  cholecystitis  with  suppuration.! 
In  1016  cases  of  tvphoid  fever  treated  during  the  two  years  1900-1901  in  the  Im- 
perial Yeomanry  'Hospitals  in  South  Africa  there  was  one  case  of  suppurative 
cholecystitis. 

Morbid  Anatomy. — The  gall-bladder  is  usually  enlarged,  sometimes 
very  considerably,  but  in  cases  where  suppuration  occurs  in  a  gall- 
bladder shrivelled  up  and  contracted  from  recurrent  attacks  of  chole- 
cystitis there  is  no  enlargement.  The  peritoneal  coat  is  inflamed,  granu- 
lar from  adherent  lymph,  and  usually  darkish  red  or  greenish  l)lack  in 
colour.  It  may  be  adherent  by  old  fibrous  adhesions  to  the  parts  around, 
or  glued  to  them  by  recent  lymph.  Inflammation  may  thus  spread  to 
adjacent  coils  of  intestine  and  cause  paralytic  distension.  The  wall  of 
the  gall-bladder  is  swollen  from  inflammatory  exudation  and  softened 
and  friable.  The  mucous  membrane  is  largely  replaced  by  granulation 
tissue,  and  the  inner  surface  is  shaggy,  red,  and  in  places  has  flakes  of 
adherent  lymph.  Ulceration  is  connnoner  near  the  fundus,  from  the 
fact  that  calculi  are  more  likely  to  gravitate  there.  The  contents  are 
bile-stained  or  sanious  pus,  and  calculi  are  often  present. 

In  cases  of  chronic  empyema  the  walls  of  the  gall-bladder  are  thickened 
from  organisation  of  the  inflanunatory  exudation. 

Clinical  Picture. — The  signs  and  symptoms  of  acute  cholecystitis 
vary  considerably.     They  may  be  local,  and  at  first  confined  to  the  region 

*  Etienne:  .\rcliiv.  gi'm'ral.  de  Mc'd.,  189C),  tome  clxxviii,  p.  284. 
t  Gillies:  Montreal  Med.  .lourn.,  Juno,  1900,  p.  422. 
I  Holscher:  Miinch.  med.  Woch..  1891. 


606  DISEASES    OF   THE    GALL-BLADDER. 

of  the  gall-bladder,  or  general,  from  wide-spread  infection  of  the  peri- 
toneum. 

The  local  manifestations  are  those  of  inflammation  in  the  situation 
of  the  gall-bladder,  pain,  tenderness,  and  increased  resistance  of  the 
overlying  rectus  abclomin  is  muscle. 

The  gall-bladder  may  be  palpable  as  a  tense  tumor,  somewhat  pear- 
shaped,  in  a  Une  between  the  tip  of  the  ninth  rib  and  a  point  one  inch 
below  the  umbihcus  in  the  middle  line  (Mayo  Robson).  The  shape  of 
the  gall-bladder  is  subject  to  considerable  variation:  when  elongated,  it 
may  appear  to  be  independent  of  the  liver,  since  it  may  be  separated  from 
the  liver  dulness  by  a  zone  of  resonant  intestines.  When  suppuration 
occurs  in  a  gall-bladder  which  has  previously  been  considerably  distended, 
the  tumor  may  be  palpable  in  the  right  iliac  fossa  and  may  suggest 
appendicitis.  In  such  cases  there  is  often  an  elongated  condition  of  the 
right  lobe  of  the  liver  (Riedel's  lobe).  In  exceptional  instances  the  gall- 
bladder is  found  in  the  middle  line  of  the  abdomen. 

When  there  is  local  peritonitis  around  the  gall-bladder,  intestinal 
paralysis  and  distension  may  prevent  its  being  felt,  but  the  hypochon- 
drium  will  be  prominent  and  exquisitely  tender.  In  other  cases  rigidity 
of  the  abdominal  muscles  prevents  the  gall-bladder  from  being  made 
out,  unless  the  examination  is  conducted  under  an  anaesthetic. 

In  many  instances  the  gall-bladder  is  contracted  from  past  attacks 
of  inflammation,  and  though  acutely  inflamed  and  containing  pus,  does 
not  project  beyond  the  margin  of  the  right  lobe. 

Pain  is  constant,  as  a  rule,  but  exacerbations  of  great  severity  resem- 
bling biliary  colic  may  occur,  and  its  intensity  is  subject  to  considerable 
variation  in  different  cases.  It  is  usually  felt  in  the  right  liA^ochondrium 
or  pit  of  the  stomach,  but  may  be  referred  to  the  right  iliac  region  and 
imitate  appendicitis.  In  acute  suppurative  cholecystitis  the  temperature 
is  raised  and  may  be  high,  and  be  accompanied  by  rigors  and  attacks 
of  shivering. 

When  pus  has  slowly  formed — chronic  emp3^ema — in  the  gall-bladder 
there  may  be  no  rise  of  temperature  and  very  little  constitutional  dis- 
turbance, though  pain,  loss  of  appetite,  malaise,  and  some  degree  of 
wasting  are  usually  present.  If  there  is  ulceration  of  the  gall-bladder, 
septic  absorption  may  give  rise  to  fever,  and  local  peritonitis  with  in- 
creased pain  will  result. 

The  pulse  is  rapid — 100-120 — in  suppurative  cholecystitis.  An  in- 
creasing pulse-rate  shows  that  operative  interference  is  indicated.  There 
may  be  vomiting,  from  the  irritation  of  the  peritoneum  around  the  gall- 
bladder, while  the  local  peritonitis  thus  produced  may  spread  to  neigh- 
bouring coils  of  the  small  intestines  or  to  the  hepatic  flexure  of  the  colon 
and  lead  to  paralysis  of  the  bowel  and  so  to  the  symptoms  of  intestinal 
obstruction.  Jaundice  is  not  a  necessary  symptom,  and  is  very  com- 
monly absent.  When  present,  it  is  usually  slight.  It  may  be  due  to 
extension  of  inflammation  into  the  common  bile  or  hepatic  ducts,  or  to 
definite  causes  of  biliar}"  obstruction,  such  as  gall-stones  or  tumors  in- 
volving the  large  extra-hepatic  bile-ducts.     It  has  been  suggested  that 


ACUTE    CHOLECYSTITIS.  607 

when  the  mucous  membrane  of  the  gall-bladder  is  ulcerated;  bile  may  be 
absorbed  from  the  gall-bladder  and  that  slight  icterus  in  the  early  stages 
of  suppurative  cholecystitis,  before  the  cavity  becomes  filled  "u-ith  pus, 
may  be  due  to  this  cause,  but  this  is  unhkely. 

The  spleen  is  occasionally  found  to  be  enlarged.  Albuminuria  may 
be  present  in  the  more  severe  cases,  and  is  due  to  the  local  action  on 
the  renal  epithelium  of  poisons  absorbed  from  the  gall-bladder.  There 
is  leucoc}i:osis  of  from  15,000  to  30,000.  In  severe  cases  there  may  be 
nothing  to  indicate  that  the  primary  lesion  is  in  the  gall-bladder,  the 
symptoms  being  those  of  general  peritonitis  or  intestinal  obstruction, 
and  thus  imitating  those  due  to  perforation  of  the  intestine  or  appendix. 

If  operation  is  delayed,  the  localising  symptoms  present  in  an  early 
stage  become  masked  by  the  spread  of  the  inflammation  to  the  general 
cavity  of  the  peritoneum. 

Complications  and  Results. — The  chief  danger  of  suppurative  chole- 
cystitis is  perforation  into  the  general  cavity  of  the  peritoneum  and  fatal 
peritonitis. 

Keen  *  has  collected  31  examples  of  perforation  due  to  typhoidal  cholecystitis; 
of  these,  26  were  not  operated  upon  and  all  proved  fatal;  5  were  operated  upon, 
and  of  these,  3  recovered. 

Perforation  of  the  gall-bladder  may  lead  to  a  local  peritoneal  abscess 
instead  of  to  general  peritonitis.  The  formation  of  a  local  abscess  is 
favoured  by  the  presence  of  previous  peritoneal  adhesions  shutting  off 
the  cavity  of  the  general  peritoneum.  The  abscess  may  open  in  a  number 
of  A^arious  situations,  and  imitate  other  forms  of  local  abdominal  sup- 
puration, such  as  a  subdiaphragmatic  abscess  due  to  disease  of  the  stom- 
ach, duodenum,  pancreas,  etc.  The  abscess  may  discharge  into  the 
stomach,  duodenum,  colon,  or  penetrate  the  diaphragm  and  set  up  an 
empyema  or  a  bronchobiliary  fistula;  or  it  may  open  through  the  skin 
of  the  anterior  abdominal  wall  close  to  the  costal  arch  or  at  the  um- 
bilicus. In  rare  instances  the  abscess  may  communicate  with  the  pelvis 
of  the  right  kidney,  or  even  the  bladder  or  vagina. 

A  suppurating  gall-bladder  may  ulcerate  directly  into  the  liver  and 
give  rise  to  an  abscess  continuous  with  the  cavity  of  the  gall-bladder. 

Weir  t  records  the  case  of  a  woman  aged  thirty-five  whose  gall-bladder  con- 
tained 3  ounces  of  pus.  Ulceration  on  the  posterior  wall  of  the  gall-bladder  led 
into  an  abscess  cavity  in  the  liver  containing  more  than  an  ounce  of  pus.  A  woman 
aged  fifty-three  died  in  St.  George's  Hospital  with  multiple  recurrent  growths  after 
removal  of  the  mamma;  the  cystic  duct  was  blocked  by  a  calculus;  the  gall-bladder 
contained  pus  and  communicated  by  two  openings  with  a  small  abscess  cavit}^  in 
the  liver. 

Concomitant  suppurative  cholangitis  may  lead  to  multiple  areas  of 
suppuration  in  the  liver;  these  readily  infect  the  hepatic  veins,  induce 
secondary  abscesses  in  the  lungs,  which  in  their  turn  may  burst  into  the 
pleura  and  set  up  empyema.  A  very  rare  event  is  profuse  haemorrhage 
into  the  gall-bladder  from  ulceration  of  the  vessels;  concomitant  jaundice 
prol^ably  increases  the  tendency  to  h£emorrhage. 

*  Keen:  Complications  and  Sequels  of  Tvphoid  Fever,  189S,  pj\  249,  325. 
t  Weir:  Medical  Record  (U.  S.  A.),  1900,  p.  1137. 


608  DISEASES    OF   THE    GALL-BLADDEE. 

Appendicitis  may  complicate  suppurative  cholec^^stitis,  and  in  oper- 
ating on  a  case  of  cholecystitis  the  condition  of  the  appendix  should  be 
investigated,  as  death  may  subsequently  occur  from  peritonitis  due  to 
perforation  of  the  appendix  in  a  case  where  suppurative  cholecystitis  has 
been  satisfactorily  operated  upon.  Dieulafoy  *  considers  that  the  infec- 
tion of  the  appendix  is  secondary  to  that  of  the  gall-bladder. 

Diagnosis. — Before  perforation  has  occurred  suppurative  cholecys- 
titis resembles  other  forms  of  local  peritonitis  in  the  neighbourhood,  such 
as  might  be  set  up  by  a  duodenal  ulcer  before  perforation,  by  a  localised 
subphrenic  pneumothorax  on  the  right  side,  clue  to  a  perforated  duodenal 
or  gastric  ulcer,  or  to  appendicitis  in  an  abnormally  situated  appendix. 

In  addition  to  the  signs  of  local  peritonitis  the  presence  of  a  tumor 
moving  with  respiration  in  or  near  the  situation  of  the  gall-bladder  is 
an  important  indication  of  cholecystitis.  The  absence  of  jaundice  must 
not  be  regarded  as  militating  against  the  existence  of  cholecystitis, 
though  the  history  of  past  attacks  of  biliary  colic  with  transient  jaundice 
strengthens  the  diagnosis. 

Differential  Diagnosis. — As  already  indicated,  suppurative  chole- 
cystitis must  be  diagnosed  from  local  peritonitis  and  subphrenic  abscess 
due  to  other  causes,  but  situated  in  the  neighbourhood  of  the  gall-bladder. 
It  must  also  be  distinguished  from  appendicitis  and  biliary  colic. 

In  duodenal  ulcer  there  should  be  a  history  of  pain  about  two  hours 
after  food,  but,  unfortunately,  the  ulcer  may  remain  latent  until  it 
perforates  and  sets  up  general  or  localised  peritonitis.  In  most  cases  of 
duodenal  ulcer  there  is  no  special  resemblance  to  suppurati^^e  cholecystitis ; 
but  in  the  following  case  a  perforating  duodenal  ulcer  imitated  acute 
influenzal  cholecystitis: 

A  man  about  fort^^  years  of  age  had  had  recurrent  attacks  of  influenza,  but 
was  improving  until  he  was  seized  with  vomiting  and  severe  pain  over  the  region 
of  the  gall-bladder.  There  was  a  rather  indefinite  history  of  biliary  colic  some 
years  before.  The  patient  had  been  slightly  yellow  during  his  illness,  but  showed 
no  jaundice  at  the  time  that  I  saw  him  in  consultation  with  Dr.  Xorman  McCaskie. 
The  man  looked  ill,  had  a  temperature  of  103°,  and  a  rapid  pulse.  There  was 
tenderness  over  the  gall-bladder,  but  nothing  like  a  tumor  could  be  felt.  Influenzal 
cholec3"stitis  was  diagnosed.  Three  leeches  were  put  over  the  tender  area.  After 
this  he  was  better  until  the  next  day,  at  1  p.  m.,  when  he  was  suddenly  seized  with 
intense  pain  and  collapse.  I  saw  him  again  with  Dr.  McCaskie,  and  felt  sure  that 
perforation  had  taken  place.  Accordingly,  Sir  W.  H.  Bennett  saw  him  and  opened 
the  abdomen  and  found  that  there  was  a  perforated  duodenal  ulcer  and  not  chole- 
cystitis.    The  patient  died  two  days  after  the  operation. 

Perforation  of  a  gastric  ulcer  with  the  production  of  a  localised  sub- 
phrenic abscess  hardly  ever  imitates  suppurative  cholecystitis,  as  the 
abscess  nearly  always  contains  air  (a  subphrenic  pyopneumothorax),  but 
in  the  following  case  the  absence  of  resonance  led  to  an  open  diagnosis : 

A  woman  aged  twenty-eight  years  had  sudden  pain  on  November  14,  1900. 
She  came  up  to  St.  George's  Hospital  on  November  16th  with  a  firm  mass,  tender 
and  dull  on  percussion,  in  the  position  of  the  gall-bladder.  She  had  no  jaumlice, 
and  there  was  no  history  of  gall-stone  colic,  but  she  had  previously  had  some  dys- 
peptic pain  one  hour  after  food.  The  pulse  was  140,  and  the  patient's  face  indicated 
grave  abdominal  mischief.     The  diagnosis  lay  between  suppurative  cholecystitis 

*  Dieulafoy :  La  Presse  M^dicale,  June  17,  1903,  p.  448. 


ACUTE    CHOLECYSTITIS.  609 

and  a  local  abscess  clue  to  a  perforated  gastric  ulcer.  My  colleague,  Mr.  Sheild, 
operated  the  same  day  and  found  a  localised  peritoneal  abscess  due  to  perforation 
of  a  gastric  ulcer  close  to  the  pylorus.  The  localised  condition  was  due  to  old 
adhesions. 

An  elongated  and  distended  gall-bladder  may  project  into  the  right 
lower  half  of  the  abdomen  and  simulate  appendicitis;  as  already  men- 
tioned, this  condition  is  frecjuently  associated  with  an  elongated  right 
lobe  of  the  liver.  Cases  of  cholecystitis  are  not  infre(|uently  regarded  as 
appendicitis;  the  converse  mistake  is  much  rarer.  The  differential  diag- 
nosis is  very  difficult,  as  both  these  conditions  may  vary  so  much  in  their 
clinical  manifestations.  Further,  as  pointed  out -above,  cholecystitis 
and  appendicitis  may  both  be  present  at  the  same  time.  It  is,  therefore, 
desirable  that  during  laparotomy  for  either  of  these  conditions  the  state 
of  the  other  viscus  should,  if  possible,  be  investigated. 

When  perforation  of  a  suppurating  gall-bladder  sets  up  general  peri- 
tonitis, the  diagnosis  must  be  made  from  other  fornxs  of  peritonitis, 
especially  that  set  up  by  fulminating  appendicitis,  which  it  often  closely 
resembles  inasmuch  as  the  pain  may  be  referred  to  the  right  iliac  fossa, 
probably  because  the  contents  of  the  gall-bladder  may  travel  down  into 
the  region  of  the  appendix.  A  careful  investigation  of  the  history  may 
])e  of  help  in  forming  an  opinion,  but  in  either  case  immediate  operation 
is  essential  and  the  surgeon  must  be  prepared  for  unexpected  conditions. 
When  the  abdomen  is  opened  the  character  of  the  exudate  may  assist 
the  surgeon  by  indicating  the  perforated  viscus ;  thus  bile  or  calculi  will 
at  once  direct  his  attention  to  the  gall-bladder;  an  acid  reaction  or  gas, 
to  perforation  of  the  stomach  or  duodenum. 

Prognosis. — In  acute  suppurative  inflammation  of  the  gall-bladder 
there  is  little  tendency  to  spontaneous  cure  by  the  discharge  of  the  puru- 
lent contents  through  the  cystic  duct,  and  subsidence  of  the  inflamma- 
tory process,  since  in  most  cases  the  cystic  duct  is  blocked  or  ol^structed. 
This  may  be  due  to  various  factors,  such  as  an  impacted  calculus,  the 
contraction  of  cicatricial  fibrous  tissue,  either  as  the  result  of  past  ulcera- 
tion or  from  pericholecystic  adhesions,  or  in  some  cases  to  new-growth 
involving  the  duct.  When  the  obstruction  of  the  cystic  duct  depends 
on  swelling  of  the  mucous  membrane,  due  to  the  spread  of  inflammation 
from  the  gall-bladder,  it  is  possible  that  the  purulent  contents  may  be 
expelled  through  the  duct.  In  cases  where  the  progress  is  less  acute,  pus 
may  be  formed  in  the  gall-bladder  and  may  remain  confined  there;  this 
is  chronic  empyema  of  the  gall-bladder.  But  in  acute  su]ipurative  chole- 
cystitis the  inflammatory  process  spreads  through  tlie  walls  of  the  gall- 
bladder, infects  the  surrounding  peritoneum,  and  leads  to  local  or  general 
peritonitis.  Under  the  circunxstances,  therefore,  the  prognosis  is  grave 
imless  operative  interference  is  invoked  before  more  wides])read  infection 
has  set  in.  A  local  abscess  may  be  treated  surgically  very  successfully, 
but  if  general  peritonitis  has  supervened,  the  outlook  is  very  glooms' 
indeed. 

Treatment. — ^The  proper  treatment  of  suppurative  cholecystitis  and 
of  the  more  chronic  condition,  empyema  of  the  gall-bladder,  is  surgical 
39 


610  DISEASES    OF   THE    GALL-BLADDER. 

and  consists  in  opening  the  gall-bladder  and  draining  it,  or,  if  it  appear 
necessary,  removing  it.  Exploratory  puncture  through  the  abdominal 
walls  with  a  syringe  to  see  whether  there  is  pus  is  dangerous,  and  should 
never  be  countenanced.  The  palliative  or  medical  treatment  is  the  same 
as  in  acute  cholecystitis. 


PHLEGMONOUS  CHOLECYSTITIS. 

This  is  a  very  acute  infective  form  of  cholecystitis,  and  differs  only 
in  degree  from  the  acute  suppurative  form  just  described,  from  which 
it  cannot  be  separated  by  any  hard-and-fast  line.  It  passes  into  gan- 
grenous cholecystitis,  from  which  again  it  can  hardly  be  separated;  in 
fact,  gangrene  is  merely  a  result  of  phlegmonous  cholecystitis. 

It  may  supervene  on  the  same  conditions  as  suppurative  cholecystitis, 
such  as  cholelithiasis,  typhoidal  cholecystitis  (v.  Wunscheim,*  Imhofer), 
and  is  due  to  a  very  virulent  infection. 

Incidence. — Very  few  cases  are  on  record.  Osier  considers  it  much 
less  rare  than  it  is  thought  to  be.  Probably  many  cases  described  as 
acute  suppurative  cholecystitis  might  be  included  under  this  heading. 
Courvoisier,  who  first  described  it  as  acute  progressive  empyema  of  the 
gall-bladder,  collected  7  cases.  Mayo  Robson  f  has  added  4  more. 

Morbid  Anatomy. — The  changes  are  the  same  as  in  acute  suppurative 
cholecystitis,  but  more  extensive  and  acute.  The  outside  of  the  gall- 
bladder is  purple,  oedematous,  and  inflamed  with  adherent  lymph.  The 
walls  are  swollen,  friable,  and  infiltrated  with  pus  and  blood;  the  mucous 
membrane  is  swollen,  and  may  show  ulceration,  necrosis,  or  be  separated 
in  flakes  from  the  underlying  coats.  The  gall-bladder  contains  pus  and 
often  gall-stones.  The  cystic  duct  is  closed  and  may  be  blocked  by  a 
calculus. 

Clinical  Features. — Symptoms  set  in  suddenl}^  with  pain  in  the 
region  of  the  gall-bladder.  Owing  to  the  intensity  of  the  inflammation 
the  peritoneum  early  becomes  involved,  at  first  locally,  but  soon  peri- 
tonitis becomes  generahsed,  unless  there  are  firm  adhesions  around  the 
gall-bladder. 

Jaundice  may  be  present  from  concomitant  inflammation  of  the 
ducts,  but  it  is  inconstant,  and  therefore  not  of  any  great  diagnostic 
value.  The  results  are  peritonitis,  ulceration,  sloughing,  and  perforation 
of  the  gall-bladder,  leading  to  localised  or  generalised  peritonitis,  and 
a  very  rare  event — gangrene  of  the  gall-bladder. 

The  diagnosis  depends  on  evidence  of  acute  inflammation  in  the 
region  of  the  gall-bladder  in  a  patient  whose  history  points  to  past  chole- 
cystitis. In  some  cases  there  may  only  be  evidence  of  general  peritonitis 
with  or  without  the  history  that  it  followed  localised  inflammation  in 
the  right  upper  quadrant  of  the  abdomen.  When  there  is  more  or  less 
localised  inflammation  of  the  peritoneum  in  the  right  upper  half  of  the 

*  V.  Wnnscheim:  Prag.  med.  Wochen.,  1898. 

t  Robson  and  Macrae :  Diseases  of  the  Gall-bladder.  Robson :  Brit.  Med. 
Journ.,  1903,  vol.  i,  p.  189. 


ACUTE    CHOLECYSTITIS. 


611 


abdomen,  the  differential  diagnosis  is  the  same  as  in  other  forms  of 
cholecystitis,  to  which  the  reader  should  refer.  It  may  be  very  difficult 
when  general  peritonitis  is  estabhshed  to  make  out  whether  it  is  due 
to  fulminating  appendicitis  or  to  cholecystitis.  Perforation  of  a  gastric 
or  duodenal  ulcer  may  be  suspected  from  the  history,  and  receives  very 
considerable  support  from  signs,  such  as  absence  of  the  hver  dulness, 
which  points  to  the  presence  of  free  gas  in  the  general  peritoneal  cavity. 
But  the  accurate  diagnosis  of  phlegmonous  cholecystitis  is  extremely 
difficult;  this  is  shown  by  the  following  case,  in  which  the  gall-bladder 
showed  a  transition  from  phlegmonous  to  gangrenous  cholecystitis. 

A  woman  aged  sixty-three  was  admitted  into  St.  George's  Hospital  with  a 
history  of  constipation  for  three  days  and  of  more  acute  symptoms  and  vomiting 
for  twenty-four  hours.  The  sac  of  an  umbiUcal 
hernia  whicli  she  had  had  for  three  years  was 
opened,  and  was  found  to  contain  adherent  omen- 
tum, coils  of  small  intestine,  and  a  piece  of  the 
colon.  The  bowel,  which  was  in  good  condition 
and  was  not  strangidated,  was  returned.  She  tem- 
porarily rallied,  but  died  with  recurrent  vomiting 
thirty  liours  after  the  operation.  At  the  post- 
mortem there  was  general  peritonitis.  The  gall- 
bladder was  adherent  to  the  colon,  and  contained 
several  gaU-stones  in  the  fundus;  its  mucous  mem- 
brane was  ulcerated  and  in  a  necrotic  condition, 
especially  on  the  anterior  surface  of  the  gall-blad- 
der. There  was  a  large  calculus  encysted  in  the 
neck  of  the  gall-bladder  which  occluded  the  com- 
mencement of  the  cystic  duct.     (Vide  Fig.  75.) 

The  prognosis  is  very  grave,  as  the  dis- 
ease may  prove  fatal  in  a  few  days,  the 
process  being  so  virulent  that  infective  peri- 
tonitis is  rapidly  set  up.  The  process  is  too 
acute  to  allow  adhesions  capable  of  localising 
the  infection  to  be  formed. 

The  treatment  is  generally  that  of  per- 
forative peritonitis,  and  though  the  pain 
may  be  relieved  by  hot  fomentations  and 
the  hypodermic  injection  of  morj^hia,  the 
only  satisfactory  measure  is  laparotomy  and 
surgical  treatment  of  the  gall-bladder.     The 

gall-bladder  must  either  be  freely  drained,  the  surrounding  space  being 
packed  with  gauze — and  this  is  probably  the  most  satisfactory  course — 
or  the  gall-bladder  must  be  removed;  this  course  is  essential  when  the 
further  stage  of  gangrene  is  threatened. 


Fig. 


75. —  Gall-bladder  with 
A  Large  Calculus  in  its 
Neck  and  Showing  Phleg- 
monous Inflammation  Pass- 
ing ON  into  Gangrene. 
(Drawn  by  Dr.  E.  A.  Wilson.) 


GANGRENOUS  CHOLECYSTITIS. 

Synonym:  Gangrene  of  the  Gall-bladder. 

This  is  a  further  stage,  or  rather  a  result,  of  the  very  acute  infective 
or  phlegmonous  inflammation  of  the  gall-bladder  just  described,  and,  as 
already  pointed  out,  no  hard-and-fast  line  of  distinction  can  be  drawn 
between  them.     The  transitional  cases  with  small  areas  of  necrosis  in 


612  DISEASES    OF   THE    GALL-BLADDER. 

the  gall-bladder  may  be  spoken  of  as  partial  gangrene,  as  in  Donoghue's  * 
case.  It  stands  in  the  same  relation  to  cholecystitis  that  gangrenous 
appendicitis  does  to  other  forms  of  inflammation  of  the  appendix,  but 
it  is  very  rare  and  thus  contrasts  with  the  frequency  of  gangrenous 
appendicitis.  It  seems  probable  that  the  rarity  of  gangrene  of  the  gall- 
bladder may  in  part  be  explained  by  its  better  blood-supply  and  by  the 
fact  that  it  is  not  prone,  like  the  appendix,  to  be  twisted  on  its  own 
axis  and  its  blood-supply  thus  interfered  with.  In  order  that  gangrene 
may  supervene  it  is  necessary  that  the  cystic  duct  should  be  occluded 
and  that  a  very  virulent  infection  should  fall  on  the  gall-bladder.  Gib- 
bon f  described  a  case  in  which  impaction  of  a  calculus  at  the  neck  of 
the  gall-bladder  probably  interfered  with  the  blood-supply;  a  similar 
condition  is  seen  in  figure  75,  but  it  must  be  remembered  that  cholecystitis 
frequently  supervenes  in  cases  where  a  calculus  is  impacted  in  the  neck 
of  the  gall-bladder  without  causing  gangrene  of  the  gall-bladder. 

Incidence. — It  is  extremely  rare,  but  probably  not  so  rare  as  the 
recorded  cases  suggest.  It  is  highly  probable  that  some  cases  have  been 
published  or  described  merely  as  very  severe  cholecystitis.  Cases  have 
been  reported  by  IIotchkiss,J  Mayo  Robson,§  Mayo,  |!  Gibbon,**  Moyni- 
han.ff 

The  morbid  anatomy  is  the  same  as  in  phlegmonous  cholecystitis, 
with  the  addition  of  gangrene  of  the  wall  of  the  gall-bladder.  The  extent 
of  the  gall-bladder  affected  by  gangrene  varies,  but  it  appears  to  begin 
at  the  fundus  and  spread  towards  the  neck  of  the  gall-bladder.  The  gan- 
grenous walls  are  dark  green  in  colour,  extremely  soft,  and  friable. 

The  cystic  duct  is  blocked,  and  there  may  be  a  calculus  imbedded  in 
the  neck  of  the  gall-bladder.  Calculi  are  present  in  the  gall-bladder  in 
Hotchkiss',  Gibbon's,  Moynihan's  cases,  and  in  a  case  described  as  phleg- 
monous cholecystitis  by  Da  Costa,  J  J  where  the  calculus  was  found  pro- 
jecting through  a  hole  in  the  wall  of  the  gall-bladder. 

The  clinical  features  are  the  same  as  those  of  ''phlegmonous"  chole- 
cystitis in  a  late  stage — viz.,  general  peritonitis.  In  fact,  as  has  already 
been  pointed  out,  gangrenous  cholecystitis  is  the  extreme  stage  of  the 
phlegmonous  form.  In  Gibbon's  case  there  was  a  leucocytosis  of  37,600, 
which  fell  to  12,600  in  twenty-four  hours  after  removal  of  the  gall-bladder. 

The  diagnosis  is  extremely  difficult,  and  cannot  be  made  frqm  per- 
forative peritonitis  due  to  other  lesions  of  the  gall-bladder.  It  is  very 
likely  to  be  confused  with  peritonitis  due  to  fulminating  appendicitis. 

The  only  real  treatment  is  surgical,  and  consists  in  removal  of  the 
gall-bladder  (cholecystectomy).  There  should  be  no  delay  in  operating 
on  any  case  which  is  thought  to  be  one  of  phlegmonous  or  gangrenous 
cholecystitis. 

*  Donoghue:  Amer.  Journ.  Med.  Sciences,  vol.  cxxiii,  p.  193. 

t  Gibbon :  Amer.  Journ.  Med.  Sciences,  vol.  cxxv,  April,  1903,  p.  592. 

j  Hotchkiss:  Annals  of  Surgery,  Feb.,  1894. 

§  Mayo  Robson:  Brit.  Med.  Journ.,  1903,  vol.  i,  p.  181. 

II  Mayo,  quoted  by  Gibbon.  **  Gibbon :  Loc.  cit. 

tt  Moynihan:  Brit.  Med.  Journ.,  1903,  vol.  i,  p.  186. 
jj  Da  Co.sta:  Proc.  Philadelphia  County  Med.  Soc,  vol.  xxiii,  p.  29. 


ACUTE    CHOLECYSTITIS. 


613 


Mayo  Robson  *  and  Moynihan  f   have   both  operated  successful!}'  in  cases  of 
partial  gangrene  of  the  gall-bladder. 

In  addition  to  surgical  treatment,  morj3hine<  should  be  given  and  the 
patient's  strength  maintained  by  strychnine  and  nutrient  enemata. 


CHRONIC  CATARRHAL  CHOLECYSTITIS. 

This  is  a  chronic  inflammatory  condition  in  which,  as  in  catarrhal 
appendicitis,  subacute  attacks  supervene  from  time  to  time  and  produce 
pain  resembling  that  of  biliary  colic. 

Causes. — It  may  be  a  legacy  left  by  a  past  attack  of  acute  inflamma- 
tion of  the  gall-bladder,  and  is  often  associated  with  gall-stones.  In 
other  cases  the  process  is  probably  chronic  from  the  first,  and  may  be 
disposed  to  by  sedentary  habits,  constipation,  tight  lacing,  and  the  other 
factors  that  favour  the  microbic  infection  of  the  gall-bladder.  Chronic 
catarrhal  cholecystitis  may 
be  part  of  a  chronic  ca- 
tarrhal state  of  the  ducts, 
and  is  then  quite  subordi- 
nate to  that  condition. 

Morbid  Anatomy. — The 
gall-bladder  is  usually  some- 
what distended  with  mucus, 
which  may  be  so  thick  and 
tenacious  as  to  resemble 
grains  of  boiled  sago  (Mayo 
Robson  J).  It  may  or  may 
not  contain  calculi;  occa- 
sionally calculi  are  em- 
bedded in  the  walls  of  the 
gall-bladder  (parietal  cal- 
culi). According  to  Mayo 
Robson,  adhesions  between 
the  gall-bladder  and  adja- 
cent organs  are  found  when 
the     gall-bladder     contains 

calculi,  but  not  otherwise.  The  walls  of  the  gall-bladder  are  thickened, 
and  the  rugous  appearance  of  the  mucous  membrane  may  be  exagger- 
ated, but  in  some  instances  the  mucosa,  though  thickened,  is  smooth 
and  has  a  white,  nacreous  appearance.  From  contraction  of  inflamma- 
tory tissue  the  gall-bladder  may  become  small  and  shrivelled  up  (chole- 
cystitis obliterans).  Secondary  calcification  of  the  walls  sometimes 
occurs.     The  cystic  duct  is  often  quite  pervious. 

Microscopically  the  thickening  of  the  wall  of  the  gall-bladder  is  due 
to  fibrosis  and  proliferation  of  connective  tissue  between  the  muscidar 

*  Mayo  Robson:  Brit.  Med.  Journ.,  1903,  vol.  i,  p.  181. 

t  Moynihan:  Brit.  Med.  Journ.,  1903,  vol.  i,  p.  186. 

t  Mayo  Robson  and  Macrae:  Diseases  of  the  Gall-bladder  and  Bile-ducts,  ]).  31. 


Fig.  76. — Drawing   of    Calcareous    Infiltration  of 
THE  Gall-bladder. 
'From    a    specimen    (Series    ix,  No.   195  A)    in    the 
Museum  of  St.  George's  Hospital.     (Drawn  by  Dr.  E. 
A.  Wilson.) 


614 


DISEASES    OF   THE    GALL-BLADDEE. 


and  serous  coats.  There  may  be  a  large  amount  of  well-formed  con- 
nective tissue  with  a  little  inten^ening  small-cell  infiltration  due  to  pro- 
liferation of  the  connective  tissue.  There  may  also  be  some  oedema  and 
swelhng,  and  sometimes  hyaline  degeneration  of  the  w^ell-formed  fibrous 
tissue.  I  have  not  obser^-ed  the  elongation  of  mucous  glands  through 
the  muscular  coat  to  the  serosa  described  by  Ries,*  and  am  inchned  to 
consider  such  a  process  as  evidence  of  early  mahgnant  disease. 

Clinically,  the  symptoms  are  practically  those  of  cholehthiasis. 
There  are  attacks  of  gall-stone  cohc  from  time  to  time.  In  the  intervals, 
when  the  subacute  attack  of  inflaimiiation  has  subsided;  there  is  no 
jaundice  and  no  tenderness  over  the  gall-bladder,  which  can  sometimes 
be  felt  as  a  pear-shaped  tumor.  The  distinction  between  chronic  chole- 
hthiasis with  periodic  at- 
tacks of  cohc  and  chronic 
catarrhal  cholecystitis  is 
an  artificial  one.  From 
academic    point    of 


,,^f^^%* 


an 


view  a  criterion  might 
be  made  of  the  presence 
or  absence  of  gall-stones; 
the  cases  of  chronic  ca- 
tarrhal cholecystitis  as- 
sociated with  gall-stones 
might  then  be  removed 
to  another  category  and 
included  under  cholehth- 
iasis. It  is  doubtful 
whether  a  diagnosis  be- 
tween chronic  catarrhal 
cholecystitis  and  gall- 
stones can  be  made  on 
the  ground  that  the 
biliar}^  colic  is  more  se- 
vere in  the  case  of  gall- 
stones, since,  after  re- 
peated attacks  of  bihary 
colic,  the  ducts  may  be  so  dilated  that  pain  is  comparatively  slight. 
When  there  are  no  gall-stones,  the  attacks  of  cohc  due  to  attacks  of 
subacute  cholecystitis  are  less  hkely  to  be  foUowed  by  jaundice,  and  no 
calculi  can  be  recovered  from  the  stools. 

Treatment. — ^The  medical  treatment  is  that  of  cholehthiasis,  viz., 
a  careful  dietar}^  with  plenty  of  water,  sahcylate  of  soda,  regular  action 
of  the  bowels,  and  exercise,  and,  if  necessary,  gentle  massage.  These 
measures  are  directed  to  prevent  stagnation  of  bile  in  the  gall-bladder 
and  to  increase  the  flow  of  bile  through  the  ducts  and  gall-bladder  so  as 
to  flush  them. 

Surgically  drainage  of  the  gall-bladder  is  followed  by  good  results. 
*  Ries:  Annals  of  Surgery,  Oct.,  1902. 


Fig.  77. — Section  of  Wall  of  Gall-bladdeb  in  Chhonic 
Cholecystitis. 
The  villosities  of  the  inner  coat  are  seen,  but  there  is  no 
epithelium  left  on  the  surface.  The  darker  longitudinal 
strands  are  smooth  muscle.  The  lighter  portion,  which 
constitutes  two-thirds  of  the  thickness  of  the  wall,  is 
fibrous  tissue  showing  oedema  and  some  small-cell  infiltra- 
tion.    Low  power.      (Photomicrograph  by  Dr.  H.  Spitta.) 


ACUTE    CHOLECYSTITIS.  615 

Excision  of  the  gall-bladder,  according  to  Ries,*  is  preferable  to  removing 
the  mucous  membrane  of  the  gall-bladder  and  leaving  the  rest  of  the 
viscus,  as  practised  by  Mayo,t  but  in  most  cases  drainage  will  prob- 
ably be  sufficient. 

ATROPHIC  SCLEROSING  CHOLECYSTITIS. 

Synonym:  Cholecystitis  obliterans. 

This  thickened,  retracted  condition  of  the  gall-bladder  is  the  result 
of  chronic  cholecystitis  and  is  often  associated  with  cholelithiasis  of  old 
standing.  The  gall-bladder  is  buried  in  adhesions  and  firmly  contracted 
on  itself,  or  perhaps  on  one  or  more  calculi.  In  such  cases  the  wall  of 
the  gall-bladder  is  often  almost  inseparable  from  the  calculi.  If  the 
calculus  is  a  large  one,  the  gall-bladder  may  be  palpable  as  a  tumor  of 
stony  hardness. 

The  walls  of  the  gall-bladder  may  undergo  calcification,  and  choles- 
terin  may  be  deposited  in  the  tissues. 

When  extensively  calcified,  the  gall-bladder  may  be  felt  through  the 
abdominal  wall  and  wdll  resemble  a  gall-bladder  filled  up  with  a  large 
gall-stone. 

Claude  %  found  a  calcified  gall-bladder  the  size  of  a  turkey's  egg  in  a  woman 
aged  ninety-four 

*  Ries:  Annals  of  Surgery,  Oct.,  1902. 

t  Mayo:  Annals  of  Surgery,  1899. 

%  H.  Claude:  Bull.  Soc.  Anat.,  1897,  p.  219. 


PARASITIC  AFFECTIONS  OF  THE  GALL-BLADDER. 

Hydatid  cysts  hardly  ever  arise  in  the  gall-bladder  itself.  Cases 
have  been  reported  in  the  last  twenty  years  by  Bowman,*  J.  K. 
Thornton,t  F-  Page,t  Langenbuch,^,  Huber,  ||  and  Barling  and  Burton.** 
McGavin's  f  f  case  was  in  a  woman  aged  thirty-two  years  and  was  removed 
during  life,  but  the  committee  of  the  Pathological  Society,  on  which  I 
was,  reported  that  the  cystic  tumor  was  not  the  gall-bladder,  but  a 
hydatid  cyst  which  had  arisen  in  its  neighbourhood  and  probably  dis- 
placed it.  A  number  of  cases  described  from  clinical  evidence,  viz., 
jaundice,  a  distended  gall-bladder,  and  disappearance  of  these  signs 
after  the  passage  of  hydatid  membranes  by  the  bowel,  as  hydatid  disease 
of  the  gall-bladder,  are  open  to  the  criticism  that  they  may  have  been 
examples  of  rupture  of  a  hydatid  cyst  into  the  bile-ducts,  with  subse- 
quent obstruction  of  the  common  bile-duct.  Cysts  have  been  said  to 
have  been  found  loose  in  the  gall-bladder.  It  is  conceivable  that  small 
daughter  cysts  which  have  passed  into  the  ducts  from  rupture  of  a  cyst 
into  the  ducts  might  pass  up  a  cystic  duct  which  had  previously  been 
dilated  by  a  gall-stone,  but  it  would  hardly  be  possible  for  them  to  work 
their  way  up  a  normal  cystic  duct  on  account  of  the  valves  of  Heister. 
As  shown  by  J.  Hutchinson,  Jr.'s,  case,  a  hydatid  cyst  in  the  liver 
may,  under  conditions  such  as  suppuration,  discharge  into  the  gall- 
bladder. So  far  as  our  knowledge  goes,  the  symptoms  of  hydatids  in 
the  gall-bladder  are  much  the  same  as  those  of  rupture  of  a  hydatid  cyst 
into  the  bile-ducts. 

Distomuin  Hepaticum. — Budd,  in  his  book  on  Diseases  of  the  Liver, 
mentions  cases  in  which  liver  flukes  have  been  found  loose  in  the  gall- 
bladder. 

Actinomycosis. — Mayo  Robson  J  J  operated  successfully  on  a  case  of 
this  nature,  which  appears  to  be  unique. 

*  Bowman :  Lancet,  1876,  vol.  i,  p.  532. 

t  Thornton,  J.  K. :  Lancet,  1891,  vol.  i,  p.  763. 

i  Page,  F. :  Lancet,  1898,  vol.  i,  p.  995. 

§  Langenbuch:  Deutsch.  med.  Wochens.,  Bd.  xxvi,  1900. 

11  Huber:  Deutsch.  Archiv  f.  klin.  Med.,  Bd.  xlviii,  S.  432. 
**  Barling  and  Burton:  Birmingham  Med.  Rev.,  vol.  xUi,  p.  234. 
tt  McGavin:  Lancet,  1902,  vol.  i,  p.  504.     Trans.  Path.  Soc,  vol.  liii,  p.  351. 
jt  Diseases  of  the  Gall-bladder  and  Bile-ducts,  p.  173,  ed.  iii. 


616 


INNOCENT  TUMORS  OF  THE  GALL-BLADDER. 

Innocent  tumors  are  rare  in  the  gall-bladder  and  are  not  nearly  so 
often  met  with  as  malignant  growths.  Practically  the  only  innocent 
tumor  met  with  in  the  gall-bladder  is  a  papilloma. 


PAPILLOMA  OF  THE  GALL-BLADDER. 

A  papilloma  of  the  mucous  membrane  of  the  gall-bladder  is  rather  a 
rare  tumor — far  rarer  than  carcinoma.  Zenker  *  has  suggested  that 
papilloma  is  the  early  stage  of  carcinoma;  this  may  be  true  for  some 
cases  of  villous  carcinomata  of  the  gall-bladder,  but  from  an  ex- 
amination of  an  extremely  early  case  of  carcinoma  I  am  convinced  it 
is  not  universally  true.  Also,  if  it  were  so,  routine  examination  of  the 
gall-bladder  would  have  shown  that  papillomata  are  commoner  than 
is  the  case. 

A  papilloma  may  be  associated  .with  the  presence  of  gall-stones,  and 
from  analogy  it  would  be  natural  to  expect  that  the  papilloma  is  secondary 
to  the  irritation  of  calculi;  but  there  may  be  no  calculi  and  nothing  to 
suggest  that  there  ever  have  been  any.  It  is  probable  that  some  of  the 
recorded  cases  of  villous  carcinoma  of  the  gall-bladder  are  really  large 
innocent  papillomata. 

Chappet  t  describes  a  large  villous  cancer  in  the  gall-bladder  attached  to  the 
mucosa  by  two  very  thin  pedicles  in  a  man  aged  seventy-nine  years;  there  was  a 
calculus  in  the  common  bile-duct. 

The  papilloma  is  a  soft  wavy  mass  which  is  extremely  friable  and 
breaks  up  on  examination  so  easily  that  it  may,  when  removed  at  an 
operation,  suggest  the  material  that  would  later  form  a  gall-stone.  When 
seen  after  death  the  tumor  is  deeply  bile-stained.  A  papilloma  of  the 
gall-bladder  may  become  detached  from  its  base  and  be  found  quite 
loose  in  the  gall-bladder.  This  was  the  state  of  affairs  in  a  female  patient 
of  Dr.  Des  Voeux's  whose  gall-bladder  was  operated  upon  by  Mr.  Ailing- 
ham,  who  removed  a  pure  cholesterin  gall-stone,  together  with  a  soft,  red 
coloured  mass  of  villous  growth  from  it.  Microscopically  there  is  a  deli- 
cate papillomatous  growth  covered  with  columnar  or  subcolumnar  cells. 
In  specimens  removed  during  life  from  the  gall-bladder  it  is  impossible, 
from  microscopic  examination,  to  say  whether  it  is  a  simple  papilloma 
or  the  superficial  part  of  a  villous  carcinoma. 

The  structure  of  the  papilloma  removed  after  death  is  difficult  to 
make  out  in  the  microscopic  sections  I  have  seen,  from  the  staining  and 
degeneration  due  to  soaking  in  the  bile.     V.  Schueppel  J  examined  niicro- 

*  Zenker:  Deutsche  Archiv  f.  klin.  Med.,  Bd.  xliv,  S.  1.59. 
t  Chappet :  Lyon  Medical,  vol.  Ixxvi,  p.  146. 

X  V.  Schueppel:  v.  Ziemssen's  Cvclopicdiaof  Practical  Medicine,  vol.  ix,  p.  56. 

617 


618  DISEASES    OF   THE    GALL-BLADDER. 

scopic  sections  of  a  myxomatous  papilloma  from  a  gall-bladder  which 
did  not  contain  any  bile. 

If  the  papilloma  becomes  oedematous  or  undergoes  mucoid  degenera- 
tion, a  succulent  tumor  (myxomatous  papilloma)  results.  No  clinical 
symptoms  can  be  correlated  with  papilloma  of  the  gall-bladder. 

The  two  following  examples  of  papilloma  of  the  gall-bladder  have 
come  under  my  notice  at  St.  George's  Hospital: 

A  man  aged  forty-five  died  in  St.  George's  with  cardiac  dilatation  secondary 
to  arteriosclerosis.  Tlae  gall-bladder  felt  rather  like  a  varicocele,  and  when  opened 
contained  a  yellow,  bile-stained,  papillomatous  mass  growing  from  the  anterior 
surface  of  the  gall-bladder  close  to  the  fundus.  The  wall  was  not  thickened  or 
invaded.  There  were  no  calculi  in  the  gall-bladder  or  bile-ducts,  but  the  common 
duct  was  dilated,  as  if  by  the  passage  of  calculi  previously.  In  a  man  who  died 
of  pulmonary  tuberculosis  at  the  age  of  thirty-nine  the  gall-bladder  contained  a 
small  bile-stained  papilloma.  There  were  no  calculi  in  the  gall-bladder  or  ducts, 
and  no  dilatation  of  the  ducts.     There  had  been  no  abdominal  symptoms. 

FIBROMA. 

A  submucous  fibroma  of  the  gall-bladder  has  been  described.*  A 
caution  may  be  thrown  out,  however,  not  to  regard  the  early  stage  of 
primary  carcinoma  of  the  gall-bladder  as  a  fibroma.  The  naked-eye 
appearance  of  early  carcinoma  may  very  closely  resemble  a  firm  fibroma. 


CYSTIC  ADENOMA. 

These  tumors  are  extremely  rare  and  are  pathological  curiosities. 
Such  a  growth  might  be  derived  from  the  mucous  glands  embedded  in 
the  wall  of  the  gall-bladder. 

Stanmore  Bishop  f  removed  a  cystic  tumor  from  the  gall-bladder  of  a  wornan 
aged  forty-two  years  who  had  had  bilious  attacks  accompanied  by  transient  jatmdice. 
The  tumor  contained  a  number  of  cavities  which  did  not  communicate  with  each 
other ;  the  cysts  were  lined  by  cylindrical  epithelium.  Terrier  and  Auvray  |  quote 
a  case  of  Wiedemann's  which  was  probably  of  the  same  nature. 

CYSTS. 

Cysts  in  the  mucous  membrane  of  the  gall-bladder  containing  choles- 
terin  and  of  small  size  are  occasionally  met  with.  Terrier  and  Auvray 
refer  to  a  case  of  Adler's  in  which  a  gall-bladder  presented  three  such 
cysts.  These  cholesterin-containing  cysts  may  develop  into  calculi  em- 
bedded in  the  wall  of  the  gall-bladder.  Hydatid  cysts  are  referred  to 
on  page  616. 

Local  oedema  under  the  peritoneal  coat  of  the  gall-bladder  is  some- 
times seen  in  cases  of  backward  pressure,  such  as  is  induced  by  morbus 
cordis  or  chronic  bronchitis  and  emphysema.  To  the  naked  eye  it  looks 
like  a  small  cyst ;  microscopically  it  is  seen  that  there  is  no  true  cavity, 
and  only  oedema  of  the  tissues. 

*  Albers,  quoted  in  v.  Ziemssen's  Cyclopaedia  of  Practical  Medicine,  vol.  ix,  p. 
567,  1880. 

t  Stanmore  Bishop:  Lancet,  1901,  vol.  ii,  p.  72. 

j  Terrier  and  Auvray:  Chirurgie  du  foie,  p.  253,  1901. 


INNOCENT   TU:M0RS   OF   THE    GALL-BLADDER.  619 

FATTY  TUMORS. 
Local  subperitoneal  masses  of  fat  are  in  rare  instances  seen  on  the 
gall-bladder.  I  have  observed  this  abnormality  in  otherwise  perfectly 
health}^  gall-bladders.  As  a  result  of  cholecystitis  it  is  conceivable  that 
an  appendix  epiploica  might  become  adherent  to  the  gall-bladder  and 
subsequently  be  detached  from  the  colon. 


PRIMARY  MALIGNANT  DISEASE  OF  THE  GALL-BLADDER. 

This  is  b}'  no  means  a  rare  disease,  and  has  attracted  quite  a  fair  share 
of  attention.  Frerichs  *  gave  an  excellent  account  of  the  disease  in  1861, 
and  in  1870  Villard  t  collected  17  cases;  Musser.J  in  1889,  100  cases; 
Cour\^oisier,^  103;  and  in  1901  Flitterer,  ||  268.  These  tables,  of  course, 
deal  largely  with  the  same  individual  cases.  The  bibUography  attached 
to  Siegert's,**  Ames's,tt  and  Fiitterer's  papers  shows  that  the  subject 
has  no  cause  to  complain  of  neglect.  Though  this  disease  has  certainly 
received  more  attention  of  late  years,  it  is  probably  actually  more  fre- 
quent now  than  formerly.  Of  Fiitterer's  268  cases,  no  less  than  195 
were  reported  since  1880.  This  is  no  doubt  in  part  due  to  the  fact  that 
the  disease  has  been  more  generally  distinguished  from  genuine  primary- 
carcinoma  of  the  liver. 

It  is  a  striking  fact  that  another  annexa  of  the  alimentary  canal,  the 
vermiform  appendix,  in  which  concretions  are  comparatively  common, 
is  verv^  rarely  attacked  b}"  primary  malignant  disease. |J  They  are  both 
frequently  inflamed,  and  are  both  very  hable  to  irritation  and  infection, 
the  appendix  more  especially.  Why  one  should  be  comparatively  im- 
mune to  mahgnant  disease  is  a  difficult  c|uestion.  Possibl}^  some  basis 
of  an  explanation  may  be  found  in  the  fact  that  the  appendix  is  an  atrophy- 
ing relic  of  part  of  the  gut,  while  the  gall-bladder  belongs  to  the  very 
extensively  developed  appendage — the  hepatic  diverticulum  from  the 
duodenum. 

HORBID  ANATOMY.  ' 

Primary  malignant  disease  of  the  gall-bladder  is  practically  always 
carcinoma.     I  have  references  to  nine  cases  of  primary  sarcoma. 

Musser,§  §  in  his  statistical  analysis,  mentions  three  cases  of  primary  sarcoma ; 
Griffon  and  Segall  ||  !|  record  a  case  of  a  spindle-celled  sarcoma,  primary  in  the  gall- 
bladder, which  contamed  two  calculi,  in  a  woman  aged  seventy-six.  Czerny  (angio- 
sarcoma), Reidel,***  and  Xeviadomski  ttt  l^ave  also  met  with  primary  sarcoma 
of  the  gall-bladder.     Becker  JJ J  has  described  a  primary  endothelioma  of  the  gall- 

*  Frerichs :  Diseases  of  the  Liver,  vol.  ii,  p.  479.     Transl.  Xew  Sydenham  Soc. 
t  Villard:  Bull.  Soc.  .\nat.  Paris,  vol.  xliv,  p.   217,  at  sitting  August,  1869. 
i  Musser,  J.  H. :  Boston  Med.  and  Surg.  Joum.,  vol.  cxxi,  p.  525,  1889. 
§  Courvoisier:  Pathologie  und  Chirurgie  der  Gallenwege.  Leipzig,  1890. 
jl  Fiitterer,  G. :  Ueber  die  Aetiologie  des  Carcinoms,  1901,  Wiesbaden. 
**  Siegert :  Virchow's  Archiv,  Bd.  cxxxiii,  S.  353. 
tt  Ames,  D.:  Johns  Hopkms  Hospital  Bulletin,  vol.  v,  No.  41,  1894. 
J  j  Within  the  last  few  years  a  number  of  cases  of  primary  carcinoma  of  the 
vermiform   appendix   have   been   described,  and   in    1903   Moschowitz  (Annals  of 
Surgery,  part  126,  p.  891)  collected  21  authentic  cases. 
§§  Musser:  Loc.  cit. 

III!  Griffon  and  Segall:  BuU.  Anat.  Soc.  Paris,  1897,  p.  586. 
***  Riedel:  Erfahrungen  liber  die  Gallensteinkrankheiten,  1892. 
ttt  Neviadomski:  Meditzinskoe  Obozrenie,  Feb.,  1900. 
j jj  Becker,  W. :  .Journ.  American  Med.  Assoc,  1903,  April  4,  p.  903 

620 


PRIMARY    MALIGNANT    DISEASE    OF    GALL-BLADDER. 


621 


bladder  associated  with  t^YO  gall-stones  which  had  almost  perforated  into  the 
stomach  near  the  pylorus.  I  have  examined  one  case  of  primary  spindle-celled 
sarcoma  of  the  gall-bladder. 

A  woman  aged  fifty-six  had  a  large  tumor  to  the  right  of  the  umbilicus  which 
entirely  replaced  the  gall-bladder;  it  contained  a  cavity  lined  by  broken-down 
gro-«i;h  which  opened  into  the  transverse  colon.  The  growth  had  tracked  along 
the  cystic  and  common  bile-ducts  and  formed  a  projection  at  the  biliary  papilla. 
Xo  gall-stones  were  found.  There  were  secondary  growths  in  the  aortic  lymphatic 
glands  and  in  a  gland  in  the  right  groin.  There  was  no  jaundice.  Microscopically 
the  growth  was  a  spindle-celled  sarcoma  somewhat  alveolar  in  arrangement.  There 
were  numerous  blood-spaces  in  the  growth.  The  case  was  under  the  care  of  Mr. 
[now  Sir]  W.  Bennett  in  St.  George's  Hospital  in  1891  and  the  autopsy  was  made 
by  me. 

The  description  of  malignant  disease  of  the  gall-bladder  is,  therefore, 
practically  that  of  carcinoma  of  the  organ. 

Histological  Structure.^ — Carcinoma  of  the  gall-bladder  varies  much, 
both  in  the  form  of  the  cells  and  in  their  structural  arrangement ;  it  may 
be  either  columnar  or 
spheroidal-celled.  The 
cells  may  undergo  colloid 
degeneration,  or  the  cavi- 
ties of  the  tubes  lined 
by  coluimiar  epithelium 
may  become  distended 
by  mucoid  material  with- 
out the  cells  showing  any 
of  the  appearances  of  col- 
loid degeneration.  The 
columnar- celled  carci- 
noma may  groAv  into  the 
cavity  of  the  gall-bladder 
as  a  villous  or  papilloma- 
tous growth;  but  the  es- 
sentially mahgnant  part, 
where  there  is  invasion 
of  the  deeper  layers, 
does  not  show  a  papil- 
lomatous arrangement, 
and  is  a  columnar-celled 

carcinoma  of  the  ordinary  type,  containing  a  fair  amount  of  fibrous 
tissue.  Freciuently  a  change  of  type  of  the  carcinoma  is  visible;  parts 
of  the  growth  may  be  columnar-celled,  others  cubical,  and  other  parts 
spheroidal-celled.  This  transition  is  seen  in  columnar-celled  carcino- 
mata  elsewhere,  especially  in  duct  cancer  of  the  breast.  In  transitional 
parts,  and  especially  when  colloid  or  allied  degenerative  changes  are 
present,  the  large  epithelial  cells  may  be  so  far  modified  as  to  appear 
flattened,  and   have   then   been   described  as  squamous    cells;*    multi- 

*  For  a  discussion  of  this  curious  change  see  Bret.  Lyon  Medical,  t.  Ixxxix, 
p.  41,  Sept.  11,  1898.  Cases  of  this  kind  are  recorded  by  Mayo  Robson:  Medico- 
Chirurg.  Trans.,  vol.  Ixxix,  p.  159;  Hebb,  R.  G. :  Westminster  Hospital  Reports, 
1895,  p.  316;  Deetz:  Virchow's  Archiv,  Bd.  clxiv,  S.  381. 


Fig.  78. — Photomicrograph  of  Columnar-celled  Carci- 
noma   OP   THE    GaLL-BLAHDER. 

Shows   dilated    spaces   lined   by   columnar   epithelium   and 
containing  mucus.     (S.  G.  Penny,  Esq.) 


622  DISEASES    OF   THE    GALL-BLADDER. 

nuclear  cells  are  also  sometimes  seen.  The  lining  membrane  of  the 
gall-bladder  is  normally  columnar  epithelium;  as  the  result  of  inflam- 
mation or  irritation  it  may  become  replaced  by  round  cells,  but 
metaplasia  never  goes  so  far  as  to  lead  to  cornification.  It  is  highly 
improbable  that  changes  of  this  kind  ever  give  rise  to  a  true  squamous- 
celled  carcinoma,  showing  keratinisation,  primary  in  the  gall-bladder, 
though  in  transitional  parts  of  the  growth  the  altered  or  colloid 
columnar  cells  and  cell  inclusions  may  closely  resemble  squamous  cells 
and  cell-nests. 

Deetz  (Virchow's  Archiv,  Bd.  clxiv,  S.  381),  in  an  examination  of  300  gall- 
bladders, including  some  with  cholelithiasis,  never  observed  transformation  of 
the  lining  epithelium  into  squamous  epithelium,  but  he  nevertheless  believes  this 
change  must  occur  to  account  for  the  appearances  of  a  primary  squamous-celled 
carcinoma  of  the  gall-bladder.  Adami  (Brit.  Med.  Journ.,  1901,  vol.  i,  p.  626)  also 
believes  that  metaplasia  of  the  columnar  into  squamous  epithelium  must  take  place 
in  the  gall-bladder. 

Degenerative  changes  besides  the  mucoid  and  colloid  changes  al- 
ready referred  to  and  fatty  degeneration  of  the  cells  of  the  growth  may 
occur,  while  in  parts  the  growth  may  become  necrotic.  Occasionally 
haemorrhages  may  take  place  into  the  tumor. 

Starting-point  of  the  Growth. — In  order  to  explain  the  origin  of 
the  two  varieties,  columnar-  and  spheroidal-celled  carcinoma,  arising  in 
the  gall-bladder,  it  has  been  suggested  that  spheroidal-celled  carcinoma 
is  derived  from  the  mucous  glands  in  the  wall  of  the  gall-bladder,  while 
columnar-celled  carcinoma  is  derived  from  the  surface  mucous  mem- 
brane of  the  gall-bladder.  This  theory  is  unnecessary,  since  the  change 
in  type  from  a  columnar-  to  a  spheroidal-celled  carcinoma  can  be  seen 
in  the  same  specimen,  and  also  because  there  is  no  essential  difference 
between  the  columnar  cells  of  the  surface  mucous  membrane  and  of  the 
mucous  recesses,  depressions,  or  "glands"  in  communication  with  it. 
It  may  be  concluded  that  carcinoma,  whatever  its  form,  arises  from  the 
mucous  membrane  as  a  whole,  and  no  statement  that  either  form  of 
carcinoma  arises  exclusively  from  the  surface  epithelium  of  the  gall- 
bladder or  from  the  epithelium  lining  the  "glands"  is  necessary  or  justi- 
fied by  our  knowledge. 

It  has  been  suggested  that  carcinoma  of  the  gall-bladder  begins  as 
a  papilloma,*  which,  like  a  pol5^us  of  the  intestine,  might  be  called  an 
adenoma.  Cases  of  pure  papilloma  of  the  gall-bladder  are  very  rare. 
There  are,  moreover,  some  cases  of  carcinoma  of  the  gall-bladder  which 
do  not  show  any  villous  projection  into  the  lumen  of  the  cavity,  but  are 
limited  to  the  infiltration  of  the  wall  and  the  surrounding  tissues.  Al- 
though it  may  happen  sometimes,  there  is  certainly  no  proof  that  the 
growth  always  starts  as  an  adenoma,  which  subsequently  takes  on 
mahgnant  growth.  Carcinoma  of  the  gall-bladder  may,  hke  carcinoma  of 
the  intestine,  occur  in  two  forms:  (1)  That  projecting  into  the  cavity  of 
the  gall-bladder  as  a  f ungating  growth;  (2)  that  limited  to  an  infiltration 

*  Zenker:  Deutsches  Archiv  f.  klin.  Med.,  Bd.  xhv,  S.  159,  1889;  Aczel:  Vir- 
chow's Archiv,  Bd.  cxliv,  S.  86,  1896:  Warthin:  Journ.  American  Med.  Association, 
Maj--  6,  1899. 


PRIMARY   MALIGNANT    DISEASE    OF   GALL-BLADDER.  623 

of  its  walls.  The  fungating  form  is  generally  papillomatous,  and  histo- 
logically a  columnar-celled  growth,  while  the  infiltrating  form,  though 
it  may  be  a  columnar-celled  carcinoma,  is  often  a  spheroidal-celled  growth. 
The  two  forms  may  be  combined. 

Situation  of  the  Growth. — The  fundus  is  the  commonest  situation 
for  the  origin  of  carcinoma,  and  the  distal  compartment  of  an  hour-glass 
gall-bladder  may  be  the  starting-point  of  the  growth.  This  is  explained 
by  the  fact  that  the  fundus  being  the  most  dependent  part,  is  specially 
exposed  to  irritation  from  the  presence  of  calculi.  The  gro^'th  may  begin 
at  the  neck  of  the  gall-bladder,  at  its  junction  with  the  cystic  duct,  and 
then  give  rise  to  obstruction,  either  by  blocking  the  lumen  or  by  spreading 
around  the  circumference  of  the  narrowed  gall-bladder  or  cystic  duct, 
and  producing  an  annular  stricture.  As  a  result  the  gall-bladder  may 
become  tense  and  distended  with  fluid.  Carcinoma  of  the  cystic  duct 
is  much  the  same  as  carcinoma  of  the  neck  of  the  gall-bladder,  and 
clinically  resembles  that  condition  rather  than  carcinoma  of  the  other 
bile-ducts.  Carcinoma  of  the  neck  of  the  gall-bladder  may  appear  to 
depend  on  the  irrita- 
tive effects  of  im- 
pacted calculi  in  that 
situation. 

The  growth  may, 
however,  involve  the 
whole  of  the  gall- 
bladder, so  that  it  is 
difficult  or  impossible 

to    say  in  what   part Fig.   79. — Drawing  of  Section  of  a  White  Growth  Replac- 

r-  ■,  ^  j_  •!.  ING    THE    GaI.L-BLADDER,  IN  THE    CeNTHE    OF    WHICH    THERE 

fundus,    neck,    etc. it  is  a  Calculous  Mass. 

arose.       In  other   cases        „     '^F^'P-   ^   specimen    (Series   ix    No.    197c)    in    St.  George's 
Hospital    Museum.     (Drawn    by  L/awrence  Jones,  iLsq.,  M.B., 

the     gall-bladder     is     f.r.c.s.) 
entirely    replaced    by 

growth.  That  the  growth  originated  in  the  gall-bladder  is  then  assumed 
from  the  complete  absence  of  that  viscus,  or  from  the  presence  of  calculi 
embedded  in  the  centre  of  a  growth  in  the  position  of  the  gall-bladder. 
This  condition  may,  indeed,  be  erroneously  regarded  as  primary  (mas- 
sive form)  cancer  of  the  liver  itself,  the  real  origin  of  the  groN\i:li  in  the 
gall-bladder,  which  has  completely  disappeared,  being  easily  overlooked. 
A  secondary  growth  in  the  gall-bladder  may,  to  the  naked  eye,  re- 
semble a  primary  neoplasm. 

There  is  a  specimen  in  St.  Bartholomew's  Hospital  Museum  (No.  2216  g)  which 
looks  like  a  primary  growtli,  but  is  really,  as  shown  by  section  of  the  walls  of  the 
gall-bladder,  a  secondary  nodule  of  round-celled  sarcoma;  the  primarj'-  growth  was 
in  the  lung. 

Behaviour  and  Appearance  of  the  Growth. — The  columnar-celled 
form  may  project  into  tlio  gall-l)Iad(l('r  and  fill  it  with  a  villous  or  papillo- 
matous growth  which  easily  disintegrates,  and  then  somewhat  resembles 
caseous  pus  or  plaster-like  material,  imitating  both  in  structure  and  in 
appearance  psorospermosis   of  the   bile-ducts   in   a   rabbit's   liver.     A 


624 


DISEASES    OF   THE    GALL-BLADDER. 


columnar-celled  carcinoma  of  the  gall-bladder  may  form  a  hard,  sohd 
growth,  and  need  not  be  in  the  least  villous  in  its  arrangement.  So, 
just  as  in  the  breast,  a  columnar-celled  carcinoma  may  occur  in  one  of 
two  forms:  (i)  villous;  (ii)  like  an  ordinary  columnar-celled  carcinoma 
of  the  bowel. 

On  comparing  the  columnar-  and  spheroidal-celled  forms  of  gall- 
bladder carcinoma  it  is  seen  that,  generally  speaking,  the  spheroidal- 
celled  grows  more  rapidly  and  generalises  more  freely.  But  a  columnar- 
celled  growth  may  spread  by  continuity  into  the  liver  substance,  and 
then  show  a  transition  to  the  spheroidal-celled  type. 

Haemorrhage  from  the  villous  growth  into  the  gall-bladder  very  rarely 
occurs;    Musser  says  that  haemorrhages  occurred  7  times  in  100  cases. 

It  has  seemed  to  me,  as 
would  naturally  be  ex- 
pected, that  colloid  change 
occurs  more  commonly  in 
the  more  chronic  columnar- 
celled  growths  than  in  the 
spheroiclal-cellecl  carcinoma. 
Carcinoma,  if  seen  in  an 
early  stage,  may  appear  as 
a  localised  thickening,  like 
a  button,  of  the  wall  of  the 
gall-bladder,  of  a  whitish 
appearance,  and  may  re- 
semble a  scar  or  a  gumma. 
Opportunities  for  examin- 
ing the  early  stage  of  such 
growths  are  rare;  as  a  rule, 
the  growth  has  extensively 
invaded    the    walls   of    the 

Fig.  80.— Primary  Carcinoma  of  the  Gall-bladder  gall-bladder.  (For  an  ex- 
ample of  an  early  case  vide 
p.  602.) 

Extension  of  the 
Growth  by  Continuity. — 
As  already  mentioned,  a 
large  growth  in  the  gall-bladder  may  directly  invade  the  liver,  and 
thus  give  rise  to  considerable  hepatic  enlargement.  In  these  cases  the 
fact  that  the  growth  arose  in  the  gall-bladder  may  be  overlooked  and 
the  condition  may  be  regarded  as  primary  carcinoma  of  the  liver. 


-Primary  Carcinoma  of  the  Gall-bladder 

OF    THE    PAPILLOM.iTOU.S    FoRM. 

The  gall-bladder  has  been  cut  up  longitudinally; 
it  is  seen  that  the  growth  does  not  occupy  the  whole 
of  the  gall-bladder,  the  fundus  and  neck  not  being 
affected.  From  a  specimen  (Series  ix,  No.  197a)  in 
St.  George's  Hospital  Museum.  (Drawn  by  Dr.  E.  A. 
Wilson.) 


In  one  case  which  I  examined  the  growth  spread  from  the  anterior  surface  of 
the  gall-bladder  into  the  liver  substance,  and  projected  so  little  into  the  cavity  of 
the  gall-bladder  that  it  was  only  on  section  and  careful  examination  that  it  became 
clear  that  the  growth  started  in  the  walls  of  the  gall-bladder.  In  this  instance 
the  primary  growth  was  confined  to  the  surface  of  the  gall-bladder  in  contact  with 
the  liver,  and  might  have  been  overlooked  on  casual  e.xamination,  and  the  numerous 
secondary  growths  in  the  liver  might,  therefore,  have  been  regarded  as  primary 
multiple  carcinoma. 


PRIMARY    MALIGNANT    DISEASE    OF    GALL-BLADDER.  625 

Generally,  however,  when  the  groT\i:h  in  the  gall-bladder  extends 
by  continuity  into  the  liver,  the  origin  of  the  tumor  is  quite  clear.  The 
growth  may  spread  by  continuity  in  the  wall  of  the  cystic  duct  into 
the  common  bile-duct,  or  along  the  hepatic  ducts  into  the  hver,  much 
in  the  same  way  that  a  growth  at  the  bifurcation  of  the  trachea  may 
track  along  the  bronchi  and  their  lymphatics  into  the  lung.  It  may 
then  be  difficult  to  say  whether  the  primary  growth  started  in  the  bile- 
ducts  and  then  extended,  or  originated  in  the  gall-bladder.  A  carcinoma 
of  the  gall-bladder  has  been  known  to  project  as  a  free  process  down 
the  lumen  of  the  cystic  duct  into  the  common  bile-duct  (Bohnstedt  *), 
in  the  same  manner  that  malignant  disease  of  the  liver  has,  in  at  least 
one  case  (Gilbert  and  Claude  f),  been  found  projecting  into  the  extra- 
hepatic  bile-ducts. 

Fistulae. — When,  as  is  more  commonly  the  case,  the  growth  begins 
in  the  fundus  of  the  gall-bladder,  it  readily  becomes  adherent  to  the 
colon  and  may  open  into  it.  Musser  refers  to  this  accident  in  10  cases. 
Fistulous  communications  between  the  colon  and  gall-bladder  may,  of 
course,  be  due  to  other  causes,  such  as  ulceration  due  to  a  gall-stone, 
but  in  9  cases  of  colocholecystic  fistulae  collected  by  Murchison  6  were 
the  result  of  cancer  of  the  gall-bladder.  In  like  manner  the  carcin- 
omatous gall-bladder  may  open  into  the  duodenum,  but  this  fistulous 
communication  is  less  often  seen  in  carcinoma  than  in  cholelithiasis. 

The  growth  may  involve  the  duodenum  so  widely  that  it  may  be 
difficLdt  to  decide  in  which  situation  it  started. 

Coupland  t  describes  a  primary  carcinoma  of  the  first  part  of  the  duodenmii 
which  grew  into  and  entirely  replaced  the  gall-bladder.  Inasmuch  as  primary 
carcinoma  of  the  first  part  of  the  duodenum  is  much  rarer  than  carcinoma  of  the 
gall-bladder,  it  is  quite  reasonable  to  raise  the  question  whether  the  growth  did 
not  arise  in  the  gall-bladder. 

In  rare  instances  a  fistulous  passage  is  established  between  the  gall- 
Ijladder  and  the  pyloric  end  of  the  stomach;  the  gro-wth  has  been  known 
to  invade  the  abdominal  wall,  then  to  set  up  an  abscess,  and  even  to 
lead  to  an  external  fistula. 

Pressure  Effects. — ^When  the  growth  involves  the  pylorus,  it  may 
lead  to  pyloric  obstruction,  and  so  clinically  simulate  carcinoma  of  that 
part  of  the  stomach.  From  the  anatomical  relations  of  the  gall-bladder 
to  the  pylorus  this  is  more  likely  to  occur  when  the  growth  is  near  the 
neck  of  the  gall-bladder. 

Rabe  and  Rey  §  found  the  fundus  of  a  carcinomatous  gall-bladder  firmly 
adherent  to  the  first  part  of  the  duodenum,  which  was  greatly  narrowed  and  had 
led  to  dilatation  of  the  stomach.  The  colon  was  also  adherent  to  the  gall-bladder, 
and  the  intestinal  obstruction  whicli  existed  in  the  case  was  thus  partly  explained. 
Lejonne  and  Milanoff  ||  have  recorded  a  somewhat  similar  case. 

*  Bohnstedt,  quoted  by  Devic  and  Gallavardin,  Rev.  de  Med.,  July,  1901,  p. 
569. 

t  Gilbert  and  Claude:  Archiv.  g6n6ral.  de  MM.,  t.  clxxv,  1895,  p.  513. 
X  Coupland,  S. :  Trans.  Path.  Soc,  vol.  xxiv,  p.  103. 
§  Rab6  and  Rey:  Bull.  Soc.  .^nat.  Paris,  1897,  p.  881. 
II  Lejonne  and  Milanoff:  Bull.  Soc.  Anat.  Paris,  1900,  p.  133. 
40 


626  DISEASES    OF   THE    GALL-BLADDER. 

The  gall-bladder  may,  in  very  rare  cases,  perforate  into  the  peritoneal 
cavity,  or  give  rise  to  a  localised  abscess.  The  notes  of  the  following 
remarkable  case  were  communicated  to  me  by  Dr.  C.  D.  Green: 

The  patient  was  a  woman  aged  sixty-two,  with  persistent  jaundice,  mahgnant 
cachexia,  and  an  enlarged  liver  from  which  there  projected  a  mass  of  stony  hard- 
ness about  as  large  as  a  bantam's  egg ;  she  was  suddenly  seized  with  acute  abdominal 
pain,  and  the  hard  mass  could  no  longer  be  felt,  but  was  replaced  by  a  general 
boggy  feeling.  Death  followed  m  a  few  hours  from  peritonitis.  At  the  autopsy 
there  was  a  large  carcinomatous  mass  involving  the  liver  in  the  region  of  the  gall- 
bladder, colon,  and  the  stomach.  An  abscess  cavity  due  to  destruction  of  the 
growth  had  ruptured  into  the  peritoneal  cavity.  No  trace  of  the  gall-bladder  could 
be  made  out;  the  abscess  cavity  contained  a  smgle  large  biliary  calculus,  obvi- 
ously what  had  been  felt  during  life. 

A  localised  abscess  around  a  carcinomatous  gall-bladder  was  operated  upon 
during  life  by  Mr.  Rushton  Parker.*  Death  occurred  ten  days  later  from  general 
purulent  peritonitis. 

Secondary  Growths. — The  liver  is  the  organ  most  frequently  af- 
fected, being  involved  in  about  50  per  cent,  of  the  cases.  Not  infre- 
quently the  tumor  grows  directly  into  the  right  lobe. 

In  Musser's  f  100  cases  there  were  metastases  in  55,  and  in  all  but  one  of  these 
the  liver  was  involved — in  52  by  metastases,  in  2  bj'  direct  extension.  The  abdom- 
inal lymphatic  glands  were  involved  in  16,  the  limgs  or  pleura  in  10,  the  peritoneum 
in  12. 

When  the  growths  are  numerous,  the  clinical  aspect  of  the  case 
becomes  that  of  malignant  disease  of  the  liver  substance.  Secondary 
growths  in  the  lymphatic  glands  may  compress  the  bile-ducts  and  portal 
vein,  thus  setting  up  jaundice  and  ascites.  Secondary  growths  may 
occur  in  other  abdominal  lymphatic  glands,  in  the  peritoneum,  in  the 
ovaries,  and  in  the  lungs. 

Infection  may  travel  up  from  the  abdomen  into  the  chest  along  the 
lymphatic  vessels,  which  pass  immediately  behind  the  sternum  to  the 
glands  in  the  anterior  mediastinum.  A  tumor  may  thus  project  from 
the  surface  of  the  chest  even  before  the  primary  growth  has  been  de- 
tected. 

Beadles  J  described  a  case  of  primary  carcinoma  of  the  gall-bladder  with  a 
secondary  growth  as  large  as  a  cocoanut  arising  near  the  second  rib  on  the  right 
side.  In  a  case  of  S.  West's  §  the  clinical  symptoms  were  those  of  mediastinal 
tumor,  which  at  the  autopsy  Avas  shown  to  be  secondary  to  a  groAAi;h  in  the  gall- 
bladder. 

In  rare  instances  the  lymphatic  glands  above  the  clavicle  may  be 
enlarged  and  readily  palpable  during  life.  To  this  phenomenon  of  intra- 
abdominal disease  the  term  "Virchow's  gland"  has  been  applied.  In 
cases  where  acute  cholecystitis  supervenes  in  a  carcinomatous  gall- 
bladder enlargement  of  lymphatic  glands  in  the  neiglibourhood  may  be 
inflammatory  and  not  necessarily  due  to  new-growth. 

The  liver  may  be  healthy,  but  usually  it  is  enlarged,  either  from 
distension  with  bile  or  from  the  presence  of  secondary  growths.     In 

*  Brit.  Med.  Journ.,  1899,  vol.  ii,  p.  1544. 

t  Musser:  Boston  Medical  and  Surgical  Jourii.,  vol.  cxxi,  LS89. 
X  Beadles,  C.  F. :  Trans.  Path.  Soc,  vol.  xlviii,  p.  119. 
§West,  S. :  Path.  Soc.  Trans.,  vol.  xxxvii,  p.  144. 


PRIMARY    MALIGNANT    DISEASE    OF    GALL-BLADDER.  627 

many  cases  the  growth  extends  directly  into  the  substance  of  the  right 
lobe,  and,  as  pointed  out  elsewhere,  the  tumor  may  resemble  a  primary 
massive  carcinoma  of  the  liver.  From  infection  of  the  bile-ducts  sup- 
puration may  occur  in  the  liver  and  give  rise  to  miliary  abscesses.  In 
60  cases  tabulated  by  Winton  *  4  showed  miliary  abscesses. 

ETIOLOGY. 
Relation  of  Primary  Carcinoma  of  the  Gall-bladder  and  Gall- 
stones.— Special  interest  attaches  to  the  association  of  gall-stones  and 
carcinoma  of  the  gall-bladder,  inasmuch  as  the  calculi  are  generally 
thought  to  be  the  cause,  whether  by  direct  irritation  or  otherwise,  of  the 
neoplasm.  That  calculi  are  commonly  met  with  in  primary  carcinoma 
of  the  gall-bladder  is  shown  by  numerous  statistics.  In  Musser's  100 
cases  gall-stones  were  stated  to  be  present  in  69,  and  in  only  three  in- 
stances was  cholelithiasis  definitely  stated  to  be  absent.  Fiitterer  f 
estimated  that  calculi  were  present  in  70  per  cent.;  Winton  J  in  81  per 
cent.;  Zenker  §  in  85  per  cent.;  Courvoisier||  in  91  per  cent.;  Siegert 
in  95  per  cent.  Janowski**  in  40  cases  of  malignant  disease  of  the  gall- 
bladder records  calculi  in  all.  Conversely,  it  appears  that  primary  car- 
cinoma of  the  gall-bladder  occurs  in  from  14  per  cent,  to  4  per  cent,  of 
all  cases  of  cholelithiasis. 

Schroeder  ft  estimated  that  14  per  cent,  of  persons  with  choleUthiasis  eventually 
became  the  subjects  of  carcinoma  of  the  gall-bladder;  in  141  cases  of  gall-stones 
there  were  20  of  primary  carcinoma.  In  149  cases  of  gall-stones  abstracted  from 
the  postmortem  records  of  Guy's  Hospital  by  Keay  %%  there  were  17  cases  of  carci- 
noma of  the  gall-bladder  or  cystic  duct,  or  11.4  per  cent.  Riedel  §§  estimated 
the  percentage  of  primary  carcinoma  in  cholelithiasis  at  from  7  to  8  per  cent.  Among 
242  cases  of  gall-stones  at  St.  George's  Hospital  there  were  10  cases  of  primary 
carcinoma  of  the  gall-bladder,  or  4.1  per  cent.;  this  low  percentage  is  possibly 
accounted  for  by  the  fact  that  in  many  instances  minute  bilirubin-calcium  calculi 
were  the  only  ones  present.  In  twenty-one  and  one-half  years  there  were  at  St. 
George's  16  cases  of  primary  carcinoma  of  the  gall-bladder;  13,  or  81  per  cent.,  of 
which  were  associated  with  gall-stones. 

It  has,  however,  been  suggested  that  the  calculi  are  secondary  to 
the  growth,  and  are  the  result  of  obstruction  to  the  passage  of  bile  or 
of  other  changes  set  up  by  the  growth  of  carcinoma  in  the  gall-bladder. 
Experimentally,  however,  it  does  not  appear  that  bile  is  more  likel}'  to 
crystallise  on  stagnation,  provided  the  gall-bladder  is  aseptic  (Mignot||  ||). 
If  calculi  were  the  result  of  obstruction  pure  and  simple,  they  would  be 
found  more  frequently  in  carcinoma  of  the  bile-ducts,  where  there  is 
much  more  biliary  obstruction  than  in  malignant  disease  of  the  gall- 
bladder.    But  they  are   less  frequent  in  the  former  condition,   being 

*  Winton,  W.  B. :  ITnpublished  Thesis  for  M.  D.,  Camliridge,  1902. 

t  Fiitterer,  G.:  Ueber  the  Aetiologie  dor  Carcinoms,  A^'i('sbadcl:,  1901. 

X  Winton,  W.  B.:  Thesis  for  M.D.,  Cambridge,  mipublishcd,  1902. 

§  Zenker,  H.:  Deutsch.  Archiv  f.  klin.  Mod.,  Bd.  xliv,  S.  159,  1891. 

II  Courvoisier :  Path.  u.  Chirurg.  der  Gallenwego,  1890. 
**  Janowski:  Ziogler's  Beitnigo,  Bd.  x,  S.  449,  1891. 
tt  Schroeder:  Quoted  by  Kcay. 
tX  Keay:  Medical  Treatment  of  Gall-stones,  p.  67. 
§§  Rieclel:  Berlin,  klin.  Woolion.,  1901,  S.  1. 
III!  Mignot:  Archiv.  general,  do  Mod.,  1898,  Aug.-Sept. 


628  DISEASES   OF  THE    GALL-BLADDER. 

present  in  23  out  of  my  62  cases,  while  in  carcinoma  of  the  gall-bladder 
the  percentage  is  about  90.  Besides  directly  obstructing  the  exit  of  bile 
and  mucus  from  the  gall-bladder,  a  growth  in  its  wall  might  interfere 
with  its  contractions.  Both  these  conditions  would  lead  to  biliary  stag- 
nation and  so  favour  microbic  infection,  cholecystitis,  and  the  production 
of  calculi.  Further,  it  is  conceivable  that  the  presence  of  a  growth  or 
its  disintegration  ixdght  modify  the  secretion  from  the  mucous  membrane 
of  the  gall-bladder. 

In  this  connexion  it  is  important  to  bear  in  mind  that  the  cholesterin 
is  derived  from  the  mucous  membrane  of  the  gall-bladder,  and  not  from 
the  bile  itself.  Siegert  *  tried  to  settle  the  question  whether  the  presence 
of  a  growth  in  the  gall-bladder  gave  rise  to  the  formation  of  calculi  by 
a  comparison  of  the  incidence  of  calculi  in  primary  and  in  secondary 
carcinoma  of  that  viscus.  In  99  cases  of  primary  disease  calculi  were 
present  in  94;  while  in  13  cases  of  secondary  growths  in  its  wall  they 
were  present  in  only  2.  In  13  other  cases  of  secondary  growths  that  I 
have  collected  or  seen,  calculi  were  present  in  one ;  so  in  these  26  cases 
of  secondary  growths  in  the  gall-bladder  gall-stones  occurred  in  3,  or 
11.7  per  cent.,  which  are  "wdthin  the  limits,  5  to  12  per  cent.  (Schroeder 
and  Naunyn  f),  of  the  incidence  of  gall-stones  in  ordinary  routine  post- 
mortem work.  These  figures,  as  far  as  they  go,  do  not  support  the 
view  that  the  presence  of  a  growth  in  the  gall-bladder  is  a  factor  of  any 
importance  in  the  production  of  gall-stones.  It  must,  however,  be  ad- 
mitted that  the  presence  of  a  secondary  growth  in  the  gall-bladder  is  not 
quite  the  same  as  a  primary  growth,  especially  as  regards  its  relation  to 
the  mucous  membrane.  A  secondary  growth  usually  starts  under  the 
serous  coat,  and  need  not  involve  the  mucous  coat,  which  produces 
cholesterin,  while  a  primary  carcinoma  is  due  to  changes  in  the  mucous 
membrane  itself. 

There  is  undoubtedly  a  very  definite  relation  between  cholelithiasis 
and  the  development  of  primary  carcinoma  of  the  gall-bladder.  But 
gall-stones  are  so  commonly  present  without  carcinoma  developing,  that 
though  they  dispose  to  its  occurrence,  some  additional  factor  is  necessary. 
Possibly  the  part  played  by  calculi  is  that  of  preparing  the  soil  for  the 
direct  cause,  whatever  it  may  be,  of  carcinoma.  That  gall-stones  may 
dispose  to  fresh  attacks  of  cholecystitis  is  undoubted,  and  by  thus  reduc- 
ing the  resistance  of  the  gall-bladder  they  may  be  an  indirect  cause  of 
carcinoma.  The  walls  of  a  carcinomatous  gall-bladder  may  show  definite 
evidence  of  chronic  inflammation,  and  even  of  calcareous  infiltration.  | 
On  the  other  hand,  gall-stones  are  due  to  catarrh  of  the  mucous  mem- 
brane of  the  gall-bladder,  and  it  might  be  suggested  that  cancer  and 
gall-stones  are  both  the  results  of  forms  of  irritation  which  have  much 
in  common. 

To  sum  up,  gall-stones  are  present  in  the  great  majority  of  cases  of 

*  Siegert:  Virchow's  Arcliiv,  Bd.  cxxxiii,  S.  353. 

t  Schroeder:  Quoted  by  Naunyn,  who  accepts  this  estimate,  On  Cliolehthiasis, 
p.  40.     Translated  by  New  Sj'denham  Soc. 

J  Beadles,  C.  F. :  Trans.  Path.  Soc,  vol.  xlvii,  p.  69. 


PRIMARY    MALIGNANT    DISEASE    OF    GALL-BLADDER.  629 

primary  malignant  disease  of  the  gall-bladder,  while  carcinoma  develops 
in  from  14  to  4  per  cent,  of  cases  of  cholelithiasis.  It  appears  that  the 
antecedent  of  the  two  conditions  is  cholelithiasis,  and  that  carcinoma 
'per  se,  whether  local  in  the  gall-bladder  or  present  elsewhere  in  the  body, 
does  not  set  up  cholelithiasis.  At  the  present  time  the  questions  whether 
carcinoma  is  due  to  a  parasite  or  to  the  cells  of  the  affected  organ  having 
acquired  a  habit  of  gro\\i:h  and  continued  proliferation  are  unsettled; 
but  from  either  point  of  view  gall-stones  would  appear  to  be  favourable 
to  the  morbid  process.  (1)  Thus  their  presence  would  reduce  the  resist- 
ance of  the  organ  and  so  dispose  to  local  infection  with  the  hypothetical 
parasite  of  carcinoma.  (2)  Wliile  on  the  non-parasitic  theory,  gall-stones 
would  irritate  the  epithelial  lining  of  the  gall-bladder  and  keep  up  the 
habit  of  proliferation,  which,  under  favourable  conditions,  viz.,  dimin- 
ished resistance  of  the  underlying  tissues,  may  become  carcinomatous. 
In  connexion  with  the  close  association  between  carcinoma  of  the 
gall-bladder  and  cholelithiasis  the  rarity  of  a  similar  association  be- 
tween renal  calculi  and  growths  of  the  pelvis  of  the  kidney  is  of  interest. 
It  must  be  remembered  that  both  renal  calculi  and  new-growths  of  the 
renal  pelvis  are  less  common  than  gall-stones  and  carcinoma  of  the  gall- 
bladder. 

Kelynack  *  refers  to  23  examples  of  associated  renal  calculus  and  growth.  In 
8  cases  of  papilloma  of  the  pelvis  of  tlie  kidney  collected  by  Drew  f  calculi  were 
present  in  4.  The  causal  relationship  of  the  irritation  of  a  calculus  to  a  villous 
growtli  of  the  renal  pelvis  would  reasonably  be  much  more  probable  tlian  to 
malignant  disease  of  the  substance  of  the  kidney. 

Sex. — Malignant  disease  of  the  gall-bladder  is  very  much  commoner 
in  women.  According  to  Fiitterer's  figures  (202  females,  52  males),  it 
is  four  times  more  often  seen  in  the  female  sex.  Musser's  cases  included 
75  females  and  23  males  (or  3  to  1);  Siegert's,  79  females  and  14  males 
(5^  to  1) ;  while  Ames  gives  the  proportion  of  females  to  males  as  4  to  1 ; 
Courvoisier,  as  5  to  1.  In  50  cases  of  Terrier  and  Auvray,J  40  were 
women  and  10  men.  In  Winton's  60  cases  43  were  females  and  17 
males  (4  to  1). 

This  predominance  of  females  in  carcinoma  of  the  gall-bladder 
corresponds  to  their  greater  liability  to  gall-stones,  which  is  calculated 
by  Schroeder  in  the  proportion  of  5  to  1,  by  Murchison  3  to  2,  Bouchard 
100  to  66,  Harley  2  to  1.  The  overwhelming  majority  of  female  patients 
among  the  subjects  of  gall-bladder  carcinoma  contrasts  with  the  sex 
incidence  in  carcinoma  of  the  bile-ducts;  thus  in  18  cases  Musser  found 
the  sexes  eciually  represented,  and  in  my  75  cases  44  were  males  and  31 
females.  In  this  connexion  it  may  be  mentioned  that  gall-stones  are 
less  frequently  associated  with  carcinoma  of  the  bile-ducts;  thus  in 
Musser's  18  cases  they  were  present  in  11,  and  in  my  62  cases  23,  times. 

The  pressure  of  the  corset  on  the  liver  may,  as  suggested  by  Fiitterer,§ 
increase  the  friction  between  calculi  and  the  walls  of  the  gall-bladder, 

*  Kelynack,  T.  N. :  Renal  Growths,  p.  27. 

t  Drew,  D. :  Trans.  Path.  Soc,  vol.  xlviii,  p.  13.3. 

X  Terrier  and  Auvray:  Rev.  de  chirurg.,  1900,  p.  143. 

§  Fiitterer,  G. :  Chicago  Medical  Soc,  April  1,  1897. 


630  DISEASES    OF   THE    GALL-BLADDER. 

and  so  may  help  to  explain  the  great  predominance  of  females  in  primary 
carcinoma  of  the  gall-bladder.  In  this  connexion  it  is  remarkable  that 
the  bile-ducts,  which  can  hardly  be  affected  in  the  same  way  by  the 
wearing  of  a  corset  or  belt,  are  more  often  the  subject  of  carcinoma  in 
men  than  in  women.  Graham  recorded  a  case  of  carcinoma  of  the  gall- 
bladder in  a  shoemaker  whose  last  pressed  upon  the  liver  much  as  a 
corset  might  do,  and  Fiitterer  is  inclined  to  think  that  pressure  of  this 
kind  may  be  a  factor  in  the  male  cases. 

While  primary  carcinoma  is  much  commoner  in  women,  Siegert's 
statistics  of  secondary  growths  in  the  bladder,  though  only  13  in  number, 
showed  that  the  male  sex  were  affected  in  10,  or  77  per  cent.,  and  the 
female  sex  in  3,  or  23  per  cent. 

Age. — Frerichs  described  the  disease  as  one  of  old  age.  In  17  cases 
collected  by  Villard  9  were  over  seventy  years  of  age.  The  average  age 
of  Flitterer's  large  series  was  fifty-eight  years,  and  curiously  enough  the 
average  age  was  the  same  in  60  cases  collected  by  Winton,  many  of  them 
from  the  unpublished  records  of  St.  George's  and  other  hospitals.  Carcin- 
oma of  the  gall-bladder  is  very  rare  before  forty  years  of  age.  Markham  * 
described  an  exceptional  case  in  a  woman  aged  twenty-eight.  At  the 
other  extreme  the  most  advanced  age  was  ninety  (Thomas  and  Noica  f). 

CLINICAL  PICTURE. 

In  considering  the  clinical  aspect  of  malignant  disease  of  the  gall- 
bladder it  may  be  well  at  the  outset  to  point  out  that  the  clinical  mani- 
festations are  roughly  divisible  into  three  groups:  (i)  Those  symptoms 
connected  with  pre-existing  cholelithiasis;  (ii)  the  local  effects  of  ma- 
lignant disease  of  the  gall-bladder;  (iii)  complications  due  to  invasion 
of  adjacent  parts  by  the  tumor  and  to  secondary  gro\vths  in  the  liver, 
peritoneum,  and  elsewhere. 

The  patient,  as  has  already  been  pointed  out,  is  generally  a  woman 
between  fifty  and  sixty  years  of  age,  who  may  have  suffered  from  symp- 
toms of  gall-stones.  Biliary  colic  may  closely  precede  the  development 
of  carcinoma,  but  in  some  instances  there  is  a  very  long  interval  between 
the  first  appearance  of  colic  and  the  development  of  carcinoma. 

Jourdan  J  recorded  a  case  where  the  coUc  began  twenty-five  years  before  the 
growth  appeared.  Bret  §  describes  a  case  where  a  woman,  who  died  at  the  age  of 
thirty-six  with  carcinoma  of  the  gall-bladder  enclosing  an  oval  calculus,  had  had 
biliary  colic  since  the  age  of  twenty. 

There  is  often,  however,  no  history  of  gall-stone  colic  in  fatal  cases 
of  carcinoma  of  the  gall-bladder;  the  calculi  may  remain  latent  in  the  gall- 
bladder and  never  pass  into  the  ducts.  Kehr  ||  says  that  clinical  evi- 
dence of  cholelithiasis  is  wanting  in  the  majority  of  the  victims  of  car- 
cinoma of  the  gall-bladder.  In  other  instances  pain  really  due  to  in- 
flammation or  adhesions  around  the  gall-bladder  is  regarded  as  d3^spepsia. 

*  Markham:  Trans.  Path.  Soc,  vol.  viii,  p.  243. 

t  Thomas  and  Noica:  Bull.  Soc.  Anat.  Paris,  1896,  p.  471. 

t  Jourdan:  Bull.  Soc.  Anat.  Paris,  1891,  p.  323. 

§  Bret:  Lyon  Medical,  tome  Lxxxix,  p.  35,  1898. 

II  Kehr:  Diagnosis  of  Gall-stone  Disease,  p.  92,  American  translation. 


PRIMARY    MALIGNANT    DISEASE    OF    GALL-BLADDER.  631 

Usually  the  first  thing  noticed  by  the  patient  is  a  feeling  of  discomfort 
and  heaviness  in  the  right  hypochondrium  and  parts  around.  According 
to  Head,*  the  eighth  dorsal  segment  is  the  visceral  area  in  connexion 
with  the  gall-bladder.  This  may  be  followed  by  loss  of  appetite,  gastro- 
intestinal disturbance  accompanied  with  definite  pain,  and  even  by 
attacks  of  colic,  indistinguishable  from  biliary  paroxysms.  A  tumor  may 
be  felt  in  more  than  half  the  cases  in  the  situation  of  the  gall-bladder, 
which  is  at  first  smooth  and  oval,  like  the  gall-bladder,  and  subsequently 
becomes  hard,  irregular,  and  may  be  tender.  Like  the  liver,  it  moves 
with  respiration  unless  fixed  by  adhesions.  The  tumor  may  reach  the 
size  of  a  cocoanut.  These  may  be  called  the  local  manifestations,  and, 
on  the  whole,  resemble  those  of  cholelithiasis.  As  time  goes  on  the 
growth  invades  neighbouring  parts,  and  secondary  growths  may  spring 
up;  additional,  or  what  may  be  called  secondary,  symptoms,  are  thus 
produced.  Carcinoma  of  the  gall-bladder  may  remain  latent  until  the 
secondary  growths  set  up  prominent  symptoms.  This  is  well  illustrated 
by  the  following  case : 

A  man  aged  sixty-eight  was  in  St.  George's  Hospital  with  ascites,  but  no  jaun- 
dice, and  was  diagnosed  as  cirrhosis.  At  the  autopsy  there  was  a  primary  columnar- 
celled  carcinoma  of  the  gall-bladder,  which  contained  gall-stones.  The  liver  was 
directly  invaded  by  the  growth,  and  there  was  a  large,  broken-down  groni,h  in 
the  glands  beliind  the  pancreas,  which  compressed  the  portal  vein. 

When  the  liver  becomes  infiltrated  with  secondary  growths,  the 
clinical  aspect  of  the  case  may  become  that  of  carcinoma  of  the  liver. 
Enlargement  of  the  liver  can  be  made  out  in  about  half  the  cases,  but 
it  may  be  obscured  by  ascites  or  by  flatulent  distension.  The  surface 
may  be  smooth  when  the  enlargement  is  due  to  distension  with  bile, 
nodular  from  secondary  growths,  or  there  may  be  a  definite  tumor  mass 
formed  by  the  cancerous  gall-bladder  and  the  adjacent  liver  substance 
infiltrated  by  gro'^lh.  The  bile-ducts  may  also  become  invaded  by 
direct  extension  of  the  growth  or  by  pressure  exerted  from  without  by 
secondary  gro-v\i:hs  or  by  enlarged  glands,  situated  either  in  the  portal 
fissure  or  in  the  neighbourhood  of  the  pancreas.  Jaundice  is  thus  set 
up,  and  the  symptoms  are  much  the  same  as  those  of  primary  carcinoma 
of  the  head  of  the  pancreas  or  of  the  bile-ducts.  Though  not  a  necessary 
result  of  carcinoma  of  the  gall-bladder,  jaundice  is  very  frequent.  In 
30  cases  collected  b}^  Meunier  f  it  was  absent  in  only  four.  In  Winton's 
60  cases  permanent  jaundice  occurred  in  33,  or  55  per  cent.,  and  in  69 
per  cent,  of  iMusser's  100  cases. 

As  Mayo  Robson  J  points  out,  jaundice  may  be  due  to  catarrh  of  the 
ducts,  but  in  that  event  it  would  not  have  the  progressive  character 
met  with  in  malignant  disease,  but  would  tend  to  vary  or  e\'en  pass 
away.  I  have  seen  several  cases  of  carcinoma  of  the  gall-bladder  in 
wliicli  jaundice  came  on  after  vomiting  and  diarrhoea,  the  characters  of 

*  Head,  H. :  Brain,  part  Ixi,  p.  75. 

t  Meunier:  Bull.  Soc.  Anat.  Paris,  LS93,  p.  585. 

t  Mayo  Kobsoii:  Brit.  Med.  .lourn.,  1897,  vol.  i,  p.  710. 


632  DISEASES    OF   THE    GALL-BLADDER. 

catarrhal  jaundice^  but  persisted  until  death,  and  at  the  postmortem 
examination  was  found  to  depend  on  definite  obstruction  to  the  ducts. 
In  such  cases  the  onset  was  probably  catarrhal,  but  obstruction  super- 
vened and  rendered  the  icterus  permanent. 

The  following  case  illustrates  this  point,  and  also  the  latency  of  gall- 
stones in  carcinoma  of  the  gall-bladder : 

A  jaundiced  woman,  aged  forty-six  years,  was  under  my  care  in  St.  George's 
Hospital  in  1897.  Two  months  before  her  deatli  she  was  attacked  with  sickness 
and  pain  after  food  without  any  sufficient  cause ;  this  lasted  for  one  week  and  was 
followed  by  jaundice,  which  persisted  until  her  death.  She  was  quite  certain  that 
there  had  been  no  biliary  cohc  at  any  time.  Her  health  had  generally  been  very 
good  and  there  had  been  no  dyspepsia.  She  was  a  wasting  but  not  emaciated 
woman,  with  the  remains  of  good  looks.  There  was  marked  jaundice,  but  no 
itching  or  eruption  of  the  skin.  The  pulse  was  90.  The  fseces  were  pale  and  the 
urine  contained  bile.  The  liver  was  much  enlarged,  but  the  gall-bladder  could 
not  be  made  out.  The  umbilicus  was  brown  and  hard;  this  was  noticed  directly 
after  the  onset  of  jaundice.  There  was  no  ascites.  A  movable  tumor  the  size 
of  one's  hand  was  palpable  in  the  left  ingumal  region.  The  patient  was  in  the 
hospital  a  month,  during  which  time  she  steadily  got  weaker;  a  week  before  death 
there  was  haemorrhage  from  the  umbilicus,  and  on  the  two  days  preceding  death 
haemorrhage  from  the  bowel.  She  died  in  a  sleepy  state.  At  the  autopsy  there 
was  a  primary  spheroidal-celled  carcinoma  of  the  gall-bladder,  which  contained 
numerous  pearl-like  calculi  and  three  large  calculi,  one  of  which  had  undergone 
spontaneous  fracture,*  probably  some  time  before  death.  The  liver  weighed  11 
pounds  3  ounces,  and  contained  numerous  secondary  growths.  The  portal  vein 
and  the  common  bile-duct  were  embedded  in  secondary  groT\-th  and  narrowed. 
There  was,  however,  no  ascites.  There  was  a  large  loose  gro'n'th  in  the  great  omen- 
tum, corresponding  to  the  movable  tumor  felt  during  life.  There  were  dilated 
veins  in  the  rectum  and  a  small  ulcer  from  which  the  haemorrhage  must  have  come. 

Jaundice  may  also  be  due  to  a  gall-stone  in  the  common  duct  either 
obstructing  it  mechanically  or  setting  up  intermittent  hepatic  fever. 

Warthin  t  describes  a  case  of  carcinoma  of  the  gall-bladder  in  which  jaundice, 
leucoderma,  and  marked  pigmentation  of  the  skin,  suggesting  Addison's  disease, 
were  all  present.  After  death  secondary  growths  were  found  in  both  adrenal 
bodies. 

Ascites  is  met  with  in  about  one-quarter  of  the  cases.  In  Winton's 
60  cases  it  was  present  in  14.  It  depends  not  on  mahgnant  disease  of 
the  gall-bladder  itself,  but  on  complications  set  up  by  secondary  growths 
or  by  extension  of  the  primary  growth.  It  may  be  associated  wdth,  but 
does  not  necessarily  follow,  pressure  on  the  portal  vein;  and  is  most 
satisfactorily  explained  by  chronic  peritonitis  set  up  by  secondary  gro^\i:hs 
on  the  surface  of  the  peritoneum.  ^Tien  there  are  numerous  gro-^'ths 
in  the  peritoneum,  the  effusion  may  be  fatty  as  the  result  of  cellular  de- 
generation (chyliform  or  fatty  ascites). 

CEdema  of  the  legs  may  occur  in  the  late  stages  of  cachexia,  and  be 
due  to  cardiac  debility,  or  possibly  to  the  pressure  exerted  on  the  inferior 
vena  cava  by  a  large  ascitic  effusion  or  by  enlarged  glands  in  the  neigh- 
bourhood.    Thrombosis  of  the  inferior  vena  cava  has  been  recorded. 

There  is  often  dyspepsia,  which  in  a  few  instances  is  clue  to  a  definite 
organic  cause — viz.,  obstruction  at  the  pylorus  from  invasion  of  the 
growth,  and  may  then  be  associated  with  a  dilated  stomach.     There  may 

*  Trans.  Path.  Soc,  vol.  xlix,  p.  135. 

t  Warthin:  Philadelphia  Medical  Journal,  July  7-14,  1900. 


PRIMARY   MALIGXAXT    DISEASE    OF    GALL-BLADDER.  633 

be  vomiting,  flatulent  distension  of  the  abdomen,  and  usually  constipa- 
tion. In  some  instances  diarrhoea  alternates  "wdth  coixstipation.  Exten- 
sion of  the  groT\i:h  to  the  colon  rasLV  give  rise  to  chronic  obstruction  or 
eventually  to  complete  intestinal  obstruction.  TMien  deep  jaundice  has 
developed,  the  patient  gradually  passes  into  the  condition  of  cholsemia. 
The  temperature  is  normal  or  subnormal  unless  there  are  complications. 
Muscular  wasting  and  loss  of  strength  steadily  develop,  and  eventually 
emaciation,  exhaustion,  and  cachexia  become  marked;  the  biliary  tox- 
aemia gives  rise  to  haemorrhages,  petechise,  epistaxis,  and  occasionally 
hgematemesis  and  melaena,  mental  failure,  delirium,  coma,  and  death. 
Terminal  infections  may  take  place  and  carry  the  patient  off,  and  this 
without  the  temperature  being  necessarily  raised. 

Complications. — ^The  gaU-bladder  ma}^  in  rare  instances  perforate 
into  the  peritoneal  cavity  and  set  up  peritonitis.  The  growth  may  ex- 
tend and  perforate  into  the  transverse  colon,  and,  as  a  result,  the  gall- 
bladder may  become  infected  and  an  abscess,  either  in  the  gall-bladder 
or  in  its  immediate  neighbourhood,  may  result.*  Suppurative  cholan- 
gitis may  occur  and  spread  into  the  liver,  the  gall-bladder,  or  Wirsung's 
duct,  and  in  the  latter  event  set  up  acute  suppurative  pancreatitis.  Pus 
may  collect  in  the  gall-bladder,  either  when  the  growi:h  is  in  a  very  early 
stage  (vide  p.  602),  or  when  there  are  numerous  secondary  growths. 

In  a  man  aged  fifty-two,  whom  I  examined  after  death  at  St.  George's  Hospital, 
the  gall-bladder  was  the  site  of  a  primary  spheroidal-celled  carcinoma  Avhich  had 
given  rise  to  numerous  secondarj^  growths  in  the  liver,  which,  with  the  stomach, 
weighed  15  pounds.  There  were  calculi  and  pus  in  the  gaU-bladder.  There  was 
a  chyliform  (fatty)  effusion  into  the  left  pleura  and  the  peritoneum. 

A  local  peritoneal  abscess  may  form  close  to  a  carcinomatous  gall- 
bladder, or  there  may  be  circunxscribed  acute  peritonitis  in  the  neighbour- 
hood of  the  growth,  due  to  microbic  infection. 

This  was  present  in  a  woman  aged  forty-five  j^ears  upon  whom  exploratory 
laparotomy  was  performed  by  my  colleague,  Mr.  Jaffrey,  for  a  large  tumor  in  the 
hepatic  region.  A  quantity  of  fibrin  was  found  around  a  carcinomatous  mass  in 
the  position  of  the  gaU-bladder,  enclosing  two  calculi. 

In  cases  where  cholecystitis  supervenes  in  a  carcinomatous  gall- 
bladder micro-organisms  may  be  absorbed  and  give  rise  to  infection 
elsewhere  in  the  body.  Lorrain  f  has  reported  a  case  of  lithiasis  and  car- 
cinoma of  the  gall-bladder,  with  cholecystitis,  and  endocarditis.  Pyloric 
obstruction  and  obstruction  of  the  transverse  colon  due  to  direct  exten- 
sion of  growi;h  have  been  already  referred  to. 

Duration. — There  is  some  difficult}^  in  determining  the  duration  of 
the  disease,  since  the  early  symptonxs  so  closely  resemble  cholelithiasis, 
with  which  it  is  almost  always  combined.  Probably  it  remaias  latent 
for  a  considerable  time,  but  when  Jaundice  and  cholsemia  have  set  in, 
the  end  is  near.  Some  cases  die  very  soon  after  the  appearance  of  definite 
symptoms.  On  the  whole,  perhaps,  the  average  duration  of  the  disease 
may  be  put  down  as  less  than  six  months. 

*  Blanc  and  Lerav:  Bull.  Soc.  Anat.  Paris,  1897,  p.  69. 
t  Lorrain:  Bull.  Soc.  Anat.  Paris,  1903,  p.  527. 


634  DISEASES    OF    THE    GALL-BLADDER. 

DIAGNOSIS. 

The  presence  of  a  hard,  nodular,  progressively  increasing  tumor  in 
the  position  of  the  gall-bladder  in  a  patient  about  the  age  of  fifty  years, 
especially  in  a  woman,  is  suggestive  of  the  disease.  Dull  pain,  loss  of 
appetite,  and  Avasting  are  in  favour  of  gro^^-th.  WTien  secondary  gro'ui:hs 
can  be  felt  in  the  liver  or  in  the  supraclavicular  fossse,  the  diagnosis  is 
practically  cUnched. 

The  only  fallacy  is,  of  course,  that  there  is  a  primary  gro^i;h  some- 
where else  which  has  given  rise  to  generalisation,  and  that  among  other 
places  a  secondary  gro-^i:h  has  developed  in  or  close  to  the  gall-bladder. 
Careful  search  for  any  primary  growth  in  the  stomach,  rectum,  oesoph- 
agus, breast,  and  uterus  should,  therefore,  always  be  made. 

Jaundice  is  not  an  early  symptom,  though  it  is  true  the  diagnosis  is 
often  not  made  until  it  appears. 

Differential  Diagnosis. — From  Gall-stones. — Malignant  disease,  espe- 
cially in  the  earlier  stages,  when  the  growth  is  confined  to  the  gall-bladder, 
is  very  like  cholehthiasis,  and  since  in  the  vast  majority  of  the  cases 
carcinoma  develops  subsequently  to  gall-stones,  it  is  very  difficult  to 
say  when  mahgnant  disease  has  begun.  The  enlargement  of  the  gall- 
bladder is  in  favour  of  growth,  especially  if  it  is  progressive  and  nodular. 
On  the  other  hand,  extensive  inflammatory  thickening  of  the  walls  of 
the  gall-bladder  may  closely  simulate  new-grovv1:h,  even  when  the  parts 
are  exposed  during  laparotomy,  and  this  impression  may  be  supported 
when  the  thick-walled  viscus  is  punctured. 

In  a  case  under  my  care  which  was  operated  upon  by  Mr.  Warrington 
Haward  in  1896  a  piece  of  tissue  of  doubtful  nature  was  removed,  and  before  the 
end  of  the  operation,  during  which  117  calculi  were  removed,  microscopic  exami- 
nation showed  that  the  tissue  was  inflammatory. 

An  inflamed  gall-bladder  may  clinically  appear  of  stony  hardness 
either  from  contained  calculi,  or,  more  rarely,  from  secondary  calcifica- 
tion of  its  walls.  In  addition  to  this  the  occurrence  of  dense  adhesions 
to  the  surrounding  parts — colon,  stomach,  omentum,  etc. — and  inflam- 
matory enlargement  of  glands  in  the  portal  fissure,  lesser  omentmn,  and 
around  the  common  bile-duct,  where  it  passes  into  relation  to  the  pan- 
creas, may  all  suggest,  even  when  the  abdomen  is  opened,  that  there  is 
malignant  disease  either  of  the  gall-bladder,  pylorus,  or  colon;  and  that 
secondary  growths  in  the  glands,  by  pressure  on  the  ducts,  have  given 
rise  to  jaundice.  The  jDresence  of  gall-stones  in  the  common  duct  may 
simulate  glands  invaded  by  carcinoma. 

In  any  case  of  doubt  the  gall-bladder  should  be  opened  and  not 
merely  punctured.  The  difficulties  of  diagnosing  between  cholehthiasis 
and  carcinoma  of  the  gall-bladder  are  well  illustrated  by  two  cases  of 
Mr.  Mayo  Robson's.* 

"In  a  doubtful  case  of  this  kind  in  a  woman  of  fifty  I  opened  the  abdomen 
and  found  what  a]:)iieared  to  be  a  mahgnant  tumor  of  the  gall-l)ladder,  which  was 
punctured  in  several  s]")ots  with  an  exploring  syringe;    finding  it  hrni  and  liard,  I 

*  Mayo  Robson  :  The  Medical  Press  and  Circular,  April  21,  1897,  p.  407. 


PRIMARY    MALIGXAXT    DISEASE    OF    GALL-BLADDER.  635 

concluded  it  was  malignant,  and  as  it  was  too  extensive  for  removal,  I  closed  the 
abdomen,  thinking  nothing  more  could  be  done.  The  patient,  however,  forthwith 
recovered  and  is  now  well,  with  no  remnant  of  her  tumor.  It  is,  of  course,  im- 
possible to  say  that  this  was  not  cancer,  but  in  all  prol^abilit}'  it  was  an  inflammator}' 
swelling  associated  with  gall-stones. 

"  In  another  case  of  tumor  where  tliere  was  a  suspicion  of  malignanc}^  I  opened 
an  abscess  of  the  liver  containing  30  gall-stones,  giving  marked  relief;  though  only 
for  a  time,  as  death  supervened  four  months  later,  when  malignant  disease  was 
found." 

In  the  second  case  carcmoma  had  probably  developed  at  the  time  of  operation. 

As  time  goes  on  the  cachexia,  the  presence  of  increasing  jaundice, 
and,  most  positive  evidence  of  all,  secondary  growths,  may  appear  and 
strengthen  or  decide  the  diagnosis. 

From  Malignant  Disease  of  the  Liver. — In  the  later  stages,  when  the 
liver  is  enlarged  and  presents  either  a  large  tumor  or  several  small  ones, 
the  diagnosis  from  primary  or  secondary  malignant  disease  is  often  very 
difficult  or  even  impossible.  The  history  of  gall-stones  would  suggest 
that  the  primary  growth  might  have  started  in  the  gall-bladder,  and  the 
original  appearance  of  a  tumor  in  that  situation  would  strengthen  the 
diagnosis  in  the  absence  of  any  evidence  pointing  to  primary  carcinoma 
of  the  stomach,  colon,  etc.  Unfortunately,  a  histor}^  of  gall-stones  is 
often  absent,  while  a  tumor  in  the  position  of  the  gall-bladder  is  felt 
only  in  about  half  the  cases. 

In  rare  instances  syphilitic  disease  of  the  liver  may  imitate  malignant 
disease  of  the  gall-bladder.  From  cicatricial  contraction  and  deformity 
a  piece  of  the  right  lobe  may  become  elongated  and  hard  and  be  thought 
during  life  to  be  a  carcinomatous  gall-bladder.     (Gerhardt.*) 

Carcinoma  of  the  Stomach. — W^ien  the  cancerous  gall-bladder  gives 
rise  to  pyloric  obstruction,  it  may  naturally  be  regarded  as  carcinoma 
of  the  pylorus.  There  is  an  absence  of  the  movable  pyloric  tumor,  but, 
unfortunately,  this  may  also  occur  in  true  pyloric  cancer.  The  history 
of  gall-stones  and  the  presence  of  jaundice  point  to  a  biliary  origin  for 
the  stomach  symptoms. 

Hartmann  f  suggests  that  when  doubt  exists  as  to  the  position  of  a 
tumor,  whether  in  the  gall-bladder  or  the  pylorus,  the  follo^^dng  means 
may  be  employed.  The  situation  of  the  tumor  is  first  accuratel}'  deter- 
mined ;  the  stomach  is  then  distended  with  gas  by  means  of  an  effervescing 
mixture.  If  the  tiunor  remains  in  the  same  position  as  before,  it  is  the 
gall-bladder;  if  it  be  found  to  have  moved  under  the  ribs,  it  is  pyloric. 

Carcinoma  of  the  transverse  colon  in  the  neighbourhood  of  the  gall- 
bladder may  closely  resemble  carcinoma  of  the  gall-bladder. 

Cancer  of  the  bile-ducts  and  of  the  head  of  the  pancreas  may  be  simulated 
by  those  cases  of  gall-bladder  carcinoma  in  which  jaundice  occurs  early. 
In  the  former  conditions  the  gall-l)ladder  is  more  often  distended  and 
smooth,  while  in  the  latter  the  tumor  is  hard  and  solid,  and  may  be 
irregular,  and  the  liver  is  more  likely  to  be  enlarged  and  show  secondary 
growths.  The  question  of  diagnosis  between  these  two  conditions  is 
discussed  at  greater  length  on  page  693.     In  malignant  disease  of  the 

*  Gerlumlt:  La  Sem.  Mod.,  1898,  p.  273. 

+  Hartnumn :  Soc.  Chirurg.  Paris,  Oct.,  1899. 


636  DISEASES    OF   THE    GALL-BLADDER. 

pancreas  a  tumor  may  sometimes  be  felt  deeper  in  the  abdomen  and 
close  to  the  spine. 

Tumors  arising  from  the  jDarts  around  the  gall-bladder,  such  as  a 
hydatid  cyst,  a  floating  kidney,  or  renal  tumor  on  the  right  side,  or 
more  rarely  a  tumor  of  the  right  suprarenal  body,  may  imitate  carcinoma 
of  the  gall-bladder;  or  one  of  these  conditions  may  be  cUagnosed  when 
the  groT^-th  is  really  in  the  gall-bladder. 

In  a  man  aged  seventy-nine  years  who  presented  a  rounded,  tender  tumor  the 
size  of  an  apple  in  the  right  liypoehondrium,  without  jaundice  or  ascites,  the 
diagnosis  lay  between  a  calcified  hydatid  cyst  and  carcinoma  of  the  gall-bladder. 
At  the  autopsy  there  was  a  columnar-celled  carcinoma  of  the  gall-bladder  with 
miliary  abscesses  in  the  liver.* 

When  a  float'ng  kidney  gives  rise  to  jaundice  by  traction  or  pressure 
on  the  bile-ducts,  the  clinical  aspect  may  closely  resemble  that  of  chole- 
lithiasis or  malignant  disease  of  the  gall-bladder.  The  free  mobility  of 
a  floating  kidne;/  and  "^he  fact  that  it  can  be  displaced  from  continuity 
mth  the  hver  are  points  that  should  prevent  its  being  regarded  as  disease 
of  the  gall-bladder.  The  lumbar  region  should  be  carefully  examined, 
and  the  abdomen  should  oe  palpated  in  the  knee-and-elbow  position. 

Under  certain  conditions  fcecal  accumulation  in  the  transverse  colon 
may,  by  the  colicky  pains  and  the  presence  of  numerous  hard  masses 
in  the  neighbourhood  of  the  gall-bladder,  suggest  carcinoma  of  the  gall- 
bladder with  secondary  growths  around.  Examination  under  an  anaes- 
thetic may  reveal  the  fact  that  these  masses  can  be  indented  by  the 
finger,  and  subsequent  examination  that  they  vari^  in  position  and  in 
number.  In  such  cases  the  effect  of  purgatives  and  massage  should  be 
tried. 

PROGNOSIS  AND  TREATMENT. 

The  prognosis  and  treatment  may  be  considered  under  two  heads: 
(1)  From  a  medical,  and  (2)  from  a  surgical,  point  of  view. 

The  disease  being  necessarily  fatal  unless  it  can  be  removed,  medical 
treatment  is  merely  palliative,  and  resolves  itseh  into  the  rehef  of  pain 
and  discomfort  by  morphia  and  opium,  lessening  vomiting  and  nausea 
by  bismuth,  hydrocyanic  acid,  and  morphia,  combating  constipation  and 
preventing  intestinal  fermentation  by  calomel,  other  preparations  of 
mercury,  salol,  or  various  f  '"' septic  remedies.  Under  such  treatment  the 
prognosis  is  of  the  gloomi' 

Surgically,  if  the  gro  \  ed  and  there  are  no  secondary 

growths,  the  prognosis  sh  hrpeful. 

In  their  tabular  state  latistics  of  operations  on  the  gall- 

bladder Terrier  and  A'l  i  rd — (i)   16  cases  in  which  the  gall- 

bladder was  removed  fc-  ^gnant  disease  ^^ith  an  operation  mortality 
of  31.25  per  cent. ;  and  (n;  a  ^  .rther  series  of  18  cases  in  which,  in  addition 
to  removal  of  the  gall-bladder,  part  of  the  liver  was  resected.  Of  these 
18  cases  3,  or  16.7  per  cent.,  died  as  the  immediate  result  of  the  operation. 

*Lejonne  et  Melanoff:  Bull.  Soc.  Anat.  Paris,  1900,  p.  133. 
t  Terrier  and  Auvray:  Chirurgie  du  Foie,  p.  303,  1901. 


PRIMARY   MALIGNANT    DISEASE    OF    GALL-BLADDER.  637 

The  high  mortahty  from  operation  mainly  depends  on  htemorrhage, 
which  occurs  so  readily  in  cases  of  chronic  jaundice.  Thus  there  ma}^  be 
constant  oozing  from  the  wound,  and  after  death  extensive  ha3morrhagic 
infiltration  may  be  found  around  the  ducts  and  pancreas.  This  tendency 
to  haemorrhage  should  always  be  guarded  against  as  far  as  possible  by 
giving  large  doses  of  chloride  of  calcium  to  jaundiced  patients  before 
operation.  Calcium  chloride  does  not  always  prevent  hsemorrhage  in 
jaundiced  patients,  and  it  is  possible,  as  suggested  by  Berg,*  that  de- 
generation of  the  vessel-walls  is  responsible  for  the  hsemorrhagic  tendency, 
either  in  addition  to  or  instead  of  diminished  coagulation  power  of  the 
blood. 

After  recovery  from  operation  a  biliary  fistula  is  sometimes  left.  In 
some  instances  there  is  temporary  improvement  after  resection  of  the 
gall-bladder,  but  in  nearly  all  cases  a  recurrence  of  the  growth  occurs 
within  six  months.  The  only  exception  to  this  in  Terrier  and  Auvray's 
statistics  is  Hochenegg's  f  case,  which  survived  cholecystectomy  with 
partial  resection  of  the  Uver  for  three  years.  Mayo  Robson's  J  case,  in 
which  a  similar  operation  was  performed,  recovered  completely.  War- 
ren §  performed  a  similar  operation  for  carcinoma  of  the  cystic  duct 
with  recovery.  The  following  case  illustrates  the  extreme  malignancy 
of  primary  carcinoma  of  the  gall-bladder,  even  when  removed  in  a  very 
early  stage  and  apparently  under  the  most  favourable  conditions. 

Heidenhain,  ||  in  the  course  of  an  operation  on  the  gall-bladder  for  the  removal 
of  sbc  calculi,  noticed  a  small,  button-like  thickening  in  its  wall  and  removed  the 
gall-bladder;  microscopic  examination  showed  that  it  was  carcinomatous.  Three 
months  later  the  patient  died  from  growths  in  the  liver,  though  at  the  operation 
it  appeared  perfectly  healthy. 

The  success  of  the  operation  depends  on  early  operation  and  on  the 
absence  of  secondary  growths,  and  this  cannot  be  positively  excluded 
before  the  abdomen  has  been  opened. 

The  diagnosis  of  carcinoma  of  the  gall-bladder  being  difficult,  cases 
occur  in  which  laparotomy  is  undertaken  with  a  view  of  relieving  chole- 
lithiasis, and  carcinoma  of  the  gall-bladder  is  fomid  perhaps  in  an  early 
stage.  Such  early  cases  are  the  most  favourable  for  cholecystectomy, 
and  the  prognosis  is  less  gloomy  than  in  more  advanced  cases. 

According  to  Carl  Beck,**  forty  per  cent,  of  the  cases  operated  upon  for  chole- 
lithiasis are  found  to  show  carcinoma  of  the  gall-bladder. 

SECONDARY  MALIGNANT  DISEASES  OF  THE  GALL-BLADDER. 

Secondary  growths  occasionally  occur  in  the  course  of  widespread 
carcinoma  or  more  rarely  in  widely  disseminated  sarcoma.  The  groAvths 
are  usually  situated  either  on  the  peritoneum,  as  in  cases  of  extensi^'e 

*  Berg:  Annals  of  Surgery,  1903,  p.  356. 
t  Hochenegg:  Wiener  klin.  Wochen.,  1890. 

J  Mayo  Robson :  Medico-t'hirurg.  Trans.,  vol.  Ixxix,  p.  159,  and  Diseases  of 
Gall-bladder,  3d  ed.,  p.  186. 

§  Warren :  Boston  Med.  and  Surg.  .lourn.,  March  15,  1900,  p.  276. 
II  Heidenhain:  Verhandl.  d.  dcutsch.  Ges.  f.  Chirurg.,  1898,  S.  126. 
**  Beck,  C. :  The  Medical  Week,  1897,  p.  137. 


638  DISEASES    OF   THE    GALL-BLADDER. 

malignant  disease  of  the  peritoneum,  or  just  under  the  peritoneal  covering 
of  the  gall-bladder.  The  growths  very  rarely  invade  the  mucous  coat 
of  the  gall-bladder,  and,  as  shown  by  Siegert's  *  and  my  own  figures 
{vide  p.  628),  are  not  specially  related  to  the  presence  of  gall-stones. 
Another  way  in  which  secondary  malignant  disease  contrasts  with 
primary  malignant  disease  of  the  gall-bladder  is  in  the  sex  incidence : 
whereas  primary  carcinoma  is  about  four  times  commoner  in  women, 
secondary  growths  were  much  more  frequent  in  the  male  sex  in  Siegert's 
figures.  As  a  rule,  secondary  growths  do  not  obstruct  the  cystic  duct, 
but  this  may,  of  course,  occur  and  give  rise  to  hydrops  of  the  gall-bladder. 
Growths  of  the  stomach,  colon,  etc.,  may  spread  into  the  gall-bladder. 

*  Siegert :  Virchow's  Archiv,  Bd.  cxxxiii,  S.  353. 


DISEASES  OF  THE  BILE-DUCTS. 


ABNORMALITIES  OF  THE  BILE-DUCTS. 

Atresia  or  complete  obliteration  of  any  part  of  the  bile-ducts  is  patho- 
logical, and  usually  due  to  inflammatory  changes  occurring  in  fcetal  life. 
The  cystic  duct  is  an  exception  to  this  general  statement,  as  it  is  fre- 
quently obliterated  by  inflammation  spreading  from  cholecystitis  and 
is  often  the  result  of  the  idceration  and  cicatrisation  in  later  life, 
associated  with  gall-stones.  Simple  stricture  and  obstruction  by  pressure 
from  without,  or  by  new-growths  in  the  walls,  by  gall-stones,  parasites, 
etc.,  are  described  elsewhere.  Abnormalities  in  the  ducts  chiefly  consist 
in  variation  in  the  length  of  the  cystic  and  common  bile-ducts,  and  in  the 
presence  of  abnormal  communications  between  the  gall-bladder  and  the 
liver  (hepatocystic  ducts).  The  left  and  right  hepatic  ducts  may  remain 
separate  for  a  considerable  distance,  and  only  join  when  the  cystic  duct 
unites  with  them;  in  such  cases  there  is  no  common  hepatic  duct.  The 
cystic  duct  may  not  join  the  common  hepatic  duct  until  close  to  the 
duodenum,  so  that  the  common  bile-duct  is  very  short.  In  cases  of 
true  congenital  absence  of  the  gall-bladder  (vide  p,  589)  the  common  bile- 
duct  may  be  dilated  in  part  of  its  course. 

Variations  in  the  method  of  opening  of  the  common  bile-duct  into 
the  duodenum  exist;  Letulle  and  Nattan-Larrier,*  in  their  description 
of  the  Vaterian  region,  or  portion  enclosing  the  biliary  papilla,  of  the 
duodenum,  have  described  four  types  of  the  openings  of  the  common 
bile-  and  Wirsung's  ducts.  In  some  instances  the  common  bile-duct 
opens  into  the  duodenum  separate  from  the  main  pancreatic  duct.  It 
very  occasionally  opens  with  the  accessory  pancreatic  duct  of  Santorini, 
the  main  pancreatic  duct  being  quite  separate  and  opening  alone  in 
the  position  of  the  normal  biliary  papilla.  In  104  cases  Schirmer  f  found 
this  four  times. 

The  effect  of  tight  lacing  on  the  biliary  apj^aratus  is  referred  to  else- 
where (p.  15). 

CONGENITAL  OBLITERATION  OF  THE  BILE-DUCTS. 

Definition, — Obliteration  of  the  bile-ducts  is  usu:ill\-  due  to  a  de- 
scending inflammation,  which  is  secondary  to  iutra-uterine  cirrhosis  of 
the  liver;  in  a  few  instances,  however,  the  ol)literation  may  possibly 
depend  on  fcEtal  peritonitis,     'j'hore  is  severe  ()l)s!ru('ti\'e  jaundice,  which 

*  Letulle  and  NaUaii-Larricr :  liull.  Hoc.  Aiiat.  Paris,  IS'.H),  p.  987. 
t  Schirmer:  Inaug.  Diss.,  Hasel,  1S<»:1 

639 


640  DISEASES   OF   THE    BILE-DUCTS. 

passes  into  cholseniia  and  is  accompanied  by  numerous  haemorrhages; 
life  is  very  seldom  prolonged  beyond  six  months. 

Nomenclature. — Most  of  the  cases  are  associated  with  cirrhosis,  and 
since,  as  "^dll  be  seen  later,  it  is  probable  that  the  cirrhosis  is  the  primary 
change  and  the  cholangitis  and  obstruction  of  the  ducts  a  secondary  and 
later  result,  the  term  ''congenital  hepatic  cirrhosis  with  obliterative 
cholangitis"  describes  the  condition  more  accurately.  But  since  con- 
genital obliteration  may  possibly  be  brought  about  in  other  ways,  it 
is  better  to  retain  the  more  familiar  and  inclusive  title  of  congenital 
obhteration  of  the  bile-ducts.  Our  knowledge  of  this  rare  and  interesting 
disease  is  chiefly  due  to  Dr.  John  Thomson,  of  Edinburgh. 

Incidence. — In  1892  Thomson's  *  monograph,  containing  50  cases, 
appeared.  I  have  notes  of  14  additional  cases,  t  which  do  not  include 
cases  of  idiopathic  dilatation  of  the  common  duct,  some  of  which  ma}^ 
depend  on  the  same  or  on  an  allied  process. 

Treves'  case  J  was  successfully  operated  upon  at  the  age  of  nineteen  years 
for  jaundice  of  sixteen  years'  duration,  and  obliteration  and  absence  of  the  lower 
end  of  the  bile-duct  were  found.  It  differs  so  markedly  from  all  the  other  cases 
that  it  is  doubtful  whether  it  belongs  to  the  same  category.  Jaundice  did  not 
begin  until  the  age  of  three  j^ears,  instead  of  either  at  or  shortly  after  birth.  Possi- 
blj^,  though  Treves  does  not  suggest  it,  the  obliteration  of  the  duct  was  due  to  the 
effects  of  a  calculus  lodging  in  the  duct  or  at  about  the  time  of  the  onset  of  jaundice. 
Thomson  §  considers  that  the  same  morbid  process  is  at  work  in  cholelithiasis  in 
infants  as  in  congenital  obliteration  of  the  bile-ducts,  and  supports  this  suggestion 
by  quoting  two  cases  of  infantile  cholelithiasis  in  which  the  biliary  apparatus  was 
abnormal  (Cuffer,  Bouisson).  Treves'  remarkable  case  may  perhaps,  therefore, 
be  considered  as  allied  to,  if  not  a  very  slightly  marked  example  of,  the  same  class. 

A  remarkable  case  of  Ashby's,  ||  a  girl  aged  seven  years  who  had  been  jaundiced 
for  two  and  one-half  years,  is  akin  to  Treves'  case.  The  common  bile-duct  was 
obliterated  near  the  duodenum,  but  the  proximal  part,  together  with  the  cystic 
duct,  formed  an  enormous  cyst  containing  sixteen  pints  of  bile-stained  mucus. 


ETIOLOGY. 

Hereditary  Influences. — As  in  other  congenital  affections,  such  as 
deformities,  and  congenital  hypertrophy  with  stenosis  of  the  pylorus, 
there  is  a  marked  tendency  for  the  disease  to  occur  in  members  of  the 
same  family.  As  mil  be  pointed  out  later,  a  peculiar  form  of  very  fatal 
cirrhosis  in  Brahmin  babies  in  Calcutta  which  is  a  family  disease,  has  a 
bearing  on  the  pathogeny  of  congenital  obliteration  of  the  bile-ducts. 
It  is  possible  that  Arkwright's  **  series  of  14  cases,  with  4  survivors, 
in  one  family,  of  dangerous  icterus  neonatorum  belonged  to  tliis  group 
of  congenital  obliteration  of  the  bile-dacts. 

Association  with  Malformations. — There  does  not  seem  to  be  any 
real  association  between  malformations  and  this  disease.     Concomitant 

*  Thomson,  J. :  Congenital  Obliteration  of  the  Bile-ducts,  1892. 

t  These  cases  are  those  of  Heneage  Gibbes,  Giese,  J.  L.  Steven,  Kynock,  F.  H. 
Hawkins,  Putnam,  Ross,  RoUeston  and  Hayne,  Wollstein,  G.  Parker,  Still,  and 
Menzies.     The  references  are  given  at  the  end  of  the  paper. 

X  Treves:  The  Practitioner,  Jan.,  1899,  p.  18. 

§  Thomson,  J.:  Edinburgh  Hospital  Reports,  vol.  v,  p.  1,  1898. 

i!  Ashby:  Medical  Chronicle,  Oct.,  1898,  p.  28. 
**  Arkwright,  J.  A.:  Edinburgh  Med.  Joum.,  Aug.,  1902. 


CONGENITAL   OBLITERATION   OF   BILE-DUCTS.  641 

deficiencies  in  the  liver  must  be  regarded  as  part  of  the  disease,  and  not 
as  true  malformations. 

Witzel's  *  case  of  a  number  of  true  malformations  and  obliteration  of  the  ducts 
probably  belongs  to  the  group  of  cases  of  congenital  cystic  disease  of  the  liver. 
{Vide  p.  445.) 

In  a  case  of  complete  absence  of  tlie  biliary  apparatus  in  an  infant  one  month 
old  there  was  a  congenital  malformation  of  the  left  upper  arm.  (Kirmisson  and 
Hebert.t) 

Syphilis  is  not  an  important  and  certainly  not  more  than  an  occa- 
sional cause  of  the  change  in  the  ducts  and  liver.  This  is  shown  not  only 
by  the  histological  character  of  the  change  in  the  liver,  but  by  the  freedom 
of  the  parents  and  patients  from  signs  of  syphilis.  Among  the  parents 
of  Thomson's  50  cases  there  was  evidence  of  syphilis  in  only  5  individuals, 
and  in  6,  or  possibly  in  9,  of  the  patients.  While  there  is  every  reason 
to  believe  that  syphilis  plays  no  part  in  the  usual  type  of  the  cases, 
it  is  possible  that  stricture  of  the  ducts  might  be  due  to  foetal  peritonitis, 
which  is  usually  connected  with  syphilis,  or  that  gummatous  inflamma- 
tion might  attack  the  walls  of  the  ducts,  as  in  Beck's  case.  J 

Sex. — In  Thomson's  cases  the  sex  was  given  in  34,  and  showed  a 
preponderance  of  males — 21  males,  13  females.  In  the  14  other  cases 
7  were  females  and  7  males,  making  in  all  28  males  to  20  females. 


PATHOGENY. 

John  Thomson,  in  his  monograph  §  on  the  subject,  believed  that 
in  the  great  majority  of  cases  there  was,  to  start  with,  a  congenital  mal- 
formation of  the  ducts  which  narrowed  the  available  lumen.  This 
obstruction  to  the  free  exit  of  bile  disposed  to  catarrh,  blocking,  and 
finally  to  obliteration  of  the  ducts.  As  a  result  of  the  obstruction  to  the 
free  passage  of  bile  into  the  duodenum  biliary  cirrhosis  was  started.  In 
a  later  article,  contributed  to  Allbutt's  System  of  Medicine,  ||  this  writer 
so  far  modifies  his  views  as  to  omit  any  reference  to  a  primary  congenital 
abnormality  as  a  factor  in  the  condition.  The  process  is  regarded  as  a 
descending  cholangitis  set  up  by  toxic  bodies  in  the  bile,  compared  to 
toluylendiamin;  when  the  disease  has  gone  so  far  as  to  interfere  with 
the  free  passage  of  bile  from  the  liver,  biliary  cirrhosis  develops,  as  in 
Charcot  and  Gombault's  experimental  ligature  of  the  bile-ducts  in  guinea- 
pigs.** 

Ford, ft  in  a  recent  paper  on  obstructive  biUary  cirrhosis,  has  collected 
24  cases  since  1882,  in  which  cirrhosis  of  the  liver  was  associated  with, 
and,  as  he  believes,  due  to,  obstruction  of  the  common  duct.  Of  these  24 
cases,  no  feAver  than  9  are  examples  of  congenital  obliteration  of  the 

*  Witzel,  O. :  Centralblatt  f.  Ciyniik.,  1880,  S.  561. 
t  Kirmisson  and  Hcbert :  Bull."  Soc.  Anat.  Paris,  1903,  p.  317. 
X  Beck:  Schmidt's  .Jahrb.,  1884,  S.  204. 

§  Thomson  :  Coiigciiital  Obliteration  of  the  Bile-ducts,  p.  38. 
II  Thomson:  All!)utt's  System  of  Medicine,  vol.  iv,  p.  253. 
**  Charcot  antl  (iombault:  Arcliivcs  de  Physiologic,  second   series,  tome  iii,  v. 
272,1876.  ^         ^    >  >  ,\ 

tt  Ford,  W.  W. :  American  .Journ.  of  Med.  Sciences,  vol.  cxxi,  p.  60,  1901. 
41 


642  DISEASES    OF    THE    BILE-DUCTS. 

bile-ducts.  In  fact,  his  statistical  proof  that  biliary  obstruction  per  se 
induces  cirrhosis  of  the  liver  rests  in  some  measure  on  cases  of  congenital 
obliteration  of  the  ducts. 

It  is  a  point  of  significant  interest  that  cirrhosis  of  the  liver  is  com- 
paratively rarely  found  in  association  with  obstruction  of  the  bile-ducts 
in  adults,  and,  when  present,  is  usually  associated  with  gall-stones  and 
infection  of  the  ducts  (vide  p.  326),  while  cirrhosis  seenxs  to  be  a  definite 
accompaniment  of  congenital  obliteration  of  the  ducts. 

In  J.  Thomson's  50  cases  a  microscopical  examination  was  only  made  in  10 
and  in  all  but  one  of  these  it  is  stated  that  cirrhosis  was  present;  in  13  other  cases 
that  I  have  notes  of  cirrhosis  was  present  in  at  least  12. 

The  question  therefore  arises  whether  there  is  any  evidence  to  support 
the  theory  that  cirrhosis  in  these  cases  is  dependent  on  the  obliteration 
of  the  larger  bile-ducts.  If  it  can  be  established  that  the  change  in  the 
bile-duct  is  older  and  more  advanced  than  in  the  liver,  there  is  fair  ground 
for  regarding  the  hepatic  lesion  as  due  to  the  obstruction  in  the  ducts. 
Ross  *  describes  obliteration  of  the  common  bile-duct  near  the  duodenum 
in  a  female  child,  aged  three  months,  whose  hver  shoM'ed  small-celled 
infiltration  around  the  bile-ducts  rather  than  fibrosis.  In  this  instance 
it  must  be  admitted  that  the  evidence  points  to  the  change  in  the  bile- 
duct  being  the  older.  On  the  other  hand,  in  the  other  cases,  as  far  as 
one  can  judge,  fibrosis  in  the  Hver  is  quite  as  old  as  the  lesion  in  the 
bile-ducts.  Thomson  refers  to  7  cases  of  infantile  jaundice  with  symp- 
toms similar  to  those  of  congenital  obliteration  of  the  bile-ducts,  but 
with  pervious  ducts;  they  proved  fatal  at  seventeen  days  of  age  on  an 
average  instead  of  at  two  and  one-half  months,  as  in  congenital  oblitera- 
tion of  the  ducts.  "This  suggests  that  they  are  merely  earlier  cases  of 
the  same  condition — ^before  the  blocking  has  occurred. "t 

The  following  hypothesis  appears  to  be  a  reasonable  ex])lanation  of 
the  pathogeny  of  so-called  congenital  obliteration  of  the  bile-ducts:  In 
the  first  instance,  poisons  pass  by  the  blood  from  the  placenta  to  the 
fcEtus  by  the  umbilical  vein;  some  of  this  blood  at  once  passes  through 
the  liver,  and,  in  virtue  of  the  toxic  effect  of  the  contained  body  or 
bodies,  induces  ordinary  portal  or  multilobular  cirrhosis  of  the  liver; 
the  rest  of  the  blood  in  the  umbilical  vein  passes  directly  into  the  general 
circulation  of  the  foetus  by  the  ductus  venosus,  and  subsequently,  by 
means  of  the  hepatic  artery,  will  convey  the  same  poison  to  the  liver. 
By  this  means  the  toxic  body,  which,  as  Thomson  suggests,  may  be 
analogous  to  toluylendiamin,  is  excreted  into  the  small  intra-hepatic 
bile-ducts  and  sets  up  cholangitis  and  monolobular  cirrhosis,  like  that 
seen  in  hypertrophic  biliary  cirrhosis.  In  this  way  a  mixed  cirrhosis 
(portal  and  biliary)  is  induced.  The  cholangitis  descends  to  the  larger 
ducts,  and  gives  rise  to  an  obliterative  cholangitis — a  process  analogous 
to  obliterative  appendicitis.  The  difference  between  this  condition  of 
congenital  (umt3ilical)  cirrhosis  with  obliterative  cholangitis  and  other 
forms  of  cirrhosis  in  post-natal  life  consists  in  the  further  change  in  the 

*  Ross,  D.:  Lancet,  1901,  vol.  i,  p.  102. 

t  Thomson :  Congenital  Obliteration  of  the  Bile-ducts,  p.  30. 


CONGENITAL   OBLITERATION   OF   BILE-DUCTS.  643 

large  bile-ducts  and  gall-bladder.  An  attempt  to  explain  this  additional 
lesion  may  be  made  as  follows:  The  bile-ducts  are  extremely  small  at 
birth,  and  any  inflammatory  change  will,  from  the  small  size  of  the  lumen, 
produce  stenosis  much  more  readily  than  in  later  Ufe.  An  analogous 
effect  is  seen  in  the  fact  that  laryngeal  obstruction  in  diphtheria  is  more 
frequent  in  young  subjects  than  in  older  patients,  quite  apart  from  the 
much  greater  frequency  of  the  disease  in  the  j^oung.  The  opposed  in- 
flamed surfaces  of  the  bile-ducts  will  also  come  in  contact  more  readily, 
and,  as  in  catarrhal  appendicitis,  obliteration  might  result. 

The  following  considerations  bear  on  the  hypothesis  that  the  disease 
is  primarily  a  congenital  cirrhosis : 

1.  The  almost  constant  occurrence  of  cirrhosis  in  these  cases  of  bile- 
duct  obstruction  in  infants  as  compared  T\ith  the  infrec^uency  and  irregu- 
larity with,  which  cirrhosis  follows  obstruction  of  the  larger  bile-ducts  in 
later  hfe.  The  mixed  character  of  the  cirrhosis  explains  the  discrepancy 
in  the  recorded  cases,  some  authors  speaking  of  biliary,  others  of  multi- 
lobular, cirrhosis. 

2.  The  large  size  of  the  liver — this  resembles  hypertrophic  biliary 
cirrhosis.  In  simple  obstruction  of  the  larger  bile-ducts  in  adults  the 
liver,  though  swollen  from  retained  bile  in  the  early  stages,  is  usually 
small  after  death. 

3.  The  large  size  of  the  spleen — a  phenomenon  not  met  with  in  un- 
comphcated  biliary  obstruction.  The  large  size  of  the  spleen  is  best 
explained  as  the  result  of  toxic  bodies  reaching  the  organ  by  the  splenic 
arter}^  In  congenital  sj^ohilis,  where  it  is  probable  that  the  poison 
reaches  the  liver  by  the  umbilical  vein  and  is  derived  from  the  maternal 
circulation  rather  than  that  the  ovum  is  infected  by  a  syphilitic  spermato- 
zoon, there  is  a  similar  splenic  enlargement.  In  both  conditions  there 
is  cirrhosis  due  to  poisons  arriving  by  the  umbilical  vein;  the  difference 
between  the  pericellular  cirrhosis  of  hereditary  s3'phiUs  and  the  mixed 
(monolobular  and  multilobular)  cirrhosis  of  so-called  congenital  oblitera- 
tion of  the  bile-ducts  must  depend  on  a  difference  in  the  poisons  in  the 
two  diseases.  This  is  at  one  with  Thomson's  statistical  proof  that  syphilis 
plays  no  part  in  the  antecedents  of  so-called  congenital  obliteration  of 
the  bile-ducts. 

4.  The  fact  that  in  some  instances  several  cases  of  this  rare  disease 
have  occurred  in  the  same  family.  Hj'pertropliic  biliary  cirrhosis  not 
infrequently  occurs  in  several  members  of  the  same  family,  and  has  been 
thought  by  Boix  *  to  be  a  water-borne  disease.  Against  the  view  that 
so-called  congenital  obliteration  of  the  bile-ducts  is  in  reality  a  form  of 
congenital  cirrhosis  it  might  with  reason  be  objected  that  the  poison  that 
sets  up  the  change  must  pass  through  the  mother,  and  that  she  should 
show  evidence  of  its  influence. 

As  bearing  on  toxic  processes  being  conveyed  from  the  mother  to  the  Uver  of 
tlie  foetus  through  the  placental  circulation,  it  is  worth  referring  to  the  experiments 
of  Nattan-Larrier.t     Inoculation  of  a  pregnant   guinea-pig  with  typhoid    bacilh 

*  Boix:  Soc.  de  biolog.,  March  12,  1898,  p.  297. 
t  Nattan-Larrier :  Soc.  de  biolog.,  Nov.  3,  1900. 


644  DISEASES    OF    THE    BILE-DUCTS. 

leads  to  inflammatory  changes  in  the  livers  of  the  offsprmg.  Degenerative  changes 
in  the  hepatic  cells  were  fomad  by  Charrm  and  Delamare  *  in  the  mfant  of  a  woman 
who  had  eclampsia  before  its  birth. 

It  is  also  noteworthy  that  the  extremely  fatal  biliary  cirrhosis  in  Brahmin 
infants  aromid  Calcutta,  which  is  also  a  family  disease,  has  been  thought  to  depend 
on  the  mother's  milk.  The  mothers  restrict  themselves  to  a  dry  diet  and  take  a 
decoction  of  black  pepper.  If  this  is  the  causal  factor,  it  evidently  affects  the 
nurslings  more  than  the  nurses,  and  might  justify  the  suggestion  that  in  foetal  life 
the  infant's  liver  maj'  be  more  susceptible  than  the  mother  to  poisons  tending  to 
produce  cirrhosis ;  just  as  the  effects  of  syphilis  may  be,  and  usually  are,  much 
more  manifest  in  the  infant  than  in  the  syphilised  mother. 

To  sum  up,  it  seems  reasonable  to  believe  that  the  disease  is  primarily 
started  by  poisons  derived  from  the  mother  and  conveyed  to  the  liver 
of  the  foetus,  and  that  a  mixed  cirrhosis  and  cholangitis  are  thus  set  up. 
The  cholangitis  accounts  for  the  jaundice,  and  by  descending  to  the 
larger  extra-hepatic  bile-ducts,  induces  an  obhterative  cholangitis  analo- 
gous to  obliterating  appendicitis.  In  some  cases,  especially  those  fatal 
early  in  life,  the  latter  change  has  not  been  effected,  and  cirrhosis  alone 
is  found.  Possibly  in  some  instances  this  change  never  occurs,  and  in 
this  way  some  of  the  cases  of  cirrhosis  in  very  early  life  are  accounted 
for.  Again  in  exceptional  instances  the  obliterative  cholangitis  might 
possibly  be  delayed  and  come  on  much  later;  such  an  event  might  bring 
Treves'  case,  already  referred  to,  into  line  wdth  the  others.  It  is  possible 
that  there  are  several  conditions  at  present  included  under  the  title 
congenital  obliteration  of  the  ducts,  and  that  some,  such  as  D.  Ross' 
case,  are  due  to  constriction  of  the  duct  by  localised  peritonitis,  and 
deserve  the  title  better  than  those  cases  that  are  intimately  associated 
with  cirrhosis. 

MORBID  ANATOMY. 

The  liver  is,  in  the  great  majority  of  the  cases,  enlarged,  and  some- 
times to  a  very  considerable  extent.  In  a  case  published  in  conjunction 
M-ith  Dr.  Hayne  (vide  p.  649)  it  weighed  t\\dce  as  nmch  as  normal.  In 
only  one  of  Thomson's  cases  was  it  definitely  stated  to  have  been  small. 
The  liver  is  bile-stained,  and  often  dark  green;  the  surface  is  usually 
irregular  and  somewhat  resembles  ordinary  cirrhosis ;  in  only  a  few  cases 
has  the  surface  been  smooth.  On  section,  the  organ  is  tough,  firm,  and 
manifestly  fibrosed.  Cirrhosis  is  met  with  in  nearly  all  the  recorded  cases, 
but  exceptionally  it  is  absent.  The  lymphatic  glands  in  the  portal  fissure 
may  be  enlarged. 

Microscopically  there  is  well-formed  fibrous  tissue  separating  the 
lobules  from  each  other.  The  arrangement  of  the  fibrous  tissue  varies: 
in  parts  it  is  monolobular  and  separates  each  individual  lobule  from  its 
feUows  (vide  Fig.  81),  in  other  parts  a  varying  number  of  lobules  are 
enclosed  in  firm  strands  of  fibrous  tissue.  There  is  thus  a  mixed  cirrhosis 
composed  of  the  monolobular  and  multilol^ular  forms.  The  small  bile- 
ducts  often  contain  plugs  of  inspissated  bile  which  give  the  liver  as  a 
whole  its  dark-green  colour.     In  some  cases  proliferation  of  the  liver 

*  Charrin  and  Delamare:  Compt.  Rend.  Acad,  des  Sciences,  July  1,  1901,  t. 
cxxxiii,  p.  69. 


CONGENITAL    OBLITERATION    OF    BILE-DUCTS. 


645 


cells,  giving  rise  to  pseuclobile  canaliciili,  has  been  seen.  The  liver  cells 
are  in  places  well  preserved,  while  elsewhere  they  are  in  a  state  of  icteric 
necrosis  and  do  not  take  the  stain. 

Condition  of  the  Bile-ducts  and  Gall-bladder. — There  is  very  con- 
siderable variation  both  in  the  situation  and  the  extent  of  the  obliteration 
of  the  ducts.  There  is  a  group  of  cases  resembling  the  present  category 
in  chnical  features  and  in  the  cirrhotic  condition  of  the  liver,  but  without 
obliteration  of  the  ducts.  Now  although  they_  cannot,  of  course,  be 
included  in  the  same  class,  some  of  them  may  with  great  probability  be 
regarded  as  an  early  stage  of  that  condition  and  may  show  commencing 
changes  in  the  ducts,  such  as  thickening. 


Fig.  81. — Monolobular     Cirrhosis    from    a    Case    of    Congenital    Obliteration    of    thb 

BiiE-DUCTs  in  a  Child  Aged  Six  Months. 
There  is  well-formed  fibrous  tissue,  with  no  sign  of  recent  proliferation,  separating  the  indi- 
vidual lobules.    X  18. 


There  is  no  one  position  in  the  course  of  the  ducts  where  obliteration 
occurs  in  such  a  jn-oportion  of  cases  as  to  justify  its  being  considered  the 
site  of  election,  but  it  appears  to  be  more  frequent  towards  the  lower 
end  of  the  common  bile-duct.  The  gall-bladder,  the  cystic,  hepatic,  or 
common  bile-ducts  may  each  be  affected  to  the  exclusion  of  the  others, 
or  there  may  be  widespread  obliteration  of  the  biliary  tract.  The  ob- 
literated ducts  may  l^e  traced  in  the  lesser  omentum  as  fibrous  cords 
which  closely  resemble  the  hepatic  artery.  These  fibrous  cords  may 
gradually  fade  off  into  the  surrounding  tissues  so  that  the  continuity  of 
the  obliterated  duct  cannot  be  traced  any  further.  In  some  instances 
dilatation  above  the  obstruction  mav  occur. 


646  DISEASES   OF  THE    BILE-DUCTS. 

In  Oxley's  *  case  of  a  female  infant  aged  six  weeks  the  common  duct,  which 
formed  a  cyst  as  large  as  a  cocoanut  and  contained  36  ounces  of  bile,  was  obliterated 
at  the  duodenal  end. 

It  is  possible  that  some  of  the  cases  of  great  cystic  dilatation  of  the 
ducts  (vide  p.  651)  are  the  outcome  of  partial  obhteration  of  the  ducts 
started  in  very  early  life.  The  gall-bladder  may  be  collapsed  and  buried 
in  adhesions,  or  thickened  and  ■^dthout  any  ca"\dty.  It  may  contain  some 
clear  mucus,  but  rarely  bile.  In  one  of  Thomson's  cases  a  calculus  was 
found  in  the  gaU-bladder. 

From  the  extreme  paucity  of  the  descriptions  of  the  microscopic  ap- 
pearances of  the  ducts  I  am  obliged  to  rely  chiefly  on  my  ovm.  observ^a- 


Fia.  82. — ^Transverse  Section  of  Common  Bile-duct  Close  to  its  Obliteration.    Under  a 

Low  Power.      (X  35.) 
Shows  altered  and  fibrosed  walls  of  duct,  and  absence  of  mucous  glands  and  of  the  lining 
epithelium.     The  small  black  spots  infiltrating  the  walls  of  the  duct  are  microscopic  masses  of 
inspissated  bUe,  not  nuclei. 


tions.  In  my  own  case  the  ducts  near  the  point  of  obhteration  showed 
very  considerable  fibrous  thickening  of  its  waUs,  with  complete  alteration 
of  its  normal  appearance,  its  muscular  tissue  and  mucous  glands  having 
chsappeared.  The  epithehal  Hning  was  lost,  and  the  lumen  contained 
debris  and  masses  of  bile-pigment  which  infiltrated  the  fibrous  walls  for 
a  short  distance.  In  this  case  there  was,  as  in  the  liver,  well-formed 
fibrous  tissue  and  no  sign  of  any  progressive  h\^oerj3lasia  or  inflammation. 
In  one  of  Thomson's  own  cases  the  gall-bladder,  which  was  partly 
obliterated,  showed  thickening  of  its  walls  and  infiltration  with  round 

*  Oxley:  Lancet,  1883,  vol.  ii,  988. 


CONGENITAL   OBLITERATION   OF   BILE-DUCTS.  647 

cells,  while,  strange  to  say,  the  lining  epithelium,  where  any  cavity  re- 
mained, was  described  as  normal. 

The  spleen  is  enlarged,  sometimes  very  greatly. 

In  a  child  aged  six  months  recorded  by  Parker  *  the  spleen  weighed  5  ounces. 

The  other  organs  are  deeply  bile-stained.  Adhesions  around  the  liver 
or  bile-ducts  are  rare,  and  probably  chiefly  occur  in  cases  with  a  S3rphilitic 
taint.  A  small  quantity  of  ascites  is  recorded  in  some  of  the  cases,  but 
is  of  no  clinical  importance. 

CLINICAL  PICTURE. 

Jaundice  ma}^  be  present  at  birth  or  it  may  succeed  on  what  is  re- 
garded as  physiological  jaundice.  In  some  instances  the  infant  does  not 
develop  jaundice  until  two  or  more  weeks  after  birth.  It  is  a  difficult 
question  whether  the  effects  of  congenital  changes  in  the  ducts,  like 
those  of  congenital  morbus  cordis,  may  be  delayed,  and  not  show  them- 
selves until  some  years  have  elapsed.  If  so,  cases  like  Treves'  and  Ashby's 
can  be  explained  as  really  belonging  to  this  category.  When  once  estab- 
lished, the  jaundice  is  progressive  and  eventually  may  become  dark 
green,  but  variations  may  occur,  jaundice  becoming  less  for  a  time  and 
then  darker  again. 

The  urine  contains  much  bile-pigment  and  stains  the  napkins.  The 
meconium  passed  by  the  infants  is  usually  normal,  and  is  only  rarely 
devoid  of  bile.  In  only  a  few  instances  have  the  subsequent  motions 
contained  oile.  As  a  rule,  normal  yellow  motions  are  never  passed  and 
the  stools  are  clay-coloured  from  the  first.  In  some  instances,  however, 
a  green  motion  has  been  described  after  calomel  has  been  given. 

This  occurrence  has  given  rise  to  some  discussion;  it  has  been  suggested  that 
the  green  colour  may  be  entirely  independent  of  bile,  and  due  to  some  chemical 
combination  of  mercury  and  sulphur  (Thudichum  t),  or  that  the  green  colour  is 
due  to  chromogenic  micro-organisms.  (Lesage.J)  There  seems  very  slender  proof 
that  green  stools  are  due  to   bacterial  pigment  alone.     (Kanthack,  Garrod,  and 

Drysdale.§) 

It  is  possible  that  in  the  few  cases  where  the  administration  of  calomel  has  been 
followed  by  a  green  stool  there  was  biliverdin  present  and  that  either  there  was  not 
complete  obstruction  of  the  bile-duct  or  that  the  administration  of  calomel  set  up 
ulceration  of  the  intestine  and  so  allowed  some  bile-stained  exudation  to  pass 
into  the  bowel. 

As  might  be  expected  from  the  absence  of  bile  from  the  intestine, 
constipation  is  the  rule,  but  in  a  few  cases  attacks  of  diarrhoea  have  been 
noticed,  and  may  be  due  to  virulent  microbic  infection  of  the  alimentary 
canal. 

Haemorrhages  from  various  mucous  surfaces  into  the  skin,  and  from 
the  umbilicus  occur  in  a  large  number  of  the  cases.  Blood  may  be  lost 
by  epistaxis  or  vomited  or  passed  by  the  bowel.     I  have  seen  fatal 

*  Parker,  G. :  Lancet,  1901,  vol.  ii,  p.  520. 
t  Thudichum:  Lancet,  1889,  vol.  i,  p.  631. 

i  Lesage:  Archives  de  Phys.  Norm,  et  path.,  fourth  series,  1888,  p.  212. 
I  Kanthack,    Garrod,    Dry.sdale :  St.    Bartholomew's    Hospital    Reports,    vol. 
xxxiii,  p.  13. 


648  DISEASES    OF   THE    BILE-DUCTS. 

haemoptysis  in  a  case  {vide  p.  649)  of  this  nature.  The  conjunctivae, 
which  are  deejoly  stained,  may  show  smaU  haemorrhages.  Bleeding  due 
to  constant  oozing  from  the  umbihcus  may  occur  soon  after  birth,  and 
is  a  very  grave  symptom,  since  death  follows  in  a  few  days.  Subcutane- 
ous haemorrhages  may  be  scattered  all  over  the  body  like  flea-bites. 

The  haemorrhages,  like  those  seen  in  other  fornxs  of  deep  obstructive 
jaundice,  in  advanced  cirrhosis,  and  in  acute  atrophy,  are  clue  to  hepatic 
insufficiency  and  the  passage  of  poisons,  which  should  have  been  stopped 
by  the  liver,  into  the  general  circulation,  and  may  conceivably  be  due 
to  diminished  coagulability  of  the  blood,  to  degenerative  changes  in  the 
vessel  walls,  or  to  both  these  factors.  It  would  be  interesting  to  know 
whether  the  coagulation  time  of  the  blood  in  this  form  of  jaundice  is 
prolonged  in  the  same  way  as  it  is  in  other  kinds.  The  liver  is  enlarged, 
sometimes  so  considerably  as  to  reach  down  to  the  level  of  the  anterior- 
superior  spine,  and  is  firm,  very  hard,  and  fairly  smooth.  The  spleen 
is  also  enlarged  and  firm. 

The  infants  are  poorly  nourished,  and  usually  become  very  much  wasted 
if  life  is  sufficiently  prolonged,  but  careful  feeding  may  delay  emaciation. 
Convulsions  may  come  on  before  death. 

Duration  and  Prognosis. — A  certain  number  of  the  cases  die  within 
the  first  few  days  of  life  from  umbilical  or  other  haemorrhages.  Of  Thom- 
son's 49  cases,  30  lived  more  than  one  month,  and  of  these,  16  survived 
for  upwards  of  four  months,  two  living  into  the  eighth  month.  Still  * 
mentions  a  case  examined  by  him  in  which  death  took  place  at  the 
age  of  nine  and  a  half  months.  It  is  clear  that  the  prognosis  is  ex- 
tremely bad.  Possibly  cases  with  only  slight  changes  survive  for  long 
periods;  this  is  suggested  by  Treves'  case.  Moreover,  other  members 
of  a  faiTiily  in  which  one  child  has  died  of  the  disease  may  recover  from 
jaundice  in  early  life. 

Tilger  f  has  reported  a  rather  doubtful  case  bearmg  on  this  point.  A  woman 
aged  forty-six  had  a  gastric  diverticuhim  near  the  pylorus.  This  was  firmly  ad- 
herent to  the  gall-bladder,  which  was  shrunken.  The  bile-ducts  were  also  abnormal. 
It  was  regarded  as  a  congenital  affection.  Cocking  %  has  reported  a  case  of  jaundice 
in  a  woman  aged  fifty  which  had  existed  since  she  was  three  weeks  old,  Her  liver 
was  large  and  smooth ;  the  gaU-bladder  was  also  enlarged.  She  had  had  two  children : 
one  died  with  jaundice  at  the  age  of  fifteen  weeks;  the  other  was  health J^  It 
was  thought  that  she  might  be  the  subject  of  congenital  obstruction  of  the  ducts 
of  a  slight  degree. 

DIAGNOSIS. 

Deep  jaundice,  haemorrhages,  with  enlargement  of  the  liver  and  spleen 
and  the  absence  of  any  evidence  of  acute  septic  infection  in  a  child  a 
few  weeks  old,  point  to  this  disease. 

Differential  Diagnosis. — Since  it  is  usually  manifest  that  the  condi- 
tion is  one  of  severe  jaundice,  it  is  hardly  necessary  to  insist  on  the  dis- 
tinctions from  the  slight  and  common  jaundice  occurring  in  the  first 

*  Still:  Clinical  Journal,  vol.  xvii,  p.  324,  1901,  March  13. 

t  Tilger:  Virchow's  Archiv,  Bd.  cxxxiii,  S.  201,  1893. 

%  Cocking:  Quarterly  Medical  Journ.,  vol.  xi,  p.  104,  Feb.,  1903. 


CONGENITAL    OBLITERATION    OF    BILE-DUCTS.  649 

few  days  of  life,  in  which  the  faeces  contain  bile  and  the  jaundice  rapidly 
fades. 

From  syphilitic  disease  of  the  liver,  the  al)sence  of  any  history  or 
signs  of  the  disease,  and  the  failure  of  mercurial  treatment  should  dis- 
tinguish the  disease.  According  to  Still,  the  liver  is  much  harder  on  pal- 
pation during  life  in  congenital  obstruction  of  the  ducts  than  it  is  in 
ordinary  cases  of  syphilis. 

From  infection  of  the  umbilical  vein  after  ]3irth  in  which  haemorrhage 
from  the  navel  also  occurs,  the  disease  should  be  distinguished  by  its 
much  slower  course,  by  the  absence  of  any  sign  of  umbilical  infection, 
and  by  the  fact  that  at  first  there  may  be  little  in  the  way  of  constitu- 
tional disturljance. 

TREATMENT. 

Treatment  is  chiefly  symptomatic.  Small  doses  of  grey  powder,  frac- 
tional doses  of  calomel,  salicylates,  or  salol  may  be  given  to  minimise 
intestinal  fermentation;  and  in  the  later  stages  chloride  of  calcium  to 
prevent  hemorrhage.  It  is  alw^ays  well  to  try  antisyphilitic  treatment 
on  the  chance  that  the  disease  is  of  this  nature.  Very  little  can  be  ex- 
pected from  operative  measures,  and  it  should  be  remembered  that  there 
is  considerable  risk  of  haemorrhage,  owing  'to  the  patient's  jaundiced 
condition.  Since  the  obstruction  may  be  in  the  hepatic  ducts,  opening 
the  abdomen  to  do  a  cholecystenterostomy  is  a  speculative  or  ''explora- 
tory" operation.  The  only  cases  in  which  it  is  really  indicated  are  those, 
and  they  are  very  rare, — Oxley's,  Ashby's,  and  one  of  Parker's,— where 
a  cyst  is  palpable  in  the  abdomen. 

Unsuccessful  operations  have  been  performed  in  two  cases  (Giese 
and  Putnam's),  while  success  follow^ed  in  Treves'  case,  referred  to  on 
page  640. 

Since  the  disease  has  a  distinct  tendency  to  recur  in  several  members 
of  the  family  and  very  probably  depends  on  poisons  generated  in  the 
mother,  it  is  reasonable  to  treat  the  pregnant  woman  with  small  doses 
of  calomel  (^-^  to  ^V  S^-)'  salol,  and  other  drugs  which  tend  to  inhibit 
intestinal  fermentation,  and  to  pay  special  attention  to  her  diet  and 
general  health  during  pregnancy. 

The  following  case,  which  was  published  by  Dr.  Hayne  and  myself, 
gives  a  good  idea  of  the  disease : 

A  male  child,  aged  six  months,  had  been  jaundiced  since  birth ;  it  was  treated 
as  an  out-patient  with  mercury  and  chalk,  magnesium  sulpliate,  and  podophyllin. 
The  jaundice  varied  from  time  to  time,  and  the  child's  nutrition  was  fairly  preserved. 
A  fortnight  before  death  tlie  jaundice  became  more  marked,  and  on  May  28,  1897, 
the  child  was  admitted.  The  child  tiien  had  universal,  but  not  extreme,  jaundice. 
There  was  some  erythema  in  the  left  axilla.  The  liver  was  much  enlarged,  and 
came  down  to  the  anterior  superior  sjiine  of  the  ilium.  The  spleen  was  also  en- 
larged, and  projected  throe  fingerl^readths  below  the  costal  arcli.  There  was^no 
ascites.  The  urine  was  Ijile-stained,  and  the  motions  claj'-coloured.  On  .June  5th 
the  temperature  went  up  to  102°,  and  the  child  died  after  bringing  up  blood  from 
the  lungs.  The  child  was  the  first-born,  and  presented  no  signs  of  congenital 
syphilis. 

The  necrops}^  was  performed  by  Dr.  Hayne.  The  body  was  thin,  and  all  the 
organs  and  tissues  were  bile-stainetl.      The  oesophagus  was  normal  and  free  from 


650  DISEASES    OF   THE    BILE-DUCTS. 

staining  by  blood.  The  pleurae  were  healthy.  The  trachea  contained  blood. 
Blood  wasfoimd  to  have  been  aspirated  into  both  lungs,  which  showed  emphyse- 
matous bullae  and  some  small  caseous  masses;  the  latter  were  chiefly  close  to  the 
surface  of  the  lung.  Microscopically  these  caseous  areas  showed  bronchopneumonia, 
with  early  caseation,  but  no  clefinite  evidence  of  tuberculosis.  One  of  the  tracheal 
glands  was  enlarged  and  caseous.  The  liver  weighed  12  ounces,  or  nearly  twice  the 
normal  weight.  (Holt  gives  7.5  ounces  as  the  normal  weight  of  the  liver  for  achild 
of  six  months,  while  according  to  Birch-Hirschfeld  6  ounces  is  the  average  weight.) 
It  was  much  enlarged,  yellow  in  colour,  and  manifestly  cirrhotic.  The  common 
bile-duct  was  small,  and  as  its  lower  half  was  transformed  into  a  slender  fibrous 
cord,  considerable  difficulty  was  experienced  in  finding  it  and  in  distinguishing 
it  from  the  hepatic  artery.  The  gaU-bladder  was  small,  thickened,  collapsed, 
and  buried  in  adhesions ;  the  cystic  duct  was  represented  by  a  thln_  fibrous  cord. 
There  were  enlarged  glands  in  the  portal  fissure,  suggesting  the  condition  found  in 
hypertrophic  biliary  cirrhosis.  The  liver  cut  like  a  cirrhotic  liver  and  showed 
fibrosis. 

Microscopic  sections  were  taken  from  various  parts  of  the  liver;  fibrosis  was 
everywhere  present,  but  the  appearances  varied  in  different  situations.  Where 
the  fibrosis  was  least  marked  there  was  monolobular  cirrhosis,  the  fibrous  tissue 
being  old  and  including  a  large  number  of  newly  formed  bile-ducts ;  in  other  situa- 
tions, where  the  cirrhosis  was  multilobular,  there  were  areas  of  extensive  fibrosis, 
including  compressed  liver  cells  and  small  bile-ducts.  Some  of  the  latter  were 
dilated  and  contained  plugs  of  inspissated  bile.  The  cirrhosis  was  everywhere 
old  and  not  progressive.  The  liver  cells  inside  the  lobules  were  in  a  very  fair  state 
of  nutrition,  the  trabecular  arrangement  was  disturbed,  and  the  columns  of  liver 
cells  were  separated  from  each  other  by  spaces,  which,  however,  appear  empty. 
The  appearances  are,  therefore,  those  of  a  mixed  monolobular  and  multilobular 
cirrhosis.  The  microscopic  appearances  of  the  bile-duct  have  already  been  de- 
scribed on  page  646. 

The  spleen  weighed  2J  ounces,  and  was  extremely  diffluent.  The  heart,  peri- 
cardium, kidneys,  and  other  organs  were  normal,  except  for  bile-staining. 


BIBLIOGRAPHY. 

The  full  bibliography  up  to  1892  is  given  by  Thomson  in  his  mono- 
graph; the  following  additional  cases  have  occurred  since  1892: 

Gibbes,  H. :  Trans.  Path.  Soc,  vol.  xxxiv,  p.  130. 

Giese:  Jahrb.  f.  Kinderheilk.,  Bd.  xliii,  1896. 

Hawkins,  F.  H.:  Trans.  Path.  Soc,  vol.  xlvi,  p.  76. 

Kjmoch:  Edinburgh  Med.  Journ.,  July,  1896. 

Menzies,  G.  D.:  The  Australas.  Med.  Gaz.,  Jan.  20,  1904,  p.  20. 

Parker,  G. :  Lancet,  1901,  vol.  ii,  p.  520  (3  cases). 

Putnam:  Archives  of  Pediatrics,  Sept.,  1898. 

Rolleston  and  Hayne:  Brit.  Med.  Journ.,  1901,  vol.  i,  p.  758. 

Ross:  Lancet,  1901,  vol.  i,  p.  102. 

Steven,  J.  L. :  Glasgow  Med.  Journ.,  Jan.,  1897. 

Still,  G.  F.:  Clinical  Jour.,  vol.  xvii,  p.  324,  March  13,  1901. 

Wollstein,  M. :  Archives  of  Pediatrics,  March,  1902. 


DILATATION  AND  CYSTIC  TUMORS  OF  THE  BILE-DUCTS. 

In  obstruction  in  the  course  of  the  common  bile-duct  backward 
pressure  leads  to  dilatation  of  the  common  and  other  bile-ducts  extending 
into  the  liver  substance.  Whatever  the  nature  of  the  obstruction,  dila- 
tation -udll  occur,  but  it  is,  generally  speaking,  less  when  due  to  gall- 
stone in  the  common  duct  than  when  the  obstruction  is  due  to  pressure 
exerted  from  \\dthout  by  a  tumor,  such  as  carcinoma  of  the  pancreas. 

Terrier,  Mayo  Robson,*  and  Swain t  have  recorded  cases  of  excessive  dilata- 
tion of  the  common  duct  due  to  gall-stones. 

This  depends  on  the  fact  that  in  gall-stones  the  obstruction  is  not  so 
complete  as  in  the  case  of  tumors.  Exceptionally  the  dilatation  is  very 
excessive  and  gives  rise  to  a  tumor  of  the  common  bile-duct  containing 
many  pints  of  fluid. 

As  a  curiosity,  Todd's  %  case  may  be  mentioned.  In  a  girl  fourteen  years  of 
age  the  common  and  hepatic  ducts  were  enormously  dilated  and  contained  more 
than  a  quart  of  bile.  The  cyst  reached  from  the  liver  to  the  sacrum  and  lay  behind 
the  duodenum,  pancreas,  and  root  of  the  mesentery.  The  cause  of  this  dilatation 
was  a  "scirrhous  state"  (chronic  interstitial  pancreatitis?)  of  the  pancreas. 


CYSTIC  TUMORS  OF  THE  BILE-DUCTS. 

In  rare  instances  great  dilatation  of  the  common  bile-duct,  forming 
a  gigantic  cyst,  occurs  in  children.  There  may  be  no  very  evident  cause 
for  obstruction,  and  the  condition  has  been  spoken  of  as  idiopathic  and 
has  been  compared  to  congenital  hydronephrosis  (Russell).  In  some  of 
the  cases  there  may  have  been  partial  congenital  obliteration  of  the 
common  duct  near  its  lower  end.  In  Oxley's  §  case,  where  the  common 
duct  was  dilated  so  as  to  form  a  cyst  the  size  of  a  cocoanut,  its  duodenal 
termination  was  obliterated.  It  is,  however,  possible  that  the  cyst 
gives  rise  to  kinking  and  obstruction  in  the  distal  part  of  the  common 
duct.  In  a  case  recorded  by  Roslowzew  there  was  a  valve-like  fold 
of  mucous  membrane  at  the  lower  end  of  the  common  bile-duct.  If, 
as  in  congenital  morbus  cordis,  changes  initiated  during  foetal  life  can 
remain  latent  for  years  and  then,  possibly  as  the  result  of  slow  cica- 
tricial contraction  of  inflammator}'-  tissue,  give  rise  to  obstruction,  a 
satisfactory  explanation  is  obtained  of  the  following  remarkable  case 
recorded  by  Ashby  || : 

*  Mayo  Robson:  Diseases  of  the  dall-bladder,  p.  196,  ed.  iii. 
t  Swain,  W.  P.:  Lancet,  1895,  vol.  i. 

JTodd:  Dublin  Hosp.  Reports,  1817,  vol.  i,  p.  .328.  Quoted  by  Legg,  Brit. 
Med.  Joum.,  1874,  vol.  i,  p.  607. 

§  Oxley:  Lancet,  1883,  vol.  ii,  p.  988. 
II  Ashby:  Medical  Chronicle,  Oct.,  1898,  p.  28. 

651 


652  DISEASES    OF   THE    BILE-DUCTS. 

A  girl  aged  seven  had  been  jaundiced  for  two  and  one-half  years,  and  more 
recently  had  been  tapped  to  the  extent  of  50  ounces  for  ascites.  She  was  emaciated 
and  had  oedema  of  the  feet.  A  cyst  on  the  right  side  of  the  abdomen  was  tapped 
and  16  pints  of  dark-green  mucus  came  away.  In  the  course  of  three  months  it 
was  tapped  ten  times,  and  on  each  occasion  8  to  10  pints  were  removed.  After 
death  the  cyst  was  found  to  be  the  dilated  common  bile  and  cystic  ducts ;  no  com- 
munication with  the  duodenum  could  be  made  out. 

Possibly  in  the  following  case  obstruction  in  the  common  duct  was 
due  to. hereditary  syphilis: 

In  the  case  of  a  deeply  jaundiced  child  aged  nine  years  there  was  very  marked 
evidence  of  hereditary  syphilis  in  the  body  generally,  and  in  the  liver  in  pericellular 
cirrhosis.  The  liver  and  biliary  apparatus  preserved  in  the  Museum  of  the  College 
of  Medicine,  Newcastle-on-Tyne  (No.  382-2),  show  the  common  bile-duct  dilated 
to  the  size  of  one's  fist,  the  cystic  and  hepatic  ducts  being  also  dilated,  while  the 
gall-bladder  is  atrophied  and  collapsed  and  the  opening  of  the  common  bile-duct 
into  the  duodenum  cannot  be  found.  There  was,  however,  no  convincing  proof 
that  the  obstruction  of  the  bile-duct  was  due  to  any  syphilitic  process,  such  as 
ulceration  and  cicatrization. 

In  some  of  the  recorded  cases  the  cysts  have  been  extraordinarily 
large,  and  when  first  seen  on  opening  the  abdomen,  have  resembled 
ovarian  or  hydatid  cysts.  The  fluid  inside  them  contains  bile-pigments. 
In  Wilks  and  Moxon's  case,*  referred  to  elsewhere  (vide  p.  681),  the  com- 
mon bile-duct  of  a  child  aged  four  years,  which  was  dilated  so  as  to  be 
as  big  as  its  head,  contained  a  number  of  pendulous  growths. 

According  to  Roslowzew,t  this  condition  has  only  been  met  with  in 
females.  The  following  case  in  a  boy,  however,  has  been  recorded  by 
Russell : 

A  boy  aged  eight  years  had  jaundice,  fever,  and  a  large  elastic  tumor  reaching 
from  the  liver  to  the  iliac  crest  and  middle  line.  It  was  thought  to  be  catarrhal 
jaundice,  which  was  prevalent  in  Melbourne  at  the  time,  in  a  child  the  subject  of  a 
hydatid  cyst.  The  cyst  was  found  to  be  the  dilated  common,  hepatic,  and  cystic 
ducts.  It  contained  some  small  bilirubin-calcium  calculi.  The  opening  into  the 
duodenum  was  small  and  valvular.  J 

Clinically  these  cases  present  themselves  as  abdominal  cysts  in 
connexion  with  the  liver  and  may  be  regarded  as  ovarian  or  hydatid 
cysts.  Jaundice  is  present.  The  prognosis  and  treatment  are  not  very 
satisfactory,  as  judged  by  the  results  of  the  recorded  cases.  Probably 
drainage  of  the  cyst  and  exploration  of  the  lower  end  of  the  common 
bile-duct  with  a  probe  so  as  to  displace  any  valvular  fold  of  mucous  mem- 
brane and  allow  a  free  passage  of  bile  into  the  duodenum  are  the  best 
means  at  our  disposal. 

Bile-containing  Cyst  in  Communication  with  the  AmpriUa  of  Voter. — As  a  path- 
ological curiosity  a  brief  description  may  be  given  of  a  specimen,  dissected  by  Dr. 
R.  S.  Trevor,  of  a  cyst  containing  bile,  the  size  of  a  tangarine  orange,  which  projected 
into  the  duodenum  in  the  situation  of  the  biliary  papilla.  It  was  lined  inside  and 
out  by  mucous  membrane  and  its  only  communication  was  with  the  cavity  of  the 
ampulla  of  Vater.  It  appeared  to  be  a  sacculus  of  the  ampulla  and  to  be  comparable 
with  a  sacculus  of  the  urinary  bladder;  the  mucous  membrane  lining  it  being  that 
of  the  ampulla  and  the  mucous  membrane  on  its  outer  surface  that  of  the  duodenum. 
It  was  found  in  the  body  of  a  man,  aged  twenty-four  years,  who  died  in  St.  George's 
Hospital  from  a  perforated  duodenal  ulcer.    There  was  no  jaundice  and  no  gall-stone. 

*  Wilks  and  Moxon :  Pathology,  p.  485,  3d  ed.,  1889. 

t  Roslowzew:  Deutsche  med.  Wochen.,  Bd.  xxvni,  S.  739,  1902. 

t  Russell:  Annals  of  Surgery,  Dec,  1897,  p.  692. 


SIMPLE  STRICTURE  OF  THE  BILE-DUCTS. 

With  the  exception  of  the  cystic  duct,  this  is  a  very  rare  condition. 
The  cases  may  be  divided  into  two  distinct  groups:  (i)  the  congenital 
cases,  described  on  page  639  in  the  section  on  Congenital  Obhteration  of 
the  Bile-ducts,  and  (ii)  those  acquired  in  later  life,  which  will  be  dealt 
with  here.  It  is  possible,  though  it  is  a  speculative  point,  that  in  some 
of  these  cases  also  a  congenital  factor  may  be  present.  A  slight  congenital 
change  in  the  ducts  might  gradually  progress  so  that  it  would  only  give 
rise  to  bad  effects  some  years  after  birth.  This  point  is  referred  to  in  the 
account  of  congenital  obliteration  of  the  ducts. 

Incidence. — It  is  generally  assumed  that  ulceration  of  the  common 
ducts  due  to  gall-stones  may,  by  cicatricial  contraction,  lead  to  stenosis, 
but  this  secjuence  is  surjorisingly  rare. 

Pye-Smith  *  has  recorded  a  case,  and  a  good  example  of  a  tight 
stricture  of  the  common  duct  with  a  soft  calculus  just  above  it,  in  a 
woman  aged  twenty-six,  is  described  in  St.  Thomas'  Hospital  Reports.f 
In  cases  of  simple  stricture  recorded  by  Holmes }  and  Moxon  |  the 
stricture  was  at  the  commencement  of  the  common  hepatic  duct  and 
therefore  not  much  exposed  to  calculi,  except  small  bilirubin-calcium 
calculi.  In  Moxon's  and  Phillips'  ||  cases  there  was  no  history  of  chole- 
lithiasis. 

In  the  following  case  the  termination  of  the  common  bile-duct  was 
obliterated,  apparently  as  the  result  of  cicatrisation  of  an  ulcer  due  to 
gall-stones : 

A  woman  aged  forty-six  years  was  operated  upon  for  recurrent  attacks 
of  biliary  colic.  The  gall-bladder  was  empty  and  contracted,  but  the  cystic  duct 
was  dilated  by  five  calculi,  which  were  removed.  The  cystic  duct  was  united  to 
the  abdominal  wound,  and  bile  was  discharged  for  ten  days.  The  patient  then  got 
worse  and  died  suddenly.  At  the  autopsy  the  common  bile-duct  was  dilated 
and  contained  several  calculi;  its  opening  into  the  duodenum  was  completely 
obliterated  by  cicatrisation  of  an  ulcer.** 

Stricture  and  obliteration  of  the  cystic  duct  in  cholelithiasis  and 
cholecystitis  are  comparatively  common,  and  thus  form  a  marked  con- 
trast to  the  other  large  bile-ducts. 

It  is  conceivable  that  in  some  cases  simple  stricture  is  due  t<>  ulcera- 
tion occurring  in  the  ducts  as  the  result  of  cholangitis  set  uj)  l)y  typhoid 
or  influenzal  infection.     Possibly  syphilitic  inflammation  may  account 

*  Pye-Smith,  P.  H.:  Trans.  Path.  Soc,  vol.  xxiv,  p.  250. 
t  St.  Thomas'  Hospital  Reports,  vol.  xxix,  p.  169. 
i  Holmes,  T.:  Trans.  Path.  Soc,  vol.  ix,  p.  130. 
§  Moxon,  W.:  Trans.  Patli.  Soc,  vol.  xxiv,  p.  129. 
II  Phillips,  S.:  Trans.  Clinic  Soc,  vol.  xxi,  p   26. 
**  St.  liartliolomew's  Hospital  Reports,  vol.  xxxv.   Surgical  Registrar's  Pvf-pnrts, 
p.  216. 

653 


654  DISEASES    OF   THE    BILE-DUCTS. 

for  some  of  the  cases.  Lazarus-Barlow  *  has  .recorded  a  case  of  stricture 
occurring  in  a  boy  the  subject  of  hereditary  syphiHs,  but  in  this  instance 
and  in  that  described  by  H.  Mackenzie  f  the  cicatricial  process  probably 
started  outside  the  ducts  and  compressed  them  from  without.  (Vide 
p.  543.) 

The  following  is  the  only  case  of  simple  stricture  of  the  common  bile- 
duct  which  has  been  detected  at  St.  George's  Hospital  in  the  last  fifteen 
years : 

A  man  aged  sixty  years,  with  chronic  jaundice,  was  admitted  with  pneumonia 
which  proved  fatal.  There  were  a  fibrous  stricture  of  the  common  bile-duct  in  its 
lower  fourth  and  great  distension  of  the  gall-bladder  and  bile-ducts.  There  was 
no  evidence  of  any  malignant  disease  or  of  gall-stones. 

It  should  be  remembered  that  some  of  the  cases  of  stricture  of  the 
bile-ducts  in  adults  may,  in  the  absence  of  microscopic  examination, 
have  been  cases  of  primary  carcinoma  of  the  ducts,  as  a  stricture  which, 
to  the  naked  eye,  appears  merely  fibrous,  may  be  undoubtedly  carcino- 
matous. 

This  was  the  case  in  a  woman  aged  fifty-seven  in  whom  the  lower  part  of  the 
common  bile-duct  was  much  stenosed  as  if  from  cicatrisation  of  an  ulcer  due  to  gall- 
stones.    Microscopically  it  was  carcinomatous.  J 

The  symptoms  are  those  of  chronic  obstructive  jaundice  and  resemble 
those  of  malignant  disease  of  the  bile-ducts.  In  Moxon's  case,  where 
jaundice  lasted  eight  months,  there  was  much  xanthelasma  on  the  hands, 
back,  and  scrotum. 

An  accurate  diagnosis  is  impossible  before  the  abdomen  is  opened 
and  the  duct  freely  exposed. 

Treatment. — If  there  is  a  suspicion  of  syiahilis,  iodides  should  be 
given.  Failing  any  improvement  from  antisyphilitic  treatment,  an 
exploratory  operation  with  a  view  of  uniting  the  gall-bladder  with  the 
intestine,  if  the  stricture  is  in  the  common  bile-duct,  should  be  under- 
taken. 

*  Lazarus-Barlow,  W.  S. :  Trans.  Path.  Soc,  vol.  1,  p.  158. 

t  Mackenzie,  H. :  Trans.  Path.  Soc,  vol.  xlvii,  p.  84. 

t  Krokiewicz:  Wien.  klin.  Wochen.,  March  31,  1898,  S.  321. 


SIMPLE    CATARRHAL    JAUNDICE    OR    ACUTE    CATARRHAL 

CHOLANGITIS. 

Definition. — Local  inflammatory  swelling  of  the  mucous  membrane 
of  the  termination  of  the  common  bile-duct  leading  to  biliary  obstruction 
and  to  the  passage  of  bile  into  the  circulation.  The  jaundice  is  preceded 
by  signs  of  gastro-intestinal  catarrh,  comes  on  without  pain,  and  lasts 
about  three  weeks. 

It  is  essentially  due  to  a  local  inflammatory  obstruction,  and  must 
be  distinguished  from  toxsemic  and  infectious  jaundice  (Weil's  disease), 
which  are  the  manifestations  of  a  general  toxaemia  or  haemic  infection. 
Catarrhal  jaundice  is  due  to  acute  catarrhal  inflammation  limited  to  the 
biliary  papilla  and  the  adjacent  portion  of  the  common  bile-duct,  and 
but  for  the  objection  to  coining  new  ternxs,  might  be  spoken  of  as  acute 
cholo-papillitis. 

While  adopting  this  view  as  to  the  nature  of  acute  catarrhal  jaundice, 
it  is  well  to  admit  that  there  is  room  for  discussion  as  to  the  part  played 
by  infection  and  inflammation  spreading  from  the  duodenum.  Gastro- 
duodenal  catarrh  ma}'  be  toxic  or  due  to  microbic  activity,  and  in  the 
latter  case  the  jaundice  might  be  spoken  of  as  being  infective.  The 
French  school,*  indeed,  includes  catarrhal  jaundice  among  the  benign 
or  innocent  forms  of  infective  jaundice.  Besides  mechanically  obstruct- 
ing the  lower  end  of  the  bile-duct,  the  morbid  process  may  extend  up- 
wards and  involve  a  greater  or  lesser  extent  of  the  common  bile-duct. 
When  a  consideral^le  extent  of  the  common  bile-duct  is  inflamed,  the 
condition  usually  becomes  one  of  chronic  cholangitis  and  clinically  pre- 
sents itself  as  one  of  prolonged  catarrhal  jaundice. 


CAUSATION. 

Gastroduodenal  catarrh  involving  the  mucous  membrane  of  the  biliary 
papilla  readily  spreads  into  the  common  channel,  or  ampulla  of  Vater, 
inside  the  biliary  papilla.  Comparatively  little  swelling  of  the  mucous 
membrane  of  the  narrow  orifice  of  the  papilla  is  sufficient  to  obstruct 
the  flow  of  bile  through  it,  while  a  jilug  of  tenacious  nuicus  ma}^  easily 
form  in  the  lumen  of  the  papilla.  Probably  this  is  what  happens  in 
the  ordinary  run  of  cases,  though  it  is  not  improbable  that  inflammatory 
swelling  spreads  a  varying  cUstance  up  the  common  bile-duct  in  more 
prolonged  examples  of  the  disease.  Some  cases,  which  apparently 
begin  as  catarrhal  jaundice,  rapidly  develop  into  acute  yellow  atrophy, 
and  it  is  possible  that  an  inflammation  of  the  lower  end  of  the  common 
duct  has  rapidly  extended  up  to  the  liver. 

*  Chauffard  :  Traito  de  Mcderino  (Bouchard,  Brissaud),  tome  v,  p.  89,  1902. 

655 


656  DISEASES    OF   THE    BILE-DUCTS. 

The  causes  of  catarrhal  jaundice  are,  therefore,  those  of  gastroduodenal 
catarrh ;  it  is  a  comphcation  of  acute  gastritis  and  may  be  due  to  alcohohc 
excess  or  indiscretions  in  diet,  and  fohows  chills. 

Since  gastritis  is  a  very  common  accompaniment  of  the  specific  fevers, 
it  is  easy  to  understand  that  jaundice  in  the  course  of  typhoid  fever  or 
pneumonia  may  depend  on  purely  local  obstruction  at  or  near  the  biliary 
papilla.  On  the  other  hand,  it  must  be  remembered  that  when  seen  in 
the  course  of  the  specific  fevers,  jaundice  may  be  toxsemic,  or  depend  on 
severe  infective  inflammation  of  the  bile-ducts  and  gall-bladder. 

In  tj^hoid  fever  jaundice  is  remarkably  rare — so  much  so  that  Sir 
W.  Jenner  *  never  met  with  it.  When  it  does  occur,  it  may  be  catarrhal, 
toxic,  or  the  expression  of  infection  of  the  biliary  passages  leading  to 
cholangitis,  etc.  When  catarrhal  jaundice  occurs  in  typhoid  fever,  it 
may  be  met  with  at  any  period  in  the  course  of  the  fever  or  in  a  relapse, 
and  in  no  way  affects  the  course  of  the  disease. 

Osier  t  records  6  cases,  2  in  relapses;  5  of  these  occurred  in  829  cases  of  typhoid 
fever  at  Johns  Hopkins  Hospital.  Da  Costa,t  in  a  review  of  52  cases  of  jaundice 
in  the  course  of  typhoid  fever,  found  4  due  to  catarrhal  jaundice.  In  244  cases  of 
typhoid,  which  I  analysed,  at  the  Imperial  Yeomanry  Hospital,  Pretoria,  there  was 
one  case  of  mild  catarrhal  jaundice. §     I  have  seen  similar  cases  in  England. 

Catarrhal  jaundice  may  supervene  in  the  course  of  portal  cirrhosis 
and  be  due  to  gastroduodenal  catarrh,  which,  of  course,  is  favoured  by 
chronic  portal  engorgement  and  may  be  lighted  up  by  alcoholic  excess. 
A  shght  icteric  tinge  of  the  skin  is  ver}^  frequent  in  advanced  cases  of 
mitral  disease;  it  is  only  exceptionalh'-  that  there  is  intense  jaundice. 
It  may  also  occur  and  be  perhaps  the  first  symptom  in  cases  of  malignant 
disease  involving  the  liver  or  bile-ducts. 

Thus  in  two  cases  under  my  care  in  St.  George's  Hospital  at  the  same  time  in 
1897  jaundice  came  on  suddenly  with  vomiting  and  signs  of  gastro-enteritis :  one 
was  a  woman  with  primary  carcinoma  of  the  gall-bladder;  the  other,  a  man  with 
primary  carcinoma  of  the  common  bile-duct.  In  both  cases  the  jaundice  lasted 
until  death. 

Catarrhal  jaundice  may  also  complicate  other  organic  diseases  of  the 
liver,  such  as  hydatid.  Emotional  jaundice  has  been  thought  to  be 
really  catarrhal  in  origin,  but  without  sufficient  grounds.  Catarrhal 
jaundice  may  be  epidemic  because  gastroduodenal  catarrh  is  epidemic. 
It  must,  however,  be  borne  in  mind  that  epidemic  jaundice  is  usually 
toxsemic  and  due  to  descending  infection  of  the  small  intra-hepatic  ducts 
set  up  by  some  microbic  infection  or  toxine.  As  examples  of  this  epi- 
demic infective  jaundice,  Weil's  disease  {vide  p.  584)  and  jaundice  follow- 
ing drain  poisoning  may  be  mentioned.  It  is  not  always  easy  to  be 
dogmatic  as  to  the  nature  of  mild  epidemic  jaundice;  probably  most 
cases  are  toxsemic  rather  than  purely  local  catarrh  of  the  lower  end  of 
the  common  bile-duct.  It  is,  however,  probable  that  mild  epidemic 
jaundice  following  influenza  may  belong  to  the  latter  category. 

*  Jenner,  W. :  On  Fevers  and  Diphtheria,  p.  35.3. 

t  Osier,  \\. :  Johns  Hopkins  Hosp.  Reports,  vol.  viii,  p.  372,  1900. 

t  Da  Costa:  American  Journ.  Med.  Sciences,  July,  1898,  vol.  cxvi,  p.  1. 

§  Rolleston:  Brit.  Med.  Journ.,  1901,  vol.  ii,  p.  976. 


SIMPLE    CATARRHAL    JAUNDICE.  657 

MORBID  ANATOMY. 

Opportunities  for  investigating  the  morbid  conditions  underlying 
catarrhal  jaundice  only  arise  when  death  occurs  from  some  other  cause, 
such  as  an  accident. 

The  mucous  membrane  of  the  duodenum  and  adjacent  part  of  the 
common  bile-duct  is  swollen,  injected,  and  covered  by  tenacious  mucus. 
A  plug  of  inspissated  mucus  may  be  found  inside  the  tennination  of 
the  common  bile-duct.  These  changes  rarely  extend  further  up  than 
the  lower  end  of  the  common  bile-duct. 

The  swelling  of  the  mucous  membrane  may,  however,  subside  after 
death,  and  because  it  is  possible  to  force  bile  into  the  duodenum  by 
pressure  on  the  gall-bladder  it  does  not  follow  that  there  was  no  obstruc- 
tion during  life.  The  same  remark  applies,  only  with  more  force,  to  the 
passage  of  a  probe  up  the  bile-duct  from  the  duodenum.  The  liver  ma}'- 
be  swollen  from  accumulation  of  bile  and  from  vascular  engorgement. 
The  lining  membrane  of  the  heart  and  vessels  is  bile-stained. 

CLINICAL  PICTURE. 

Incidence. — In  an  analysis  of  215  cases  of  simple  catarrhal  jaundice 
Neumann  *  found  that  42  per  cent,  occurred  in  the  first  ten  years  of 
life,  and  here  it  may  be  mentioned  that  sucklings  appear  to  be  rarely 
affected  by  this  particular  form  of  jaundice;  between  ten  and  twenty 
years  10  per  cent,  of  the  cases  occurred,  while  the  percentage  rose  to 
27  per  cent,  in  the  third  decade.  It  is  commoner  in  the  winter  than  in 
the  summer  months. 

Premonitory  Symptoms. — Before  jaundice  appears  there  are  usually, 
though  not  invariably,  signs  of  gastro-intestinal  disturbance  which  may 
last  for  a  few  days  to  a  week.  There  are  vomiting,  loss  of  appetite,  furred 
tongue,  foul  breath,  bitter  taste  in  the  mouth,  headache,  vertigo,  and 
dyspepsia,  some  general  malaise,  and  occasionally  flying  pains  in  the 
limbs.  Diarrhoea  from  extension  of  the  catarrh  to  the  intestines  is  often 
seen.  The  motions  become  clay-coloured  and  free  from  bile-pigment 
before  the  appearance  of  icterus  and  markedly  offensive  from  fermenta- 
tion. The  fseces  may  remain  pale  for  a  considerable  time;  this  need  not 
always  be  due  to  the  absence  of  bile,  but  may  depend  on  milk  taken  as 
food,  and  on  the  fseces  containing  gas  in  a  finely  divided  state.  Jaundice 
may  not  be  noticed  by  the  patient  until  his  attention  is  directed  to  it 
by  his  friends. 

The  conjunctiva  is  the  first  part  of  the  body  to  show  the  icteric  tint, 
but  the  presence  of  bile-pigment  can  be  detected  in  tlie  urine  even  before 
this.  The  sclerotics  under  the  conjunctivse  are  one  of  the  most  suitable 
sites  for  recognising  tlio  jaundice,  but  the  fatty  and  often  slightly  yellow 
masses  (pinguecula;)  mulerneath  the  conjunctivae  must  not  be  mistaken 
for  icteric  tingeing. 

The  skin  of  the  face  becomes  jaundiced  soon  after  the  conjunctivse. 
'I'his  is  more  manifest  in  lilonds  than  in  dark-skinned  persons,  who  are 

*  Nciuiuiuii :   Dciitschri  UK'd.  Wdcln'ij.,  Auiz;.  .'^1     1X99. 
41 


658  DISEASES   OF   THE    BILE-DUCTS. 

often  naturally  somewhat  sallow.  The  mucous  membrane  of  the  mouth, 
especially  under  the  tongue  and  on  the  inner  surface  of  the  lips,  appears 
yellow  when  the  blood  is  pressed  out  of  the  superficial  vessels.  From 
the  face  the  yellow  tint  spreads  to  the  trunk  and  extremities,  reaching 
the  legs  last;  the  whole  of  the  body  finally  becomes  jaundiced,  and  some- 
times of  a  bright  yellow  colour.  The  dark  green  colour  seen  in  obstruc- 
tive jaundice  due  to  malignant  disease  is  never  seen  in  catarrhal  icterus; 
but  the  skin  may  show  the  effects  of  jaundice  for  a  considerable  time. 

Osier  *  mentions  a  case  in  which  stigmata  or  spider  angiomata  appeared  on 
the  face  during  catarrhal  jaundice. 

By  the  time  that  jaundice  has  made  its  appearance  the  gastric  symp- 
toms have  usually  begun  to  subside.  This,  however,  is  by  no  means 
universal.  Obstinate  vomiting  may  persist  when  the  diet  is  not  carefully 
restricted  and  supervised.  At  the  onset  there  may  be  slight  fever  from 
the  gastro-enteritis,  but  otherwise  the  temperature  is  either  normal  or 
considerably  below  the  normal.  It  is  often  stated  that  there  may  be 
fever  in  catarrhal  jaundice.  It  is  probable  that  cases  which  otherwise 
resemble  catarrhal  jaundice  but  show  a  raised  temperature  are  rather 
to  be  classed  as  mild  cases  of  toxemic  or  infective  jaundice. 

Symptoms  when  the  Disease  is  Fully  Developed. — The  pulse  is 
slowed;  this  is  usually  referred  to  the  action  of  bile  salts  on  the  cardiac 
ganglia.  It  is  often  60  or  less  per  minute,  and  is  of  low  tension,  soft, 
and  may  be  dicrotic.  The  slowing  of  the  heart's  action  is  much  less 
marked  in  children  than  in  adults.  Pruritus  is  often  a  troublesome 
feature;  the  scratching  may  lead  to  traumatic  eczema,  or  even  to  an  urti- 
carial rash.  Pruritus  is  rare  in  children,  as  shown  by  the  fact  that  Still  f 
has  never  met  with  an  example.  It  is  by  no  means  certain  how  the 
itching  is  brought  about ;  it  may  be  absent  when  jaundice  is  very  marked, 
and  may  appear  before  any  icterus  is  perceptible;  so  it  cannot  be  very 
satisfactorily  explained  by  the  action  of  the  bile  on  the  cutaneous  nerves. 
Yellow  vision  (xanthopsia)  is  sometimes,  though  rarely,  present;  its 
existence  is  seldom  a  cause  of  complaint,  but  the  patients  may  be  found 
to  have  noticed  it  on  being  questioned.  It  is  thought  to  be  due  to  bile 
in  the  vitreous  humour.  Owing  to  the  action  of  the  bile  constituents 
in  the  brain  there  are  depression  of  spirits  and,  sometimes,  a  melancholic 
condition.  There  may  be  much  mental  irritability  and  incapacity  for 
transacting  the  ordinary  affairs  of  life  efficiently. 

The  urine  contains  bile-pigment  On  shaking  it  in  a  white  porringer 
the  foam  becomes  characteristically  yellow.  During  the  first  few  days 
and  even  before  jaundice  has  appeared  on  the  surface  of  the  body  bile 
acids  as  well  as  bile-pigment  may  be  present  in  the  urine.  During  the 
period  of  the  disease  when  the  patient  feels  worst  there  may  be  a  distinct 
excess  of  nitrogen  in  the  urine  as  compared  with  that  taken  in.  During 
this  time  the  patient  loses  weight.  J  While  there  is  bile  in  the  urine  casts 
may  be  found,  but  not  albumin. 

*  Osier:  Johns  Hopkins  Hosp.  Bull,  vol.  xii,  p.  337,  1901. 
t  Still,  G.  F. :  Clinical  Jour.,  vol.  xvii,  p.  324,  March  13,  1901. 
.t  Schmidt:  Centralbl.  f.  innere  Med..  Feb.  5,  1898 


SIMPLE    CATARRHAL   JAUNDICE.  659 

The  occurrence  of  bile-pigment  in  the  saUva  in  cases  of  jaundice  has 
been  recorded  by  various  authors,  especially  when,  as  a  result  of  mercurial 
treatment,  inflammatory  changes  in  the  mouth  are  superadded.  W. 
Legg,*  who  paid  special  attention  to  this  point,  always  found  the  saliva 
colourless  in  cases  of  uncomplicated  jaundice.  The  sweat,  especially 
from  the  armpits,  may  contain  bile-pigment,  and  the  linen  may  be  stained, 
but,  generally  speaking,  the  perspiration  is  colourless.  The  secretion  of 
the  alimentary  canal,  the  tears,  nasal  mucus,  and  in  women  the  milk, 
are,  in  spite  of  statements  to  the  contrary,  free  from  bile.  In  inflamma- 
tory conditions  the  altered  secretions  and  exudations  become  bile-stained; 
this  is  shown  in  pneumonic  sputum  and  in  pleural  and  peritoneal  effu- 
sions. 

The  blood-senmi  contains  bile-pigment,  but  there  is  no  change  in  the 
corpuscles.  As  has  been  pointed  out  above  (p.  535),  the  serum  of  jaun- 
diced patients  has  been  said  to  agglutinate  typhoid  bacilli.  Dr.  H.  Spitta 
has  kindly  given  me  the  notes  of  the  agglutination  reactions  in  eight 
cases  of  catarrhal  jaundice.  In  two  cases  there  was  slight  clumping  of 
tjq^hoid  bacilli  in  a  dilution  of  1  :  10;  in  none  of  the  cases  was  there  any 
clumping  of  Gartner's  bacillus.  Bacillus  coli  was  agglutinated  in  all  the 
cases  in  dilution  of  1  :  10,  and  in  six  of  the  cases  in  a  dilution  of  1  :  100. 

As  a  rule,  there  is  no  hepatic  enlargement  or  tenderness  on  palpation. 
Many  authors  state  that  the  liver  may  be  enlarged  in  simple  catarrhal 
jaundice  as  the  result  of  distension  of  the  intra-hepatic  ducts  with  bile, 
but  if  the  enlargement  is  at  all  marked,  it  is  probable,  though  it  is  im- 
possible to  speak  with  any  certainty  on  this  point,  that  inflammation  of 
the  common  bile-duct  has  spread  to  the  ducts  in  the  liver  substance. 

The  gall-bladder  is  sometimes  palpably  enlarged  in  cases  of  catarrhal 
jaundice,  but  definite  enlargement  should  always  raise  the  question 
whether  the  disease  is  not  in  reality  cholecystitis  with  some  inflammation 
of  the  common  bile-duct. 

Duration. — The  jaundice  gradually  fades  in  the  course  of  four  to 
six  weeks,  but  the  skin  often  remains  tinged  for  a  considerable  period. 
In  slight  attacks  the  icteric  tint  may  pass  away  in  a  couple  of  weeks. 
Occasionally  cases,  which  begin  like  ordinary  catarrhal  jaundice  and 
eventually  clear  up,  hang  fire  and  last  for  months;  Chauffard  f  quotes 
cases  lasting  from  ninety-two  to  one  hundred  and  fifty- five  days.  These 
cases  are  very  prol^ably  examples  of  chronic  catarrhal  cholangitis,  and 
are  allied  to  the  chronic  inflammation  of  the  common  bile-duct  set  up 
by  calculi  {vide  p.  750),  as  is  shown  by  the  fact  that  interirdssions  may 
occur.  Thus,  though  beginning  like  catarrhal  jaundice,  these  cases  must 
be  regarded  as  complicated  by  an  extension  of  the  inflammatory  process 
and  as  belonging  to  another  category.  If,  in  a  case  regarded  as  catarrhal 
jaundice,  the  disease  does  not  clear  up,  there  is  either  some  complication 
or  the  diagnosis  is  wrong.     Relapses  of  catarrhal  jaundice  may  occur. 

Effects. — Considerable  loss  of  flesh  and  weight  occur  in  a  well-marked 
case  of  catarrhal  jaundice.     The  loss  of  appetite  and  the  resulting  defi- 

*  Legg,  W. :  St.  Bartholomew's  Hospital  Reports,  vol.  xiii,  p.  12. 

t  Chauffard:  Trait6  de  M6d.  (liouchard,  Brissaud),  tome  v,  p.  97,  1902. 


660  DISEASES    OF    THE    BILE-DUCTS. 

ciency  in  the  intake  of  food  largely  accounts  for  this,  but  the  diminished 
absorption  of  fats  must  also  be  considered  as  an  important  factor,  since 
it  obliges  the  patient  to  live  on  his  own  tissues. 

Calcuh  and  bihary  cohc  may  follow  ordinary  catarrhal  jaundice,  but 
in  order  to  explain  cholelithiasis  as  a  sequel  of  ordinary  catarrhal  jaundice 
it  must  be  assumed  that  the  gall-bladder  was  involved  and  that  chole- 
cystitis of  a  mild  degree  was  present  in  addition.  Cholelithiasis  might 
thus  be  a  result  of  a  complication  of  catarrhal  jaundice  and  subsequently 
give  rise  to  bihary  colic.  Dilatation  of  the  lower  end  of  the  common  bile- 
duct  has  been  thought  to  be  a  result  of  catarrhal  inflammation,  but  it 
is  probable  that  when  this  sequence  is  noted,  the  inflammation  has  been 
•of  considerable  duration  or  intensity,  or  that  there  has  been  a  gall-stone 
there.  Just  as  the  inflammation  of  the  papilla  may  spread  into  the 
common  bile-duct  and  give  rise  to  chronic  cholangitis,  so  the  catarrhal 
process  may  extend  into  Wirsung's  duct  of  the  pancreas  and  set  up 
acute  or  chronic  pancreatitis,  which  may  therefore  be  regarded  as  pos- 
sible complications  or  sequelae  of  catarrhal  jaundice. 


DIAGNOSIS. 

The  presence  of  gastro-intestinal  disturbance,  vomiting,  diarrhoea, 
loss  of  appetite,  and  dyspepsia  before  the  onset  of  jaundice,  the  absence 
of  severe  constitutional  disturbance  and  of  pain,  and  the  comparatively 
mild  jaundice  fading  within  a  few  w^eeks  are  the  important  points  in 
the  diagnosis.  In  some  instances  gastro-intestinal  symptoms  are  absent 
and  it  is  then  difficult  to  ehminate  at  once  more  serious  forms  of  jaundice; 
it  must  also  be  remembered  that  catarrhal  jaundice  may  comphcate 
grave  forms  of  hepatic  disease.  The  age  of  the  patient  has  some  bearing, 
as  catarrhal  jaundice  in  late  middle  life  may  be  the  first  indication  of 
malignant  disease  involving  the  ducts.  The  duration  and  character  of 
the  jaundice  are  very  important;  when  jaundice  lasts  more  than  six 
weeks,  the  diagnosis  of  simple  catarrhal  jaundice  should  be  seriously 
questioned,  and  some  other  cause  sought  for.  Deep  green  or  ''black" 
jaundice  excludes  simple  catarrhal  jaundice.  Constantly  recurrent  at- 
tacks point  to  intermittent  hepatic  fever  and  the  presence  of  a  calculus 
in  the  lower  end  of  the  common  duct. 

Cases  of  mild  toxaemic  jaundice  are  readily  confused,  especially  those 
with  only  slight  fever  and  enlargement  of  the  liver,  with  catarrhal  jaundice. 
In  well-defined  toxemic  or  infective  jaundice  there  are  signs  of  general 
nfection,  such  as  fever,  albuminuria,  splenic  and  hepatic  enlargement, 
but  in  the  milder  cases  some  of  these  manifestations  may  be  absent  and 
there  is  a  transition  to  catarrhal  jaundice. 

From  gall-stone  colic  the  condition  is  distinguished  by  the  gradual 
and  painless  onset  of  jaundice  and  by  preceding  gastro-intestinal  irri- 
tation. 

The  jaundice  accompanying  the  presence  of  gall-stones  in  the  common 
duct  is  much  more  prolonged  than  in  catarrhal  jamidice,  and  is  usually 
characterised  by  periodic  outbursts  of  fever,  pain,  and  exacerbations  in 


SIMPLE    CATARRHAL    JAUNDICE.  661 

the  degree  of  jaundice  {vide  p.  750).  It  may  be  preceded  by  biliary  colic, 
but  this  is  by  no  means  alwa3^s  the  case,  and  it  may  come  on  cpite  gradu- 
ally. It  occurs  in  older  persons  than  catarrhal  jaundice,  especially  in 
women. 

PROGNOSIS. 

In  orcUnary  cases  the  prognosis  is  extremely  good,  there  being  no 
danger  to  hfe  and  very  seldom  any  after-results  of  importance.  On 
the  other  hand,  it  must  be  borne  in  mind  that  what  at  first  appears  to 
be  catarrhal  jaundice  may  be  the  initial  manifestation  of  severe  organic 
disease  of  the  liver,  such  as  malignant  disease  or  acute  3^ellow  atrophy. 
It  is,  therefore,  advisable  to  avoid  giving  a  dogmatic  prognosis  in  the 
early  stages,  if  this  can  be  done  -vdthout  creating  alarm.  In  the  vast 
majority  the  result  of  the  case  justifies  a  prognosis  of  complete  and  rapid 
recover}',  given  at  the  very  outset;  but  in  rare  instances  the  clinical 
picture  radically  changes  and  nervous  sjanptonxs  rapidly  usher  in  coma 
and  death  from  acute  yellow  atrophy,  or,  in  less  exceptional  cases,  the 
jaundice,  instead  of  gradually  disappearing,  deepens  into  that  of  ma- 
hgnant  obstruction  of  the  common  bile-duct.  When  catarrhal  jaundice 
is  prolonged,  the  prognosis  alters,  as  the  possibility  of  some  grave  cause 
of  obstruction  must  be  considered,  but  some  of  these  protracted  cases 
recover  udthout  any  definite  developments. 


TREATMENT. 

In  the  early  stage,  while  there  is  evidence  of  gastro-intestinal  catarrh, 
the  patient  should  be  kept  warm  in  bed  and  on  a  milk  diet.  As  absorption 
of  fat  is  greatly  diminished,  skimmed  milk  containing  one  per  cent,  of  fat 
is  preferable  to  ordinary  milk.  In  the  presence  of  nausea  and  complete 
loss  of  appetite  it  is  unnecessary^  to  press  even  milk,  and  for  a  few  days 
the  patient  should  be  allowed  to  take  or  leave  it ;  thirst  is  usuaUy  present, 
and  water,  lemonade,  Apollinaris,  Vichy,  or  Vals  water  should  be  pro- 
vided. The  gastric  irritation  may  be  allayed  by  draughts  of  warm  water 
containing  bicarbonate  of  soda,  and  by  the  application  of  poultices  to 
the  upper  part  of  the  abdomen.  Nausea  and  vomiting  are  readily 
excited  by  food,  and  rest  to  the  stomach  by  temporary  starvation  is 
followed  b}^  improvement  and  is  well  borne.  Bismuth  in  the  form  of  a 
lozenge  or  in  a  mixture  with  bicarbonate  of  soda  and  dilute  h3^drocyanic 
acid  may  also  be  given. 

The  bowels  should  be  kept  open  either  by  enemata  or  by  a  small 
dose  of  calomel  (^-1  gr.)  given  at  night  and  followed  next  morning  by 
Carlsbad  salts.  Vigourous  purgatives  may  set  up  or  increase  gastro- 
intestinal catarrh  and  should,  therefore,  be  avoided. 

WTien  the  gastro-intestinal  catarrh  has  subsided,  the  bland  milk  diet 
should  be  relaxed,  and  clear  thin  soup,  eggs,  fish,  and  white  meat  given 
as  the  patient's  condition  allows.  Minute  doses  (4V-2V  S^-)  ^^  calomel, 
salicylate  of  bismuth,  and  salol  are  useful  to  inhibit  intestinal  fermenta- 
tion;   while   /3'-naphthol,  benzo-naphthol,   resorcin,  and  iodoform   have 


662  DISEASES    OF   THE    BILE-DUCTS. 

been  employed  with  the  same  object.  The  action  of  the  bowels  must  be 
maintained  by  the  purgative  waters  or  by  salines,  such  as  Epsom  or 
Carlsbad  salts,  phosphate  of  soda,  and,  if  necessary,  by  blue  pill. 

Rectal  injections  of  cold  water  to  stimulate  peristaltic  action  of  the 
gall-bladder  and  so  induce  flushing  of  the  bile-ducts  by  the  bile  have 
been  recommended.  Massage  to  the  liver  has  been  advocated  by  Gilbert 
and  Lereboullet,*  and  can  be  carried  out  at  a  spa  by  the  liver  douche. 

During  convalescence  a  tonic  containing  dilute  nitrohydrochloric  acid 
and  nux  vomica  is  useful  in  improving  the  appetite  and  digestion. 

For  the  pruritus,  alkaline  baths  or  sponging  with  carbolic  acid  lotion, 
1  :  40,  often  give  relief,  while  the  internal  administration  of  chloride  of 
calcium  in  20-grain  doses,  or  antipyrin,  which  acts  as  a  nerve  sedative, 
should  be  tried. 

If  the  jaundice  persists  and  there  is  no  reason  to  suspect  any  grave 
underlying  condition,  such  as  malignant  disease,  the  patient  will  probably 
receive  benefit  from  a  visit  to  a  spa,  such  as  Harrogate,  Leamington 
Llandrindod  Wells,  Vichy,  Neuenahr,  Carlsbad,  or  Bertrich. 

*  Gilbert  et  Lereboullet:  Gaz.  hebdomin.    1901.  p.  913. 


SUPPURATIVE  CHOLANGITIS. 

ETIOLOGY. 

The  exciting  cause  of  suppurative  inflammation  of  the  bile-ducts 
is  a  virulent  microbic  infection;  the  varieties  of  bacteria  which  have  been 
found  to  give  rise  to  this  affection  are  referred  to  below  {vide  p.  665). 
The  conditions  and  diseases  which  dispose  to  suppurative  cholangitis  are — 
(i)  Local;  and  (ii)  general. 

(i)  The  local  conditions  are: 

(a)  Those  which  diminish  the  resistance  of  the  ducts,  such  as  new- 
growth,  past  inflammation,  etc.,  and  (&)  render  infection  more  easy,  svich 
as  biliary  stagnation,  gall-stones,  rupture  of  hydatid  cysts  into  the  ducts, 
the  presence  of  worms  in  the  ducts,  etc.  Bihary  obstruction  and  stagna- 
tion prevent  the  ducts  being  flushed  out.  Hence  micro-organisms  which 
have  got  into  the  ducts  either  from  the  liver  and  general  circulation 
(descending  infection)  or  from  the  duodenum  (ascending  infection)  have 
a  better  chance  of  multiplying  and  setting  up  inflammatory  changes  in 
the  ducts,  especially  since,  owing  to  dilatation,  the  ducts  are  probably 
less  resistant  than  in  health. 

Cholelithiasis  is  the  commonest  antecedent  of  suppurative  cholangitis ; 
this  was  so  in  18  out  of  20  cases  collected  by  L.  Rogers.*  The  acute 
suppurative  inflammation  may  supervene  on  old-standing  infective 
cholangitis  {vide  Intermittent  Hepatic  Fever,  p.  750)  or  may  occur  in 
a  patient  who  has  never  had  any  manifest  signs  of  cholelithiasis.  When 
suppurative  cholangitis  supervenes  on  chronic  catarrhal  inflammation  of 
the  ducts,  the  more  vindent  microbic  infection  may  be  supposed  to  be 
favoured  by  the  diminished  resistance  of  the  ducts. 

Rupture  of  hydatid  cysts  into  the  bile-ducts,  though  not  nearly  so 
frequent  a  cause  of  suppurative  cholangitis  as  gall-stones,  is  a  well- 
estabhshed  factor.  Possibly  in  the  first  instances  the  hydatid  fluid  may 
produce  a  change  in  the  mucous  membrane  of  the  ducts,  analogous  to 
urticaria.  The  presence  of  hydatid  membranes  in  the  ducts  favours 
ascending  infection  from  the  duodenum,  and  it  is  probably  to  this  that 
suppurative  cholangitis  is  due.  The  subject  of  rupture  of  hydatid  cysts 
into  the  bile-ducts  is  considered  more  fully  in  the  section  on  "Hydatid 
Disease  of  the  Liver." 

In  hepatic  abscess  the  inflammation  may  spread  to  the  bile-ducts,  or 
the  abscess  may  open  into  the  larger  bile-ducts.  Cholangitis  may  thus 
be  secondary  to  hepatic  abscess,  and  by  giving  rise  to  multiple  foci  of 
suppuration,  renders  a  fatal  issue  almost  certain. 

Round  worms  and  hver  flukes  may  pass  up  the  common  bile-duct 
from  the  duodenum  and  carry  with  them  micro-organisms.  The  ducts 
thus  become  infected,  and  suppuration,  either  diffuse  or  localised,  of  the 

*  Rogers,  L. :  Brit.  Med.  Jour.,  1903,  vol.  ii.  p.  706. 
663 


664  DISEASES    OF   THE    BILE-DUCTS. 

ducts  will  readily  result.  When  localised,  the  worm  may  be  found  in 
an  abscess  cavity  in  the  liver.  ( Vide  Parasitic  Affections  and  Bile-ducts, 
p.  676.) 

A  new-growi:h — ^jDapilloma  or  carcinoma — arising  on  the  duodenal 
surface  of  the  biliary  papilla  is  not  common,  but  is  very  prone  to  set  up 
suppurative  cholangitis.  The  tendency  to  the  development  of  suppura- 
tive inflammation  of  the  bile-ducts  in  carcinoma  of  the  duodenal  surface 
of  the  biliary  papilla  depends  on  the  following  factors:  (1)  Obstruction 
to  the  outflow  of  bile  and  dilatation  of  the  ducts  diminish  their  resistance. 
Owing  to  ulceration  and  necrosis  of  the  growth,  the  obstruction  may 
intermit,  and  this  intermission  very  probably  favours  an  ascending 
infection  from  the  duodenum.  (2)  The  presence  of  the  growth  favours 
duodenal  catarrh  and  thus  renders  ascending  infection  of  the  common 
bile-duct  easy.  (3)  Stagnation  of  bile  in  the  ducts  favours  microbic 
infection. 

The  gro'ni^h  in  the  duodenum  in  the  region  of  the  papilla  may  be  either  a  papil- 
loma or  a  carcinoma;  in  some  instances  it  appears  to  the  naked  eye  to  be  a  papilloma, 
but  microscopic  examination  shows  invasion  of  the  duodenal  waU  and  therefore 
malignancy,  as  in  the  specimens  in  the  Museums  of  Guy's  and  St.  Bartholomew's 
Hospitals* 

Besides  mahgnant  disease  of  the  duodenum,  carcinoma  of  the  diver- 
ticulum of  Vater  and  of  the  lower  part  of  the  common  bile-duct  may  also 
lead  to  suppurative  cholangitis.     (Vide  p.  692.) 

In  malignant  disease  of  the  liver  pressure  on  the  ducts  disposes  to 
and  may  lead  to  suppurative  cholangitis. 

A  woman  aged  forty-four  years  in  St.  George's  Hospital  under  the  care  of  my 
colleague,  Sir  I.  Owen,  with  jaimdice,  was  operated  upon  and  found  to  have  multiple 
growths  on  the  surface  of  tlie  liver.  She  had  a  febrile  temperature  until  her  death, 
one  week  later.  The  postmortem  revealed  primary  carcinoma  of  the  splenic 
flexure,  which,  however,  had  not  given  rise  to  any  symptoms,  and  secondary  growth 
in  the  liver  and  in  the  portal  fissure.  The  latter  compressed  the  hepatic  ducts. 
The  intra-hepatic  bile-ducts  showed  suppurative  cholangitis.  The  gall-bladder 
was  collapsed,  showed  a  secondary  growth  in  its  wall,  but  was  not  inflamed  or 
occupied  by  any  gall-stones. 

In  rare  instances  an  aneurysm  of  the  hepatic  artery  ma}^  lead  to 
multiple  abscesses  in  the  liver.  Osier  and  Ross  *  have  recorded  a  case. 
The  abscesses  may  be  due  to  infective  emboli,  but  they  ma}^  also  be  the 
abscesses  of  suppurative  cholangitis.  As  bearing  on  the  occurrence  of 
suppurative  inflammation  of  the  ducts  in  association  \\dth  aneurj^sm  of 
the  hepatic  artery,  it  is  interesting  to  note  that  Dujarier  and  Castaigne  t 
have  found  that  experimental  ligature  of  the  hepatic  artery  leads  to 
stagnation  of  bile  in  the  ducts  and  so  favours  infection. 

(ii)  The  General  Diseases  which  Dispose  to  Suppurative  Cholan- 
gitis.— Suppurative  cholangitis  may  occur  after  infective  diseases  attack- 
ing either  the  l)ody  generally  or  the  alimentary  canal. 

General  blood  infections  or  intoxications  may  set  up  inflammation 
of  the  small  ducts  in  the  liver  in  the  same  way  that  toluylendiamin,  when 
employed  experimentally,  gives  rise  to  a  descending  cholangitis.    Micro- 

*  Osier  and  Ross:  Canadian  Med.  Journ.,  vol.  vi. 

t  Dujarier  and  Castaigne-  Bull.  Soc.  Anat.  Paris,  1899,  p.  329 


SUPPURATIVE    CHOLANGITIS.  665 

organisms  or  poisons  may  reach  the  liver  by  the  blood  stream,  and  if 
the  bile-duets  are  previously  damaged,  micro-organisms  may  gain  an 
entrance  into  the  ducts  and  so  set  up  cholangitis. 

Influenza  and  pneumonia  have  in  rare  instances  been  precursors  of 
suppurative  cholangitis.  In  both  these  diseases  it  is  possible  that  the 
cholangitis  might  be  an  extension  of  inflammation  from  the  duodenum, 
since  there  is  a  well-known  gastro-intestinal  form  of  influenza,  and,  in 
rare  instances,  pneumococcal  gastritis. 

Suppurative  cholangitis  after  influenza  has  been  recorded  by  Mayo  Robson  * 
and  Remy  f;  in  the  latter  case,. cultivations  showed  the  presence  of  a  colon  bacillus. 

The  diseases  of  the  alimentary  canal  that  may  be  followed  by  sup- 
purative inflammation  of  the  bile-ducts  are  tyiDhoid  fever  and  cholera.  J 

A  great  deal  has  been  written  about  the  typhoid  affections  of  the 
biliary  system.  Usually  the  gall-bladder  bears  the  brunt  of  the  disease. 
It  is  very  rare  for  suppurative  cholangitis  to  occur  independently  of 
cholecystitis,  though  the  two  are  often  combined.  In  fact,  tj^phoidal 
suppurative  cholangitis  is  practically  subordinate  to  the  concoixiitant 
affection  of  the  gall-bladder.  Experimentally  cholangitis  has  been  set 
up  by  the  injection  of  cultures  of  the  comma  bacillus  into  the  bile-ducts 
of  rabbits.     (Gilbert  and  Dominici.§) 

Bacteriology  of  Suppurative  Cholangitis. — A  large  number  of 
micro-organisms  have  been  found  by  different  observers  to  be  associated 
with  suppurative  cholangitis.  In  some  of  the  cases  where  the  colon 
bacillus  has  grown  in  the  cultures  it  is  not  unlikely  that  other  micro- 
organisms were  present,  but  were  crowded  out  by  the  vigourous  growth  of 
the  colon  bacillus,  and  that  either  a  mixed  infection  was  present  or  that 
subsequent  contamination  with  the  colon  bacillus  occurred. 

The  chief  organisms  found  are  streptococci,  staphylococci  (albus, 
aureus),  pneumococcus,  typhoid  bacillus,  comma  bacillus,  and  colon 
bacillus. 

The  comma,  typhoid,  and  coli  bacilli  being  motile,  ascend  the  ducts 
from  the  intestine  more  readily  than  the  non-motile  streptococci  and 
staphylococci. 

The  Bacillus  aerogenes  capsulatus,  which  usually  invades  the  tissues 
during  the  death  agony,  may,  however,  be  present  during  hfe  in  the 
circulation  and  may  even  be  a  primary  infection. 

In  a  case  of  multiple  abscesses  of  the  liver  in  carcinoma  of  the  lower  end  of 
the  common  bile-duct  a  pure  culture  of  Bacillus  aerogenes  capsulatus  was  ob- 
tained by  Pratt  and  Fulton.  || 

MORBID  ANATOMY. 

The  mucous  membrane  of  the  ducts  is  swollen  from  inflammatory 
exudation  and  irregular  from  ulceration.     The  outer  walls  of  the  duct 

*  Mayo  Robson:  AUbutt's  System  of  Medicine,  vol.  iv,  p.  251. 

t  Remy:  Congres  de  chirurg.,  1.S96,  p.  485. 

:{:Galliard:  La  Cholera,  liibhotheque  Charcot-Debove,  IS94. 

§  Gilbert  and  Dominici:  Mem.  Soc.  de  biolog.,  1894,  p.  11. 

II  Pratt  and  Fulton:  Boston  Medical  and  Surgical  Journ.,  June  7,  1900,  p.  599. 


666  DISEASES    OF   THE    BILE-DUCTS. 

are  also  thickened  and  inflamed,  and  by  extension  there  may  be  local 
peritonitis,  which  may  lead  to  obliteration  of  the. foramen  of  Winslow, 
or,  by  extension  to  the  portal  vein,  to  pylephlebitis.  The  glands  in  the 
portal  fissure  are  enlarged  and  soft.  What  part  the  lymphatic  vessels 
play  in  the  upward  spread  of  the  inflammatory  process  into  the  liver  it 
is  hard  to  say,  inasmuch  as  any  process  of  this  kind  would  be  against 
the  lymph  stream.  Possibly  some  of  the  areas  of  suppuration  in  the 
liver  may  arise,  as  pericholangitic  abscesses  in  connexion  with  the  lym- 
phatics. The  suppurative  process  in  the  ducts  may  be  associated  with 
an  empyema  of  the  gall-bladder. 

When  the  inflammation  has  spread  to  the  liver,  that  organ  is  nearly 
alwa3''s  greatly  enlarged,  swollen,  and  of  a  greyish  colour,  with  yellowish- 
green  areas  around  the  portal  spaces.  These  foci  are  softening  down 
into  suppuration.  In  early  stages  these  areas  may,  to  the  naked  eye, 
resemble  secondary  nodules  of  new-growths  or  even  the  rarer  condition 
of  lymphadenoma.  When  the  disease  is  fully  developed,  the  bile-ducts 
may  be  enormously  dilated  so  as  to  be  as  large  as  the  small  intestine,  or 
to  be  opened  during  laparotomy  under  the  idea  that  the  case  is  one 
of  suppurative  cholecystitis.     (Rogers.*) 

The  dilated  and  suppurating  ducts  may  terminate  in  small  abscesses 
on  the  surface  of  the  liver,  somewhat  resembling  the  condition  of  the 
lung  in  acute  bronchiectasis.  Numerous  biliary  abscesses  may  be  scat- 
tered throughout  the  liver,  both  on  the  surface  and  in  the  substance  of 
the  organ,  and  adjacent  abscesses  may  run  together  and  form  a  confluent 
or  areolar  abscess  which  shows  septa  of  fibrous  tissue.  On  the  other 
hand,  there  may  be  a  single  localised  abscess,  or  only  quite  a  few  small 
abscesses  formed  of  ampulla-like  dilatations  of  the  ends  of  the  ducts. 
The  pus  is  often  bile-stained,  and  may  contain  soft,  calculous  matter.  The 
small  abscess  may  leak  into  the  peritoneum  and  set  up  general  peritonitis 
or  a  local  peritoneal  abscess.  In  the  substance  of  the  liver  abscesses 
may  form  outside  the  ducts,  possibly  in  the  lymphatics,  and  suppuration 
may  extend  into  the  branches  of  the  portal  vein,  setting  up  pylephlebitis. 
When  this  occurs,  there  is  diffuse  suppuration  of  the  portal  spaces  in  the 
liver. 

The  suppurative  process  may  extend  into  Wirsung's  duct  and  set  up 
suppurative  pancreatitis,  and  by  a  further  extension  of  infection  to  the 
peritoneum  covering  the  pancreas  a  local  abscess  in  the  lesser  sac  of 
the  peritoneum — the  omental  bursa  of  American  writers.  Pancreatitis 
due  to  gall-stones  in  the  common  duct  is  referred  to  on  page  755.'  Sup- 
puration may  spread  from  the  pancreas  into  the  portal  vein  and  set  up 
pylephlebitis. 

The  suppurating  bile-ducts  may  leak  into  the  peritoneum  and  set  up 
either  general  peritonitis  or  a  local  peritoneal  abscess.  When  on  the 
convex  surface  of  the  liver,  the  abscesses  may  perforate  the  diaphragm 
and  set  up  an  empyema  or  bronchobiliary  fistula,  while  abscesses  on  the 
under  surface  may  open,  into  the  colon  or  set  up  a  perinephritic  abscess 
(Rogers). 

*  Rogers,  L. :  Brit.  Med.  Jour.,  1903,  vol.  ii,  p.  706. 


SUPPURATIVE    CHOLANGITIS. 


667 


Microscopically  the  larger  portal  spaces  are  dilated,  and  relics  of 
their  fibrous  tissue  are  visible,  but  it  may  be  difficult  to  distinguish  the 
remains  of  the  large  bile-ducts  from  those  of  the  portal  veins,  since  both 
may  be  involved  in  the  same  suppurative  process.  The  walls  of  the 
ducts  may  be  destroyed  and  replaced  by  small  cells  which  extend  into 


Fig.  83. — Photomicrograph  of  a  Microscopic  Section  of  Liver  in  Suppurative 

Cholangitis. 
Shows  numerous  abscess  cavities  surrounded  by  condensed    fibrous   tissue,  which  appears 
more  darkly  stained.       It  is  impossible  to  make  out  and  distinguish   the  bile-ducts  from  the 
branches  of  the  portal  vein,  since  both  are  involved.     (By  Dr.  Spitta.    Low  magnification.) 


the  surrounding  liver  substance.  There  may  be  comparatively  well- 
formed  fibrous  tissue  from  chronic  pericholangitis,  but  the  chief  feature 
is  diffuse  small-cell  infiltration.  In  places  the  liver  cells  can  barely  be 
recognised,  and  the  condition  is  that  of  a  commencing  abscess. 


668  DISEASES    OF   THE    BILE-DUCTS. 

CLINICAL  PICTURE. 

• 

The  patient  is  feverish,  has  rigors,  and  suffers  from  loss  of  appetite, 
nausea  and  vomiting,  marked  prostration,  and  loss  of  fiesh.  The  liver, 
which  is  found  to  be  much  enlarged,  smooth,  and  tender,  progressively 
increases  in  size  as  the  disease  goes  on.  The  spleen  is  also  enlarged. 
Jaundice  is  often  present,  but  depends  more  on  the  cause  of  the  cholan- 
gitis than  on  the  disease  itself.  Thus  jaundice  accompanies  suppu- 
rative cholangitis  due  to  gall-stones,  worms  in  the  ducts,  rupture  of 
hydatid  cysts  into  the  ducts,  and  is  often  present  when  the  suppurative 
process  is  associated  with  new-growth  involving  the  ducts.  But  when 
there  is  no  independent  local  condition  sufficient  to  produce  jaundice, 
suppurative  cholangitis  may  run  its  course  without  jaundice.*  This  is 
difficult  to  explain  at  first  sight,  since  in  catarrhal  cholangitis  jaundice 
is  such  a  prominent  feature.  It  seems  reasonable  to  believe  that  the 
absence  of  jaundice  may  depend  on  the  hepatic  lymphatics,  which  should 
carry  the  bile  into  the  general  circulation,  being  impermeable  from  in- 
flammatory changes. 

In  the  following  case  there  was  only  very  slight  jaundice: 

A  man  aged  twenty-nine  years  was  admitted  mider  my  colleague,  Dr.  Penrose, 
to  St.  George's  Hospital  in  May,  1897,  in  an  extremely  grave  condition,  with  a 
large  tender  liver,  an  anaemic,  sallow  complexion,  slight  ascites,  and  a  history  that 
two  weeks  ago  ho  had  had  fever  and  jaundice.  Two  and  a  half  years  ago  he  had 
had  appendicitis.  The  temperature  was  subnormal."  At  a  consultation  various 
opinions  were  expressed,  such  as  pylephlebitis  secondary  to  appendicitis,  suppura- 
tive cholangitis  associated  with  calculi,  abscess,  and  rapid  new-growth  of  the  liver. 
The  following  day  an  exploratory  operation  was  performed,  and  a  nodule,  which 
might  have  been  either  new-growth  or  early  inflammatory  change,  was  cut  into. 
Microscopic  examination  showed  altered  liver  cells.  The  patient  died  two  days 
later.  At  the  autopsy  the  liver  Aveighed  7  pounds  and  showed  suppurating  areas 
around  the  bile-ducts  in  the  liver;  the  larger  extra-hepatic  bile-ducts  contained 
mucus.  There  were  no  calculi  in  the  gall-bladder.  The  portal  vein  was  normal. 
The  spleen  was  large  and  soft,  weighing  17  ounces.     The  appendix  was  quite  normal. 

Pain  may  be  due  to  peritonitis  on  the  surface  of  the  liver  set  up  by 
suppuration  in  the  ducts  under  the  capsule,  and  is  worse  on  respiration 
and  on  movement.  Colicky  pain  may  be  set  up  by  factors  underlying 
the  acute  infection,  such  as  gall-stones,  the  rupture  of  hydatids  into  the 
ducts,  or  worms  in  the  ducts.  Pseudo-gall-stone  colic  may  also  occur 
when  malignant  disease  involves  and  obstructs  the  ducts.  In  some  in- 
stances pain  is  entirely  absent. 

Septic  absorption  which  gives  rise  to  the  severe  constitutional  symp- 
toms may  lead  to  diarrhoea.  From  local  or  general  peritonitis  secondary 
to  leakage  of  abscesses  on  the  surface  of  the  liver  abdominal  distension 
may  come  on  before  death. 

Complications. — In  addition  to  local  or  general  peritonitis  from 
leakage  or  rupture  of  the  suppurating  areas,  general  haemic  infection  may 
occur.  Pus  and  micro-organisms  may  pass  into  the  hepatic  veins  and 
so  reach  the  lungs  and  give  rise  to  pytemic  abscesses,  pleurisy,  and  em- 
pyema.    Infective  endocarditis  may  be  induced  in  the  same  way,  and 

*  Vide  Gilbert  and  Lereboullet :  Bull,  et  Mem.  Soc.  Med.  d.  Hop,  Paris,  1900. 
[Les  angiocholitis  Anicteriques],  3d  series,  xvii,  477. 


SUPPURATIVE    CHOLANGITIS.  669 

when  the  infective  agents  have  g'ot  into  the  general  circulation,  the  joints, 
meninges,  etc.,  may  be  affected. 

Duration. — Suppurative  cholangitis  may  supervene  in  chronic 
catarrhal  cholangitis,  so  that  the  duration  is  difficult  to  fix  with  accuracy. 
In  most  cases  where  the  disease  comes  on  acutely  it  lasts  about  three 
weeks.  In  exceptional  instances  where  the  suppurating  ducts  have  dis- 
charged into  the  colon,  bronchus,  etc.,  the  course  of  the  disease  is  much 
prolonged.  Thus  Rogers  *  describes  cases  which  lasted  eighteen  and 
six  months  respectively.  The  importance  of  drainage  in  the  duration  of 
the  disease  is  shown  by  the  prolonged  course  of  bronchobiliary  fistulas 
which  in  the  majority  of  cases  are  due  to  suppurative  cholangitis. 

DIAGNOSIS. 

Fever  with  signs  of  grave  constitutional  disturbance  in  a  patient 
whose  liver  progressively  increases  in  size  and  who  has  had  symptom? 
in  the  past  pointing  to  gall-stones  are  the  features  of  importance.  Jaun- 
dice is  not  essential,  but  its  presence  is  in  favour  of  suppurative  cholan- 
gitis as  against  suppurative  pylephlebitis  and  tropical  abscess. 

The  differential  diagnosis  must  be  made  from  chronic  catarrhal 
cholangitis,  from  the  two  other  forms  of  intra-hepatic  suppuration, — 
pylephlebitis  and  tropical  abscess, — from  some  cases  of  new-growt,h  asso- 
ciated with  fever,  and  possibly  from  cases  of  acute  cirrhosis  with  jaundice. 

In  chronic  catarrhal  cholangitis  there  are  periodic  attacks  of  fever, 
pain,  and  intensification  of  jaundice,  while  in  the  intervals  the  patient 
is  comparatively  well.  In  suppurative  cholangitis  the  fever  is  continuous 
and  there  are  no  intervals  of  relief:  jaundice  is  less  marked,  while  the 
patient's  general  condition  is  much  graver. 

Pylephlebitis  is  accompanied  by  the  same  general  symptoms  and 
hepatic  enlargement  as  suppurative  cholangitis.  Jaundice  is  more  fre- 
quent, appears  earlier,  and  is  more  marked  in  cholangitis,  while  splenic 
enlargement  is  more  often  prominent  in  suppurative  pylephlebitis.  It 
must  be  remembered  that  these  two  conditions  may  be  combined.  In 
tropical  abscess  there  is  often  a  history  of  dysentery  and  there  may  be 
fluctuation  or  local  bulging  with  oedema  of  the  chest-wall.  In  cases 
where  the  abscess  is  deeply  situated  the  diagnosis  is  difficult.  The  history 
of  past  dysentery  or  gall-stones  is  in  favour  of  single  abscess  or  cholangitis 
respectively;  jaundice,  if  present,  makes  cholangitis  more  pr()])able.  But 
in  case  of  doubt,  the  rarity  of  suppurative  cholangitis  and  the  relative 
frequency  of  abscess  must  have  their  due  Aveight.  Very  rapid  new- 
growth  in  the  liver  accom]:>anie(l  by  fever  and  jauncUce  may  very  closely 
resemble  suppurative  cholangitis;  in  fact  in  some  cases  of  new-growth 
involving  the  ducts  suppurative  inflammation  of  the  ducts  occurs.  In 
the  absence  of  any  definite  evidence  of  new-growth,  such  as  a  palpable 
tumor,  the  diagnosis  may  be  possible  only  when  the  liver  is  freely  exposed. 
In  cases  of  acute  cirrhosis  with  fever,  jaundice,  and  enlargement  and 
tenderness  of  the  liver  the  resemblance  to  su]:)]mrative  cholangitis  is  very 

*  Rogers,  L. :  lirit.  Med.  Jour.,  19(«,  vol.  ii,  p.  70C). 


670  DISEASES    OF   THE    BILE-DUCTS. 

considerable.  In  cirrhosis  of  this  type  there  are  usually  a  marked  alco- 
holic history,  splenic  enlargement,  and  bsematemesis,  while  the  consti- 
tutional symptoms  are  less  severe  than  in  suppurative  cholangitis. 

PROGNOSIS. 

The  prognosis  depends  on  the  course  of  the  disease;  if  it  remains 
limited  to  the  large  ducts  or  is  operated  on  early  before  it  has  spread 
to  the  Hver  or  pancreas,  recovery  may  occur;  probably  some  cases  of 
empyema  of  the  gall-bladder  began  as  suppurative  cholangitis,  the 
original  lesion  having  passed  away.  If  it  invades  the  liver  and  sets  up 
multiple  abscesses  and  diffuse  suppuration  of  the  portal  spaces,  a  fatal 
termination  is  inevitable;  but  there  may  be  only  a  single  local  area  of 
suppuration  in  the  liver  and  the  outlook  is  then  much  better.  In  addi- 
tion to  its  course  and  complications,  much  depends  on  early  operation 
and  free  drainage.  When  a  bronchobiliary  fistula  or  a  communication 
between  the  biliary  abscess  and  other  hollow  viscera,  such  as  the  colon 
or  pelvis  of  the  kidney,  forms,  the  free  drainage  greatly  prolongs  hfe  and 
a  cure  may  even  result.  These  cases  of  fistulse  in  fact  differ  so  much  from 
the  rapid  course  of  suppurative  cholangitis  that  they  are  usuaUy  con- 
sidered as  a  separate  condition. 

TREATMENT. 

The  proper  treatment  is  surgical,  and  consists  in  obtaining  free  drain- 
age for  the  pus;  this  may  be  done  by  opening  the  dilated  ducts,  by  chole- 
cystotomy,  or  by  opening  biliary  abscesses  on  the  surface  of  the  liver. 

Medical  treatment  is  only  palliative,  but  it  may  be  combined  with 
surgical  treatment  and  then  be  of  distinct  use.  Salicylate  of  soda  should 
be  given,  inasmuch  as  it  is  a  cholagogue,  and  by  increasing  the  flow  of 
bile  tends  to  wash  out  the  bile-ducts. 


CHRONIC  CATARRHAL  CHOLANGITIS. 

Chronic  infective  or  catarrhal  cholangitis  may  be  diidded  into  two 
forms:  (i)  That  associated  with  and  largely  due  to  cholehtliiasis,  and 
(ii)  that  due  to  other  causes. 

The  form  of  chronic  cholangitis  associated  with  the  presence  of  a 
rail-stone  in  the  common  bile-duct  is  so  intimately  related  to  chole- 
lithiasis that  it  is  described  in  connexion  with  that  disease.  (Vide  In- 
termittent Hepatic  Fever,  p.  750.)  Non-calculous  chronic  catarrhal 
cholangitis  will  be  described  under  two  headings:  (A)  Chronic  catarrhal 
cholangitis  of  the  large,  extra-hepatic  bile-clucts,  and  (B)  chronic 
catarrhal  cholangitis  of  the  intra-hepatic  bile-ducts  (angiocholitis). 

(A)   CHRONIC   CATARRHAL   CHOLANGITIS   OF   THE    EXTRA-HEPATIC 
DUCTS  DUE  TO  CAUSES  OTHER  THAN  GALL-STONES. 

It  may  depend  on  chronic  gastro-duodenal  catarrh,  such  as  is  seen  in 
drunkards.     It  mav  occur  in  the  course  of  malignant  disease  of  the  Ywer 


CHRONIC    CATARRHAL    CHOLANGITIS.  671 

or  of  the  bile-ducts,  and  in  the  latter  condition  is  more  likely  to  supervene 
when  the  growth  is  at  the  biliary  papilla.  Suppuration  in  the  Uver  or 
hydatid  cysts  rupturing  into  the  bile-ducts  may  set  up  cholangitis  which 
may  be  catarrhal  at  first,  but  is  more  likely  to  become  suppurative.  In- 
fectious diseases,  such  as  tyjDhoid,  influenza,  pneumonia,  etc.,  may  play 
some  part  in  the  production  of  chronic  catarrh  of  the  bile-ducts.  Ty- 
phoid fever  and  influenza  may  set  up  an  acute  cholangitis,  and  probably 
this  may  leave  behind  it  a  chronic  catarrh.  How  often  they  may  set  up 
a  slight  degree  of  chronic  catarrh  without  any  previous  acute  inflamma- 
tion it  is  difficult  to  say.  In  these  cases  the  cholangitis  is  ascending  and 
'due  to  the  spread  of  inflammation  or  microbic  infection  from  the  duo- 
denum. There  are  some  cases  of  prolonged  catarrhal  jaundice  *  which, 
after  hanging  fire  for  weeks  and  months  'with  intermissions  and  exacer- 
bations, eventually  clear  up  completely.  It  seems  probable  that  in  these 
cases  there  may  be  an  underlying  chronic  infianmiation  of  the  common 
duct. 

Clinical  Aspect. — "When  supervening  on  acute  catarrh  the  jaundice 
remains  and  may  arouse  the  suspicion  of  malignant  disease  or  of  an 
impacted  calculus  in  the  common  duct.  The  chronic  jaundice  leads  to 
some  wasting  from  malnutrition.  It  varies  in  intensity  from  time  to 
time,  becoming  more  marked  after  attacks  of  fever  and  pain.  The  gen- 
eral features  are  those  of  chronic  relapsing  jaundice,  and  are  in  miniature 
the  same  as  those  of  intermittent  hepatic  fever  (vide  p.  752),  to  which 
the  reader  should  refer. 

The  inflammation  may  spread  u]3wards  to  the  liver,  and  in  very  rare 
instances  be  followed  by  acute  yellow  atrophy,  while  from  increased 
virulence  of  the  microbic  infection  suppurative  cholangitis  may  develop. 

The  diagnosis  of  chronic  catarrhal  inflammation  of  the  larger  bile- 
clucts  from  hypertrophic  biliary  cirrhosis  with  chronic  jaundice  must  be 
made  on  the  absence  of  the  marked  hepatic  and  splenic  enlargement. 

From  a  gall-stone  in  the  common  duct  with  chronic  infective  cholan- 
gitis the  diagnosis  is  very  difficult,  inasmuch  as  the  two  conditions  are 
much  the  same,  with  the  exception  of  the  presence  of  a  gall-stone.  In 
cholelithiasis  with  infective  cholangitis  there  tends  to  be  more  pain,  and 
the  attacks  of  intermittent  hepatic  fever  to  be  better  marked,  but  not 
uncommonly  there  is  no  history  of  cholelithiasis,  and  a  differential  diag- 
nosis between  these  two  closely  allied  conditions  may  not  be  justified. 
It  is  so  much  commoner  to  find  a  gall-stone  in  the  lower  end  of  the  com- 
mon duct  in  chronic  catarrhal  or  infective  cholangitis  tliat  this  condition 
should  be  diagnosed  in  an}^  doubtful  case. 

Treatment. — The  diet  should  be  simple,  and  milk  should  form  a 
large  amount  of  the  food.  Irritating  articles  of  diet  and  alcohol  must 
be  forbidden.  Calomel  and  saline  purges  should  be  giA'en  to  ])revent 
constipation  and  minimise  gastro-intestinal  catarrh;  for  tlic  latter  pur- 
pose alone  calomel  should  be  given  in  very  minute  doses  (^'y-  to  tjL-  gr.) 
three  or  four  times  daily,  while  salicylates  and  plenty  of  water  should  l)e 
taken  so  as  to  flush  out  the  bile-ducts.  Benefit  will  result  U-<^'a\  a  \isit 
*  Vide  Diculafoy:  Sem.  M<5d.,  1888,  p.  270. 


672  DISEASES    OF   THE    BILE-DUCTS. 

to  a   spa,  such  as  Harrogate,   Llandrindod,  Leamington,  Bath,  Vichy, 
Neuenahr,  Homburg,  Carlsbad,  etc. 

In  prolonged  cases  in  which  no  benefit  follows  medical  and  spa  treat- 
ment, the  question  of  operating  with  a  view  to  draining  the  ducts  should 
be  considered.  This  course  is  also  indicated  by  the  difficulty  of  elimi- 
nating the  presence  of  a  calculus  in  the  common  duct. 

Lejars  *  and  Quenu  t  report  cases  of  persistent  chronic  cholangitis,  which  were 
not  associated  with  cholehthiasis,  as  cured  by  operation. 

It  is  possible  that  some  of  the  cases  regarded  as  hypertrophic  bihary 
cirrhosis  in  which  cholecystostomy  and  drainage  have  been  followed  by 
a  cure  may  have  been  cases  of  chronic  infective  cholangitis. 

Guillot  t  gives  a  list  of  13  cases  of  chronic  hypertrophic  biliary  cirrhosis  or 
closely  allied  conditions  in  which  cholecystostomy  and  drainage  were  performed, 
mainly  by  Delageniere.     Recovery  followed  in  10. 

(B)    CHRONIC  CATARRHAL  CHOLANGITIS  OF  THE  SMALL  INTRA- 
HEPATIC BILE-DUCTS. 

Our  knowledge  of  chronic  cholangitis  of  the  intra-hepatic  bile-ducts 
(or  angiocholitis)  is  very  deficient  and  is  largely  theoretical.  It  may  be 
assumed  that  poisons  conveyed  to  the  liver,  either  by  the  portal  vein, 
in  cases  of  intestinal  autointoxication  or  by  the  hepatic  artery  in  general 
hsemic  infections  and  intoxications,  may  give  rise  to  catarrh  of  the 
intra-hepatic  ducts;  and  that  this  condition  complicates  other  diseases  of 
the  hver,  such  as  portal  cirrhosis,  chronic  venous  engorgement,  hepatitis, 
and  malignant  disease.  This  condition  occurs  in  hypertrophic  biliary 
cirrhosis  with  chronic  jaundice,  but  all  cases  of  chronic  catarrh  of  the 
intra-hepatic  ducts  do  not  conform  to  the  type  of  Hanot's  disease,  though 
the  conditions  are  allied  and  rec|uire  the  same  general  treatment.  The 
small  ducts  show  proliferation  of  the  lining  epithelium,  which  may  block 
up  the  lumen ;  there  may  be  some  dilatation  of  the  small  bile-ducts,  and 
there  is  pericholangitic  fibrosis. 

The  following  conditions  were  thought  to  be  due  to  chronic  angiocholitis,  but 
at  present  their  pathological  nature  requires  confirmation. 

Klippel  and  Vigouroux  §  describe  a  case  of  chronic  angiocholitis  with  hepatic 
insufficiency,  diarrhoea,  no  jaundice  or  enlargement  of  the  spleen,  in  which  signs 
of  acromegaly  developed.  The  authors  suggest  that  this  was  due  to  hepatic  in- 
sufficiency in  the  same  way  that  clubbed  (hippocratic)  fingers  develop  in  hyper- 
trophic biliary  cirrhosis.  The  liver  showed  angiocholitis  and  fibrosis  of  the  portal 
spaces. 

Lereboullet  ||  has  described  a  somewhat  similar  condition  under  the  name 
meta-icteric  splenomegaly.  Jaundice  due  to  angiocholitis  occurs  first,  gind  sub- 
sequently, as  it  recedes,  the  spleen  becomes  enlarged.  The  enlargement  of  the 
spleen  is  supposed  to  be  due  to  passive  venous  engorgement  produced  by  pressure 
on  the  branches  of  the  portal  vein  by  sclerosing  angiocholitis. 

Under  the  title  simple  family  cholsemia,  or  acholuric  jaundice  Gilbert  and 
Lereboullet  **  describe  a  common  condition  often  affecting  several  members  of  a 

*  Lejars:  Medical  Week,  1S97,  p.  139.        t  Quenu:  Medical  Week,  1897,  p.  1()3. 
%  Guillot:  Gaz.  hebdom.  de  Md^d.  et  de  Chirurg.,  Jan.  16,  1902,  p.  49. 
§  Klippel  and  Vigouroux:  La  presse  Medicale,  March  21,  1903. 
|l  Lereboullet:  Sem.  Med.,  1903,  p.  180. 
**  Gilbert  et  Lereboullet:  Bull,  et  Mem.  de  la  Soc.  des  Hop.,  May  30,   1901. 
Gaz.  hebdom.  de  Med.  et  de  Chirurg.,  Sept.  21,  p.  809.     . 


PERICHOLANGITIS.  673 

family,  especially  Jews  and  eastern  races,  in  which  jamidice  is  slight  and  bile-pig- 
ment is  present  in  the  blood  serum,  but  not  in  the  urine  (acholuria).  It  is  thought 
to  be  due  to  an  attenuated  chronic  biliary  infection  (vide  p.  39). 

The  clinical  manifestations  ascribed  to  this  diathesis  are  numerous,  and  include 
slow  pulse,  melancholia,  and  dyspepsia,  pigmentation  of  the  skin,  a  tendency  to 
xanthelasma,  pruritus,  hsemorrhages,  albuminuria,  and  other  manifestations,  such 
as  arthritis.  In  fact,  in  its  catholicity  the  condition  recalls  Murchison's  conception 
of  lithsemia. 

Cases  thought  to  be  due  to  chronic  catarrhal  inflammation  of  the 
small  intra-hepatic  ducts  should  be  treated  Avith  plenty  of  water  and 
occasional  courses  of  salicylate  of  soda,  so  as  to  wash  out  the  ducts  and 
remove  catarrh.  Minute  doses  of  calomel  (-^-^  gr.)  may  be  given  twice 
or  three  times  a  day  to  minimise  intestinal  fermentation,  and  the  bowels 
should  be  kept  freely  open  and  the  diet  should  be  simple  and  nourishing. 
Alcohol  should  be  forbidden.  Spa  treatment  on  the  same  lines  as  in 
chronic  catarrhal  cholangitis  of  the  larger  ducts  may  be  adopted.  The 
cases  of  simple  family  cholseinia  described  by  Gilbert  and  Lereboullet 
probably  require  httle  more  than  dietetic  treatment  and  the  general 
directions  necessary  to  prevent  constipation  and  dyspepsia. 


PERICHOLANGITIS* 

Pericholangitis  may  be  divided  into :  (a)  Extra-hepatic,  affecting  the 
larger  bile-ducts;  and  (5)  intra-hepatic.  Extra-hepatic  pericholangitis 
may  accompany  changes  in  the  larger  ducts,  but  is  entirely  subordinate 
to  that  condition. 

INTRA-HEPATIC  PERICHOLANGITIS. 

This  is  chiefly  of  pathological  interest,  since  it  either  occurs  as  part 
of  other  morbid  lesions  or  has  no  definite  clinical  associations.  It  is 
met  with  under  different  conditions  and  may  be  acute,  as  in  suppurative 
cholangitis,  of  which  it  forms  part,  or  may  be  chronic. 

Acute  pericholangitis  cannot  be  recognised  apart  from  acute  in- 
flammation in  the  portal  spaces,  such  as  suppurative  cholangitis  or  pyle- 
phlebitis, to  which  it  is,  as  far  as  is  known,  practically  always  secondary. 
It  is,  however,  quite  conceivable  that  an  acute  inflammation  of  the 
lymphatic  vessels  around  the  bile-ducts  might  occur  independently  of 
cholangitis.  It  might  be  set  up  by  an  abscess  in  the  liver.  But  there 
is  no  certain  knowledge  on  this  point. 

Chronic  Pericholangitis. — This  occurs  in  several  conditions  de- 
scribed elsewhere;  thus  pericholangitis  forms  part  of  hyioertrophic  biliary 
cirrhosis,  there  being  fibrosis  around  the  smaller  bile-ducts  from  extension 
of  inflammation  from  their  interior.  In  gall-stone  obstruction  with  in- 
fection of  the  ducts  there  is  a  varying  amount  of  fibrosis  surrounding 
the  ducts. 

In  a  case  of  enormous  dilatation  of  the  intra-liepatic  bile-ducts  in  which  the 
liver  was  like  a  hydroneplirotic  kidney,  there  was  very  marked  chronic  pericholan- 
gitis.     (Raynaud  and  Sabourin.*) 

*  Raynaud  and  Sabourin:  Archiv.  de  Physiol,  norm,  et  path.,  1878,  p.  37. 
43 


674 


DISEASES   OF  THE    BILE-DUCTS. 


In  the  condition  described  as  tuberculous  cavities  in  tlie  liver  the 
tuberculous  processes  begin  in  the  loose  tissue  surrounding  the  bile-ducts 
— ^tuberculous  pericholangitis. 


Fig.  84.— Drawing    of  Naked-eye  Appearance  of  a  Section  of  Liver  with  Chronic 
Pericholangitis  with  Secondary  Pylephlebitis. 


Material     Occupying 


Portal 


Fig.    85. — Photomicrograph    of    the    White-looking 

Space. 

It  is  composed  of  granulation  tissue.     The  central  space  represents  the  remains  of  the  portal 
vein,  which  in  this  instance  was  destroyed  by  secondary  suppurative  pylephlebitis. 


In  very  rare  instances  pericholangitis,  which  is  not  an  entirely  sub- 
sidiary part  of  cholangitis,  is  seen.  To  the  naked  eye  the  portal  spaces 
are  occupied  by  white  material  which  has  a  very  close  resemblance  to 


PERICHOLANGITIS.  675 

tubercle.  Strangeways  Pigg  and  I  *  described  a  case,  and  Morley 
Fletcher  f  has  since  given  an  account  of  another.  In  the  first  it  appeared 
probable  that  catarrhal  cholangitis  had  set  up  chronic  pericholangitis, 
while  Fletcher  took  the  view  that  the  pericholangitis  was  primary.  In 
our  case  there  was  secondary  suppurative  pylephlebitis,  while  in  Fletcher's 
the  portal  vein  was  healthy.  It  appears  probable  that  the  inflammation 
involves  the  portal  lymphatics;  in  our  case  the  glands  in  the  portal  fissure 
were  much  enlarged,  and  to  the  naked  eye  there  was  some  resemblance 
to  lymphadenoma. 

The  white-looking  material  in  the  portal  spaces  is  composed  of  granu- 
lation tissue  in  various  stages  of  development,  and  in  these  two  cases 
were  certainly  not  tuberculous.  It  contained  numbers  of  bile-ducts, 
many  of  which  were  proliferating  and  dilated. 

Clinically,  these  cases  showed  no  characteristic  features.  In  Morley 
Fletcher's  case  there  was  bronchiolectasis,  and  in  our  case  the  patient 
had  advanced  renal  disease  and  several  attacks  of  haemorrhage  from  the 
bowels. 

In  neither  of  these  cases  was  there  jaundice;  this  can  to  some  extent 
be  explained  by  supposing  that  blocking  of  the  lymphatics  prevented  the 
absorption  of  bile  by  the  lymph-channels. 

*  Rolleston  and  Strangeways  Pigg:  Journ.  Path,  and  Bacteriol.,  vol.  v,  p.  221, 
1898. 

t  Morley  Fletcher:  Trans.  Path.  Soc,  vol.  Hi,  p.  193. 


PARASITIC  AFFECTIONS  OF  THE  BILE-DUCTS. 

ASCARIS  LUMBRICOIDES. 

A  round  worm  in  the  duodenum  may  work  its  way  into  the  bihary 
papilla  and  common  bile-duct  and  give  rise  to  biliary  obstruction  and 
infection  of  the  ducts.  Cases  have  been  described  in  which  jaundice  has 
disappeared  after  the  passage  of  a  bile-stained  round  worm;  and  it  has 
been  reasonably  assumed  that  in  some  instances  the  head  of  the  worm 
has  temporarily  blocked  the  lower  end  of  the  bile-duct. 

Mertens  *  collected  48  cases  of  round  worms  in  the  bile-ducts,  and 
more  recently  Sick  f  has  brought  together  64  cases.  From  the  frequency 
of  ascarides  in  the  young  it  is  natural  that  some  of  the  cases  of  bile-duct 
infection  are  in  children. 

The  worms  dilate  the  bile-ducts,  carry  micro-organisms  with  them, 
and,  by  infecting  the  bile-passages,  give  rise  either  to  suppurative  cholan- 
gitis or  to  single  or  multiple  abscesses  in  the  liver. 

Roud  I  described  a  case  where  streptococci  and  colon  bacilli  were  found  in 
the  hepatic  abscesses,  which  also  contained  air. 

In  five  of  Mertens'  cases  gall-stones  were  associated  with  the  presence 
of  round  worms.  Hanot§  regards  the  cholelithiasis  as  due  to  the  infective 
agency  of  the  worms.  In  his  own  case  Mertens  believed  that  the  passage 
of  a  calculus  assisted  the  entrance  of  the  worm  by  dilating  the  passage. 

The  foUowLng  case,  recorded  by  Dr.  John  Davy,  1|  is  one  of  the  earliest  and 
illustrates  the  condition  well.  A  Maltese  boy  aged  two  years  who  died  from  dysen- 
tery was  found  to  have  numerous  round  worms  in  the  stomach,  small  intestines, 
colon,  and  liver.  The  common  and  hepatic  ducts  were  distended  with  worms,  and 
there  were  several  abscesses  in  the  liver,  containing  worms. 

There  is  an  excellent  specimen  (No.  533)  in  the  Cambridge  Pathological  Museum 
showing  the  common  bile-duct  distended  with  Ascaris  lumbricoides.  The  patient 
was  a  child.  The  duct  is  so  tightly  distended  that  jaundice  must  have  been  pro- 
duced, though  there  is  no  history  of  the  case. 

The  clinical  aspects  are  those  of  enlarged  liver,  jaundice,  fever, 
attacks  of  bihary  colic,  and,  in  a  word,  are  those  of  infective  cholangi- 
tis with  biliary  obstruction.  In  only  2  of  48  cases  collected  by  Mertens 
was  a  diagnosis  made  during  hfe.  The  diagnosis  depends  on  finding  the 
worms  or  their  ova  in  the  dejecta;  otherwise  the  cases  are  likely  to  be 
regarded  as  due  to  gall-stones. 

Treatment. — Santonin  should  be  given  if  the  presence  of  round 

*  Mertens:  Deutsch.  med.  Wochen.,  Bd.  xxiv,  S.  358,  1898. 
fSick:  Inaug.  Dissert.,  Tubingen,  1901.      Quoted  by  Neugebauer:   Archiv  f. 
klin.  Chirurg.,  Bd.  Ixx,  S.  584,  1903. 
J  Roud:  Thdse,  Lausanne,  1896. 

§  Hanot:  Archiv.  General,  de  Med.,  tome  cbcxvii,  p.  74. 
II  Davy,  J. :  Diseases  of  the  Army,  p.  423,  1862. 

676 


PARASITIC    AFFECTIONS    OF    THE    BILE-DUCTS.  677 

worms  is  suspected.  In  the  presence  of  signs  of  infection  of  the  common 
duct  the  duct  should  be  cut  down  upon  and  drained.  In  a  case  diagnosed 
as  a  calcukis  in  the  common  duct  recovery  followed  choledochotomy. 
(Neugebauer.*) 

DISTOMA. 

Several  species  of  distomida  may  be  met  with  in  the  bile-ducts  of  the 
liver  in  man. 

Distomum  hepaticum  is  commonly  found  in  sheep,  and  gives  rise  to 
the  disease  known  as  sheep-rot,  which  has  proved  disastrous  to  so  many 
sheep-farms.  In  very  rare  instances  men  have  become  infected  from 
taking  water  or  vegetables  containinated  with  the  dejecta  of  sheep  suf- 
fering from  the  disease.  Infection  with  Distomum  hepaticum  may  arise 
in  this  country,  which  is  not  the  case  with  the  other  varieties  of  distoma. 

As  far  back  as  1857  Budd,  who  added  an  appendix  to  his  work  on  the  liver, 
dealing  with  distoma  and  their  morbid  effects  in  sheep,  quoted  three  cases  of 
distoma  in  the  biliary  tract  of  man. 

Invasion  of  the  ducts  by  distoma  is  much  commoner  in  tropical  coun- 
tries, such  as  China,  Japan,  and  India.  Distomum  sinense  is  found  in 
India,  China,  Japan,  and  Tonkin.  In  Japan  20  per  cent,  of  the  inhabi- 
tants in  certain  low-lying  districts  are  affected.  (Baelz.f)  Distomum 
lanceolatum  and  Distomum  conjunctivum  have  been  met  with  in  the  bile- 
ducts  of  human  beings,  but  are  of  no  real  pathological  importance. 

Morbid  Anatomy. — The  distoma  cling  by  their  suckers  to  the  mucous 
membrane  of  the  bile-ducts,  which  become  dilated  and  inflamed  and 
contain  mucus  and  the  ova  of  the  wornxs.  Cystic  dilatations  varying 
from  the  size  of  hazel-nut  to  a  walnut  may  form  in  the  course  of  the 
ducts.  Fibrosis  from  pericholangitis  spreads  out  from  the  portal  spaces 
and  the  liver  cells  may  be  compressed.  Suppuration  may  occur  in  the 
dilated  bile-ducts.  The  liver  is  enlarged.  Scheube  J  suggests  that  the 
form  of  biUary  cirrhosis  so  common  in  native  Indian  children  around 
Calcutta  is  due  to  distoma,  but  does  not  give  any  proof  in  support  of 
this  view. 

Clinical  Aspect. — Though  sometimes  the  worms  remain  latent,  some 
of  the  following  symptoms  and  signs  may  be  expected:  Hepatic  pain 
and  enlargement  of  the  liver,  jaundice,  gastro-intestinal  disturbance, 
vomiting,  diarrhoea,  or  constipation,  fever,  enlargement  of  the  spleen, 
ascites,  oedema  of  feet,  and  anaemia.  The  cases  may  terminate  as  sup- 
purative cholangitis  or  abscess  in  the  liver,  and  the  prognosis  is,  therefore, 
bad.  The  diagnosis  depends  on  the  detection  of  the  ova  in  the  stools. 
The  treatment  consists  in  giving  vermicides,  such  as  Fihx-mas  and 
purgatives.  When  there  are  signs  of  suppurative  cholangitis,  the  com- 
mon bile-duct  should  be  opened. 

*  Neugebauer:  Archiv  f.  klin.  Chirurg.,  Bd.  Ixx,  S.  584,  1903. 

t  Berlin,  klin.  Wochen.,  1883,  S.  2.34. 

t  Scheube:  Diseases  of  Warm  Climates,  p.  304.     English  translation,  1903. 


678 


DISEASES   OF   THE    BILE-DUCTS. 


PSOROSPERMOSIS. 

The  invasion  of  the  bile-ducts  of  the  rabbit  by  psorosperms  or  the 
Coccidium  oviforme  is  extremely  common,  and  leads  to  the  production 
of  papillomatous  growths  from  the  mucosa  of  the  dilated  ducts,  which 
are  a  beautiful  demonstration  of  the  irritating  effects  of  a  parasite.  On 
section,  the  hver  shows  a  number  of  wliite,  caseous  areas  closely  resem- 
bling tubercles  to  the  naked  eye.  These  appearances  have  been  often 
described,  and  reference  may  be  made  for  a  detailed  account  of  the 
parasite  and  its  effects  to  Delepine's  *  paper.  Sometimes,  as  the  result 
of  secondary  infection,  acute  inflammation  is  set  up  in  the  ducts  and 
the  mucous  membrane  becomes  replaced  by  granulation  tissue — psoro- 
spermial  cholangitis. 


Fig.  86.— Shows  Section  of  Rabbit's  Liver  Under  a  Low  Power,  with  Papillomatous 
Growths  in  the  Dilated  Bile-duct  due  to  the  Irritation  of  Psorosperms.  (Photo- 
micrograph by  S.  G.  Penny,  Esq.) 

Psorospermial  invasion  of  the  human  liver  is  very  rare,  but  it  has 
been  more  often  described  in  the  liver  than  in  any  other  internal  organ 
of  the  human  body.  McFarlane  f  cohected  20  cases  of  human  psoro- 
spermosis, and,  omitting  supposed  psorospermial  affections  of  the  skin, 
such  as  Darier's  disease,  found  that  the  liver  was  affected  11  times,  the 
intestines  5  times,  the  kidneys  twice,  and  the  pleura  and  spleen  once 
each. 

A  case  of  calcification  of  a  psorospermial  tumor  removed  during  life  from  a  pa- 
tient who  was  thought  to  have  a  calcified  gall-bladder  is  put  on  record  by  Carrel.  J 
In  Silcock's  §  case  there  was  considerable  enlargement  of  the  liver,  which  weighed 
83  oimces.  The  spleen  and  intestines  were  also  affected,  and  psorosperms  were  cul- 
tivated for  two  months.     Podwyssozki  ||  has  reported  4  cases. 

*  Del^pine :  Trans.  Path.  Soc,  vol.  xli,  p.  348. 

t  McFarlane:  Journ.  of  Apphed  Microscopy  (Rochester,  U.  S.  A.),  1898,  vol.  i, 
p.  41.  %  Carrel:  Lyon  Medical,  tome  xciii,  p.  89,  1900. 

§  Silcock:  Trans.  Path.  Soc,  vol.  xh,  p.  320. 
II  Podwyssozki:  Centralbl.  f.  Bakt.  u.  Parasit.,  1889,  Bd.  vi,  S.  41. 


PARASITIC    AFFECTIONS    OF    THE    BILE-DUCTS. 


679 


It  is,  however,  not  unlikely  that  some  cases  have  been  overlooked 
and  the  lesions  regarded  as  caseous  tubercle,  and  that  a  microscopic 
examination,  if  undertaken,  would  have  revealed  the  presence  of  psoro- 
sperms.  The  coccidia  are  taken  in  food,  multiply  in  the  stomach,  and 
invade  the  common  bile-duct. 

Clinical  Aspect. — In  the  human  subject  the  symptoms  are  obscure. 


Fig.  87. 


-The  Same  Section  under  a  High  Power,  Showing  the  Coccidia  Loose  by  the 
Dilated  Bile-duct.     (Photographed  by  S.  G.  Penny,  Esq.) 


In  some  cases  there  have  been  fever,  enlargement  and  tenderness  of  the 
liver  without  jaundice,  and  prostration.  In  rabbits  increase  in  the 
number  of  eosinophile  leucocytes  has  been  observed  (Federici  *),  but  I 
am  not  aware  that  this  has  been  observed  in  man. 


PENTASTOMA  CONSTRICTUM. 

This  parasite  gains  entrance  to  the  alimentary  canal,  and,  reaching 
the  liver,  gives  rise  to  cysts,  especially  in  the  neighbourhood  of  the  fal- 
ciform Hgament,  which  are  thought  to  be  dilated  bile-ducts.  The  cysts 
contain  clear  fluid  and  a  single  coiled-up  parasite,  which  may  be  alive 
at  the  time  the  liver  is  examined  after  death.  The  walls  of  the  cyst  are 
composed  of  firm  fibrous  tissue  and  have  a  great  tendency  to  undergo 
calcification.  The  peritoneum  in  the  neighbourhood  of  the  cysts  may 
show  considerable  inflammation,  and  infection  of  the  lungs  may  occur. 
It  is  remarkable  that  though  the  parasite  gives  rise  to  inflammation  of 
the  peritoneum  and  lungs,  it  does  not  appear  to  irritate  the  intestines 
and  liver. 

Cysts  containing  the  parasite  have  been  observed  in  the  liver  by 

*  Federici:  Rivista  crit.  di  Clin.  Med.,  Aug.  23,  1902. 


680  DISEASES    OF   THE    BILE-DUCTS. 

Primer,*  Aitken,t  Girard,t  Chalmers. |  It  is  said  to  occur  only  in  negroes, 
but  this  is  not  correct,  as  there  is  a  specimen  of  a  hver  shoT\dng  five  cysts 
containing  the  parasite,  in  the  museum  at  Netley  (No.  1244),  taken  from 
an  Enghsh  soldier  who  died  of  spinal  caries.  Similar  cysts  containing  the 
Pentastoma  denticulatum  have  occasionally  been  met  vnth.  in  patients 
djdng  from  other  causes. 

PARAMCECIUM  COLI. 

Synonym:  Balantidium  eoli. 

This  parasite  is  very  common  in  the  colon  of  the  pig,  and  has  been 
found  in  the  intestines  of  man  in  association  with  diarrhoea.  In  the 
following  unique  case  the  parasite  was  found  in  the  liver  of  man: 

In  a  man  aged  fifty-nine  years  who  died  with  carcinoma  of  the  pylorus  Russell 
and  Buzzard  ||  found  a  dozen  cysts  the  size  of  peas  and  containing  living  paramoecia 
in  the  liver.  The  cysts,  which  had  firm  fibrous  walls,  were  probably  derived  from 
the  bile-ducts  and  due  to  the  irritation  set  up  by  paramoecia  which  had  travelled 
up  the  bile-ducts  from  the  duodenum.  The  cysts  did  not  show  any  papillary 
growths  resembling  those  in  psorospermosis  of  the  liver.  Inasmuch  as  the  patient 
died  from  gastric  carcinoma,  it  is  not  improbable  that  an  absence  of  HCl  in  the 
gastric  juice  allowed  these  organisms  to  develop  in  the  stomach.  No  proof  of 
this,  however,  is  forthcoming,  as  the  vomit  was  not  examined. 

*  Pruner:  Krankheiten  des  Orient,  1847,  S.  245.  _ 

t  Aitken:  Science  and  Practice  of  Medicine,  vol.  i,  p.  650,  1868. 

t  Girard:  Compt.  rend.  Soc.  biolog.  Paris,  1896,  tome  x,  p.  469. 

§  Chahners:  Lancet,  1899,  vol.  i,  pp.  1715,  1729. 

II  Trans.  Path.  Soc,  London,  vol.  1,  p.  149. 


INNOCENT  TUMORS  OF  THE  BILE-DUCTS. 

Innocent  tumors  of  the  bile-ducts  are  both  rare  and  of  httle  impor- 
tance. It  is  noteworthy  that  while  innocent  groA^1:hs  are  almost  eciually 
rare  in  the  bile-ducts  and  in  the  gall-bladder,  primary  mahgnant  disease 
is  much  commoner  in  the  gall-bladder. 

PAPILLOMA. 

Very  few  examples  of  papillomata  of  the  larger  extra-hepatic  bile- 
ducts  are  on  record,  but  it  is  probable  that  the  condition  is  not  quite 
so  exceptional  as  the  number  of  instances  put  on  record  would  lead  one 
to  beheve.  Some  of  the  cases  described  as  mahgnant,  but  not  examined 
microscopicall}^,  may  have  been  innocent. 

Chappet  *  speaks  of  a  case  as  carcinoma,  but  goes  on  to  say  that  the  growth 
was  developed  at  the  expense  of  the  mucosa,  which  was  not  ulcerated,  and  that 
the  other  coats  of  the  duct  were  httle  or  not  at  all  affected,  so  that  it  may  have 
been  an  innocent  papilloma. 

As  the  result  of  extensive  mucoid  change  taking  place  in  papillomata 
of  the  bile-ducts  a  condition  might  be  produced  such  as  that  described 
by  Wilks  and  Moxonf  in  a  cliild  aged  four  years  whose  common  bile- 
duct,  dilated  to  the  size  of  its  head,  contained  pendulous  myxomatous 
growths  with  muscular  fibres  in  them.  The  small  fatty  growths  de- 
scribed by  Wardell  J  as  obstructing  the  cystic  and  common  bile-ducts 
might  also  be  regarded  as  originally  papillomata  of  the  bile-ducts,  which 
subsequently  underwent  myxomatous  degeneration  and  then,  from  bile- 
staining,  took  on  a  yellowish  tinge,  suggesting  fat;  for  no  microscopic 
examination  appears  to  have  been  made.  Devic  and  Gallavardin  § 
quote  similar  cases  of  lipomata  arising  from  the  mucosa  of  the  bile-ducts 
recorded  by  Ehrmann  and  by  Dickmann.  Submucous  hpomata  occa- 
sionally arise  in  the  intestines,  so  it  is  quite  possible  that  the  same  growi;h 
might  be  found  in  the  bile-ducts. 

A  papillomatous  groA^i^h  from  the  inside  of  the  common  bile-duct,  analogous 
to  a  duct  papilloma  in  the  breast  or  to  a  polypus  of  the  intestine,  was  removed  by 
Sir  W.  Bennett  from  a  patient  at  St.  George's  Hospital.  It  was  close  to  a  gall- 
stone that  had  been  impacted  for  two  months.  ||  It  was  a  branching  papilloma, 
composed  of  a  basis  of  fibrous  tissue  covered  over  by  columnar  epitheliuni.  In 
places  the  connective  tissue  had  undergone  mucoid  degeneration.  The  after-history 
of  the  patient,  however,  rather  suggested  that  she  had  malignant  disease.  {Vide 
p.  684.) 

The  papillomatous  growths  in  rabbits'  intra-hepatic  bile-ducts,  due 
to  the  irritation  of  psorospeniLS,  are  extremely  common  and  well  known, 
but  a  similar  lesion  in  man  is  a  pathological  curiosity.     A  case  of  cystic 

*  Chappet :  Lvon  Medical,  t.  Lxxvi,  p.  146. 

t  Wilks  and  Moxon:  Pathology,  p.  485,  3d  ed.,  1889. 

t  WardeU:  Lancet,  1869,  vol.  ii,  p.  407. 

I  Devic  and  Gallavardin:  Rev.  de  Mdd.,  July,  1901,  p.  570. 

II  RoUeston :  Trans.  Path.  Soc,  vol.  xlv,  p.  S3,  and  Medical  Chronicle,  Jan.,  1896. 

681 


682 


DISEASES    OF   THE    BILE-DUCTS. 


tumors  of  the  bile-ducts  in  man  due  to  the  irritation  of  these  coccidia 
has  been  recorded  by  Podwyssozki.* 

Papillomatous  growths  of  the  intra-hepatic  ducts  are  the  same  as 
adenomata,  under  which  name  they  are  sometimes  described.  They  may 
be  multiple  and  give  rise  to  no  symptoms.  On.  the  other  hand,  there 
may  be  a  single  tumor,  and  in  either  case  they  may  become  cystic.  (Vide 
Adenoma  of  Bile-ducts.) 

Simple  papillomata  are  occasionally  seen  around  the  biliary  papilla 
in  the  duodenum,  but  are  growths  of  the  intestinal  surface  of  the  papilla 
and  not  of  the  bile-duct.  Papillomata  may,  however,  arise  in  the  cavity 
of  the  diverticulum  of  Vater.     Macphedran  f  has  described  a  case  which, 


Fig.  88. — Drawing  of  Papilloma,  of  the  Common  Bile-duct. 

There  is  some  adherent  mucus  on  the  surface  of  the  growth.     There  is  myxomatous  degeneration 

of  the  fibrous  core  of  the  papilloma.     (From  the  case  referred  to  in  the  text,  p.  681.)     X  40. 


like  most  of  the  cases  of  papillomatous  growths  around  the  duodenal 
orifice  of  the  biliary  papilla,  gave  rise  to  suppurative  cholangitis. 

Hydatid  Cysts. — Devic  and  Gallavardin  J  quote  three  cases  where 
hydatid  cysts  arose  in  the  walls  of  the  bile-ducts,  recorded  by  Cadet  de 
Gassicourt,  Ignatieff,  Macread3^ 

A  fibroma  the  size  of  a  bean  obstructing  the  lumen  of  the  bile-duct 
has  been  described,§  but  the  condition  is  practically  unique,  and  it  is 
possible  that  it  was  carcinomatous. 

*  Podwyssozki :  Centralbl.  f.  Bakt.  u.  Parasit.,  1889,  Bd.  vi,  S.  41. 
t  Macphedran,  A.:  Sajous'  Annual,  1899,  vol.  iv,  p.  422. 
i  Devic  et  Gallavardin:  Rev.  de  Med.,  July,  1901,  p.  571. 

§  Albers,  quoted  in  von  Ziem.ssen'.s  CyclopEedia  of  Practical  Medicine,  vol.  ix, 
p.  569,  1880. 


MALIGNANT   DISEASE   OF   THE   LARGER  (EXTRA-HEPATIC) 

BILE-DUCTS. 

Under  this  heading  primary  malignant  disease  of  the  extra-hepatic 
bile-diicts  will  be  dealt  with.  Wlien  carcinoma  arises,  as  it  probably 
does  in  an  appreciable  number  of  instances,  in  the  small  intra-hepatic 
bile-ducts,  the  condition  is,  for  all  practical  purposes,  primary  carcinoma 
of  the  liver.  Secondary  growths  very  rarely  occur  in  the  bile-ducts, 
though  in  multiple  malignant  groAvths  of  the  peritoneum  the  bile-ducts 
may  be  invaded  from  without.  Extension  of  growth  to  the  bile-ducts 
from  the  hilum  of  the  liver,  from  carcinomatous  glands  in  the  neighbour- 
hood, from  the  lesser  omentum,  or  from  the  pancreas  are  referred  to 
elsewhere.  Primary  carcinoma  of  the  ampulla  or  diverticulum  of  Vater, 
into  which  the  common  bile-duct  and  Wirsung's  duct  of  the  pancreas 
open,  is  very  much  the  same  as  primary  carcinoma  of  the  lower  end  of 
the  common  bile-duct,  but  a  separate  description  of  this  condition  is 
given  on  page  697. 

Incidence. — Malignant  disease  of  the  large  or  extra-hepatic  bile- 
ducts  is  probably  not  so  rare  as  has  been  thought,  or  as  might  be  gathered 
from  the  cases  put  on  record  in  the  past.  It  is  noticeable  that  within 
the  last  fifteen  years  the  number  of  cases  described  has  increased  four- 
fold. 

In  1889  Musser  *  collected  18  cases;  in  1897  P.  Claisse  t  tabulated  50;  in  1901 
Devic  and  Gallavardin,J  after  excludin.s;  doubtful  cases,  analysed  55  examples,  and 
I  have  notes  of  SO,  about  which  there  seems  no  doubt. 

The  disease  is  doubtless  commoner  than  is  thought,  since  it  ma3''be 
overlooked  or  more  probably  described  as  something  else.  Thus  some 
of  the  cases  recorded  as  malignant  disease  of  the  lesser  omentum  probably 
originated  in  the  bile-ducts.  Carcinoma  of  the  pylorus  may,  of  course, 
spread  up  into  the  gastro-hepatic  omentum,  but  if  there  is  no  primary 
source  such  as  this  for  carcinoma  of  the  lesser  omentum,  the  common 
bile-duct  should  be  suspected  and  carefully  examined. 

•Again,  in  some  of  the  cases  described  as  primary  malignant  disease 
starting  in  the  portal  fissure  and  involving  the  bile-ducts  the  growth 
may  well  have  started  in  their  walls. 

In  other  instances  a  slow-growing  fibrous  carcinoma  of  the  Ijile-ducts 
has  probably  been  described  as  a  simple  cicatricial  stricture.  In  fact, 
to  the  naked  eye  there  may  be  so  close  a  resemblance  that  a  microscopic 
examination  is  necessary  to  settle  the  question. 

*  Musser,  J.  H. :  Boston  Med.  and  Surg.  Journ.,  vol.  cxxi,  p.  581. 
t  Claisse,  P.:  Gaz.  des  Hop.,  1897,  p.  1279. 
X  Devic  and  Gallavardin:  Rev.  de  Med.,  1901,  p.  557. 

683 


684  DISEASES    OF   THE    BILE-DUCTS. 

ETIOLOGY. 

Zenker  *  believes  that  in  the  case  of  the  gall-bladder  a  papilloma  or 
an  adenoma  first  develops  and  subsequently  becomes  transformed  into 
an  adenocarcinoma.  I  have  seen  one  case  which  suggests  that  the  same 
sequence  might  occur  in  the  bile-duct, 

A  papilloma  was  remoA'ed  during  a  choledochotomy  from  the  bile-duct  of  a 
woman,  the  growth  being  in  immediate  contact  with  a  gall-stone  which  had  been 
impacted  for  about  two  months.  Some  months  later  the  patient  returned  with 
signs  compatible  with  the  view  that  the  gro'niih  had  recurred  in  the  region  of  the 
operation  woimd,  but  did  not  remain  under  observation.  I  showed  the  specimen 
to  the  Pathological  Society  f  as  an  example  of  a  papilloma  due  to  irritation  of  a 
gall-stone ;  later  on,  after  the  patient's  return,  the  question  arose  whether,  suppos- 
ing the  recurrence  to  be  carcinomatous,  the  growth  had  been  malignant  from  the 
first,  or  whether  the  growth  had  subsequently  invaded  the  duct-walls  after  the 
manner  of  a  duct  carcinoma  in  the  breast.  At  the  time  of  the  operation  there 
was  no  sign  of  any  infiltration  of  the  bile-duct,  so  that  if  the  recurrent  growth  Avas 
carcinomatous,  it  would  appear  that  a  transformation  from  a  simple  to  a  malignant 
adenoma  had  taken  place. 

It  is  quite  conceivable  that  carcinoma  may  siiper^^ene  on  an  ulcer 
of  the  bile-duct,  just  as  it  does  on  an  old  gastric  ulcer. 

In  a  woman  aged  fifty-seven  there  was  marked  stenosis  of  the  lower  end  of  the 
bile-duct,  thought  to  be  due  to  cicatrisation  of  an  ulcer  set  up  by  a  gall-stone. 
Microscopically  there  was  some  carcinomatous  invasion  of  the  wall.  (Krokiewicz.J) 
On  the  other  hand,  there  is  no  proof  that  it  was  not  a  carcinoma  from  the  first 
which  had  subsequently  ulcerated. 

Relation  to  Gall-stones. — In  carcinoma  of  the  gaU-bladder  there  is 
a  very  close  association  between  the  presence  of  gall-stones  and  carcinoma 
of  the  organ.  The  percentage  of  gall-stones  in  cases  of  carcinoma  of 
the  gall-bladder  has  been  put  as  high  as  95  per  cent.  (Siegert§.)  In 
primary  carcinoma  of  the  bile-ducts  there  is  a  marked  contrast,  gall-stones 
being  much  less  frequently  met  \vith. 

Thus  in  40  cases  collected  by  Devic  and  GaUavardin  ||  gaU-stones  were  present 
in  only  nine  instances — six  times  in  the  gall-bladder  and  on  three  occasions  in  the 
bile-ducts;  in  one  case  only  was  the  growth  found  to  surround  a  calculus.  In  62 
of  my  cases  in  which  a  definite  statement  as  to  the  presence  or  absence  of  gall- 
stones was  made  they  were  present  m  23  and  absent  in  39.  It  is  probable  that  in 
a  high  proportion  of  the  cases  where  no  statement  was  made  gaU-stones  were  absent. 

The  fact  that  gall-stones  are  not  so  commonly  met  with  in  bile-duct 
carcinoma  strongly  supports  the  conclusion,  formed  on  experimental 
grounds  (Mignot**),  that  calculi  are  not  formed  simply  as  a  result  of 
stagnation  of  bile  due  to  obstruction  set  up  by  the  growth.  Stagnation 
is  much  more  marked  in  bile-duct  carcinoma  than  in  similar  disease  of 
the  gall-bladder,  and  calcuh  are  less  common. 

Sex. — In  75  cases,  in  which  the  sex  is  recorded,  44  males  and  31 
females   were   affected.     This   contrasts    with   carcinoma   of  the  gall- 

*  Zenker:  Deutsch.  Archiv  f.  klm.  Med.,  Bd.  xliv,  S.  159. 
t  Trans.  Path.  Soc,  vol.  xlv,  p.  83. 

t  Krokiewicz:  Wien.  klin.  Wochen.,  March  21,  189S,  S.  320. 
§  Siegert :  Virchow's  Archiv,  Bd.  cxxxiii,  S.  353. 
II  Devic  et  GaUavardin:  Rev.  de  M6d.,  July,  1901,  p.  575. 
**  Mignot:  Archiv.  general,  de  Med.,  Aug.-Sept.,  1898. 


IMALIGNANT    DISEASE    OF    THE    LARGER    BILE-DUCTS.  685 

bladder,  in  which  females  are  attacked  four  times  more  frequently  than 
males. 

Age. — Primary  mahgnant  disease  of  the  bile-ducts  usually  occurs  after 
fifty  years  of  age.  This  was  so  in  52  of  my  73  cases.  In  Musser's  18 
cases  the  average  age  was  56.6  years,  and  in  my  73  cases  55.7  years;  in 
my  series  the  average  age  was  practically  the  same  in  the  two  sexes 
(55.7  in  males,  55.6  in  females) ;  the  extremes  were  81  years  in  a  woman 
and  29  in  a  man. 

MORBID  ANATOMY. 

Situation  of  the  Groioth. — Carcinoma  may  arise  in  any  part  of  the 
larger  bile-ducts,  but  it  is  very  rarely  observed  in  either  of  the  two  hepatic 
ducts. 

'  In  80  cases  the  situation  of  the  growth  was  as  follows : 

Common  bile-duct : 

Lower  end 21 

Middle  part 11 

Junction  of  common   bile-duct,  cystic,  and   common  hepatic 

ducts 25 

Conamon  hepatic  duct 18 

Right  or  left  hepatic  ducts 3 

In  cystic  duct 1 

In  cystic  duct  and  in  lower  end  of  bile-duct 1 

For  the  group  of  cases  in  which  the  growth  is  limited  to  the  conmion 
hepatic  duct  or  its  two  branches,  the  right  and  left  hepatic  ducts,  P. 
Claisse  *  has  suggested  the  term  juxtahepatic. 

Of  this  form  of  primary  carcinoma  of  the  ducts  Lecene  and  Pagniez  t  have  been 
able  to  collect  only  12  examples.  Ingebrans,t  dealing  with  practically  the  same  cases, 
tabulated  16.  When  juxtahepatic  carcinoma  attacks  the  lower  end  of  the  common 
hepatic  duct,  it  readily  spreads  to  and  occludes  the  cystic  duct  and  so  becomes 
carcinoma  of  the  junction  of  the  common,  cystic,  and  hepatic  ducts.  Devic  and 
GaUavardin  §  adopt  a  slightly  different  classification  and  divide  their  54  cases  into 
two  groups :  (a)  Those  where  the  gro^i;h  was  in  the  common  duct,  or  supraduodenal, 
22  cases;  and  (b)  juxta,  or  subhepatic,  32  cases;  among  this  latter  category  are 
included  cases  of  growth  at  the  junction  of  the  common  bile,  common  hepatic,  and 
cystic  ducts,  of  which  they  give  no  less  than  fifteen. 

When  the  cystic  duct  alone  is  affected,  the  condition  is,  both  anatomi- 
cally and  clinically,  much  the  same  as  carcinoma  of  the  neck  of  the  gall- 
bladder, and  is,  therefore,  more  conveniently  grouped  with  carcinoma 
of  the  gall-bladder.  Very  few  cases  of  carcinoma  limited  to  the  cystic 
duct  have  been  recorded;  this  is  probably  due  to  the  facts  that  it 
either  begins  close  to  the  gall-bladder  and  so  spreads  to  it,  or  that  it 
has  extended  into  the  junction  of  the  common  hepatic  and  common 
bile-duct  by  the  time  that  the  anatomical  facts  can  be  investigated. 

Appearance  of  the  Growth. — The  growth  is  firm  and  white,  and 
nearly  always  small — not  larger  than  a  cherry. 

*  Claisse,  P. :  Presse  Medicalc,  Nov.  6,  1897. 

t  Lecene  and  Pagniez:  Archiv.  general,  de  M6d.,  1901,  t.  clxxxvii,  p.  176. 

t  Ingebrans:  Archiv.  general,  de  Mod.,  Sept.,  1902,  t.  cxc,  p.  268. 

§  Devic  and  GaUavardin:  Rev.  de  M^>d.,  August,  1901,  p.  661. 


686 


DISEASES   OF  THE    BILE-DUCTS. 


Large  growths  are  most  exceptional — I  have  seen  one  as  big  as  an 
orange.  In  rare  instances  the  growtli  may  form  a  rather  diffuse,  infil- 
trating mass  around  the  structures  in  the  portal  fissure,  as  in  a  case 
described  by  Planteau  and  Cochez.* 

The  growth  may  be  villous  on  its  internal  surface,  but  this  appearance 
may  be  removed  l3y  ulceration;  in  connexion  with  this  villous  nature 
of  the  tumor  it  is  of  interest  to  refer  again  to  the  possibility  that  it  may 
start  as  an  innocent  papilloma  of  the  hning  membrane  of  the  duct.  Car- 
cinoma infiltrates  the  walls  of  the  duct  and  forms  a  firm  annular  stricture; 
this  locahsed  form  is  the  one  usually  met  with.     Occasionally  the  growth 

extends  in  the  walls  of 
the  ducts,  and  then 
transforms  them  into 
thick,  rigid  tubes.  By 
this  process  a  consider- 
able extent  of  the  com- 
mon bile-duct  or  even  of 
the  cystic  or  common 
hepatic  ducts  as  well 
may  be  converted  into 
carcinomatous  tubes. 

In  some  instances  the 
growth  projects  consid- 
erably into  the  lumen, 
and  may  thus  produce 
obstruction  rather  than 
by  an  annular  stricture. 
In  one  instance  two 
apparently  independent 
gro^\i:hs  were  found  at 
the  same  time  in  the  ex- 
tra-hepatic bile-ducts. 

Carcinoma  of  the 
common  bile-duct  pro- 
duces complete  biliary 
obstruction  during  life; 
after  death,  however,  the 
stricture  does  not  always 
appear  to  be  absolutely 
impervious.  It  is  probable  that  during  hfe  added  muscular  spasm 
makes  the  obstruction  absolute. 

Haemorrhage  occasionally  takes  place  in  connexion  with  the  growth. 
It  may  be  due  to  cholsemia,  to  erosion  of  a  blood-vessel,  or  possibly  to 
acute  hsemorrhagic  pancreatitis.  In  the  following  case,  which  I  exam- 
ined postmortem,  there  was  a  terminal  haemorrhage  in  the  neighbour- 
hood of  the  pancreas: 


^^ 


Fig.   89. — Drawing    of  Section    of   Common    Bile-duct 
WITH  Primary  Carcinoma. 
The  growth  projects  into  the  lumen  of   the  duct  and 
narrows  it.     The  muscular  walls  of  the  duct  are  infiltrated 
with  growth.      X  6. 


*  Planteau  and  Cochez:  Rev.  de  M6d.,  Jan.,  1903,  p.  70. 


MALIGNANT    DISEASE    OF    THE    LARGER    BILE-DUCTS.  687 

A  man  aged  forty-one  began  to  suffer  from  flatulence  in  1891  without  any  colic. 
In  the  autumn  of  1892  he  gradually  became  thin,  weak,  and  jaundiced.  He  was 
admitted  to  St.  George's  Hospital  under  the  care  of  Dr.  Whipham  on  December 
17,  1892,  deeply  jaundiced,  with  itching  of  the  skin,  distaste  for  fatty  food,  and 
general  weakness.  The  liver  was  enlarged,  and  the  motions  devoid  of  bile.  During 
May,  1893,  his  legs  became  cedematous  and  the  loss  of  strength  more  apparent. 
On  JNIay  18th  he  was  attacked  with  abdominal  pain,  the  abdomen  became  distended 
and  tender;  delirium  supervened,  and  haemorrhages  appeared  on  the  legs  before 
death.  At  the  autopsy  there  was  a  columnar-celled  carcinoma  of  the  lower  end 
of  the  common  bile-duct,  which  projected  down  into  the  duodenum  and  extended 
upwards  as  far  as  the  cystic  duct.  There  were  no  gall-stoiies  in  the  gall-bladder. 
There  were  secondary  nodules  of  growth  under  the  serous  coat  of  the  gall-bladder 
and  in  the  aortic  lymphatic  glands,  but  none  elsewhere.  The  liver  was  enlarged, 
and  the  ducts  dilated  and  full  of  greenish,  watery  fluid.  The  gall-bladder  was 
greatly  dilated  with  greenish  fluid,  unlike  bile.  There  was  a  large  recent  haemor- 
rhage aroiind  the  head  of  the  pancreas  and  the  bile-duct,  which  had  dissected  its 
way  up  between  the  layers  of  the  mesentery. 

Behaviour  of  the  Growth. — The  growth  is  usually  small,  and  does 
not  tend  to  infiltrate  adjacent  parts  widely.  It  may  grow  into  the  sub- 
stance of  the  pancreas,  liver,  or  the  portal  vein.  When  the  pancreas  is 
invaded,  the  resemblance  to  primary  malignant  disease  starting  in  the 
head  of  that  gland  is  very  close.  Histologically,  the  primary  pancreatic 
growth  is  almost  always  spheroidal,  while  that  in  the  ducts  is  columnar- 
celled  carcinoma. 

Carcinoma  of  the  duct  may  directly  infiltrate  the  portal  vein  and  give 
rise  to  portal  thrombosis.  As  already  mentioned,  the  growth  may  project 
into  the  lumen  of  the  duct  and  thus  obstruct  it.  It  may  extend  along 
the  walls  of  the  ducts  so  as  to  involve  widely  the  mucous  membrane  of 
the  biliary  tract,  or  it  may  spread  along  the  lymphatics  in  the  outer  coats 
of  the  ducts  and  thus  pass  into  the  liver. 

In  one  case  under  the  care  of  my  colleague.  Dr.  Penrose,  in  St.  George's  Hospital, 
a  growth  at  the  junction  of  the  common  bile,  cystic,  and  common  hepatic  ducts 
spread  up  along  the  side  of  tlie  hepatic  ducts  into  the  liver  and  produced  a  second 
stricture  of  the  left  hepatic  duct  inside  the  transverse  fissure.  In  Planteau  and 
Cochez's  *  case,  which  was  of  much  the  same  nature,  a  gro^viih  inside  the  left 
lobe  of  the  liver  was  shown  to  be  an  expansion  of  a  continuous  carcinomatous  in- 
filtration spreading  along  the  ducts. 

Naked-eye  Diagnosis  of  Primary  Carcinoma  of  the  Bile-ducts. — 

Wherever  it  starts,  the  growth  may  spread  along  the  ducts;  thus  a  con- 
siderable extent  of  the  common  duct,  together  with  the  common  hepatic 
duct  and  its  branches,  may  be  affected  at  the  same  time,  or  the  gall- 
bladder, cystic  duct,  and  the  common  bile-duct  may  be  infiltrated  in 
continuity.  In  such  cases  it  is  difficult  or  impossible  to  determine  its 
starting-point. 

Carcinoma  of  the  lower  end  of  the  bile-duct  may  spread  to  the  head 
of  the  pancreas,  and  so  present  much  the  same  naked-eye  appearances 
as  carcinoma  of  the  head  of  the  pancreas  involving  the  common  bile- 
duct.  It  is  probable  that  some  cases  described  as  carcinoma  of  the  head 
of  the  pancreas  in  reality  started  in  the  bile-duct.  ]\Iicroscopic  examina- 
tion shows  that  pancreatic  carcinoma  is  spheroidal-celled,  while  that  of 

*  Planteau  and  Coclioz:  Rev.  de  Mod.,  Jan.,  1903,  p.  70. 


688  DISEASES    OF   THE    BILE-DUCTS. 

the  bile-duct  is  almost  always  columnar-celled,  and  thus  provides  a  cri- 
terion for  deciding  the  origin  of  the  growth  in  any  doubtful  case. 

As  pointed  out  above,  carcinoma  of  the  bile-ducts  at  their  exit  from 
the  hver  merges  into  primary  carcinoma  of  the  hver;  carcinoma  of  the 
cystic  duct  resembles  malignant  disease  of  the  gall-bladder;  some  cases 
of  carcinoma  of  the  common  bile-duct  have  probably  been  described  as 
cancer  of  the  gastro-hepatic  omentum;  and  carcinoma  of  the  lower  end 
of  the  bile-duct  may  closely  resemble  disease  of  the  head  of  the  pancreas. 
The  disease  is  probably,  therefore,  less  rare  than  is  usually  thought. 

On  the  other  hand,  it  must  not  be  forgotten  that  mahgnant  disease 
of  the  gall-bladder,  or  more  rarely  of  the  pancreas,  may  spread  for  a  very 
considerable  distance  along  the  course  of  the  bile-ducts. 

Thus  in  a  remarkable  case  of  a  woman  aged  fifty-six  years  under  the  care  of 
my  colleague,  Mr.  (now  Sir)  W.  H.  Bennett,  in  St.  George's  Hospital,  a  spindle- 
celled  sarcoma  which  began  in  the  gall-bladder  spread  down  along  the  cystic  and 
common  bile-ducts  as  far  as  the  biliary  papilla.  In  a  case  of  Rose  Bradford's  * 
carcinoma  extended  from  the  gall-bladder  along  the  cystic  duct  into  the  common 
bile-duct  and  hepatic  duct,  the  growth  terminating  abruptly  in  all  directions. 

"WTien  carcinoma  arising  in  the  head  of  the  pancreas  involves  the  common 
bile-duct  and  spreads  along  its  walls  bej^ond  the  confines  of  the  pancreas,  it  may  be 
difficult  or  impossible  to  be  certain  of  the  starting-point  of  the  growth  until  a  micro- 
scopic examination  is  made,  a  spheroidal-celled  carcinoma  indicating  its  pancreatic 
origin.  Durante  f  describes  such  a  case  in  which  the  growth  appeared  to  invade 
the  duct  from  without. 

Microscopical  Appearances. — Primary  mahgnant  disease  of  the 
bile-ducts  is  always  a  carcinoma,  and  in  the  great  majority  of  instances 
a  columnar-celled  growth  derived  from  the  surface  epithelium. 

In  38  cases  which  I  have  analysed  the  tumor  was  a  columnar-ceUed  carcinoma 
in  33;  spheroidal-ceUed  in  4;  and  colloid  in  one  (Leith's  1).  In  many  cases  the 
description  is  too  vague  to  base  any  opinion  on,  the  growth  being  spoken  of  as 
"scirrhus,"  "  encephaloid,"  or  merely  as  carcinoma. 

It  is  possible  that  spheroidal-celled  carcinoma  of  the  bile-duct  may 
be  derived  from  mucous  glands  in  its  wall.  Mucoid  degeneration  of  the 
columnar  cells  leading  to  distension  of  the  alveoh  is  not  uncommon. 

In  a  certain  number  of  the  cases  of  columnar-celled  carcinoma  there 
is  a  transition  to  a  spheroidal-celled  character ;  this  change  is  commonly 
seen  in  carcinoma  of  other  organs,  such  as  the  mamma  and  gall-bladder, 
and  probably  depends  on  increased  rate  of  growth.  It  is  often  described 
as  an  atypical  carcinoma.  In  rare  cases  mucoid  or  allied  degenerative 
changes  in  the  epithehal  cells  induce  a  swoUen,  flattened  appearance, 
and  as  a  result  of  the  invagination  of  these  cells  an  appearance  closely 
resembling  squamous-celled  carcinoma  is  presented.  A  similar  condition 
occurs  in  primary  carcinoma  of  the  gall-bladder,  where  it  is  discussed. 
(Vide -p.  621.) 

I  am  indebted  to  Dr.  W.  C.  Bosanquet  for  the  section  from  which  the  accom- 
panying drawing  was  made.  In  some  parts  of  this  section  alveoli  formed  by  flat- 
tened epithelial  cells  contained  cholesterm  crystals. 

*  Bradford,  J.  R. :  Brit.  Med.  Journ.,  1898,  a-oI.  ii,  p.  1555. 

t  Durante :  Bull.  Soc.  Anat.  Paris,  1893,  p.  342. 

1  Leith:  Trans.  Med.-Chirurg.  Soc,  Edinburgh,  vol.  xv,  p.  59. 


:\L\LIGNANT    DISEASE    OF   THE    LARGER    BILE-DUCTS. 


689 


The  supporting  stroma  of  the  gro^\i:h  is  formed  of  well-formed  fibrous 
tissue,  shoT^ing  that  it  is  a  slow-gromng  tumor. 

Condition  of  the  Bile-ducts. — Below  the  growth  the  ducts  are  of 
their  normal  calibre;  it  is  possible  that  an  impacted  calculus  might  be 
situated  below  the  growth  and  distend  the  distal  portion  of  the  duct. 
Above  the  growi:h  the  ducts  are  dilated,  sometimes  to  such  an  extreme 
degree  as  to  allow  a  finger  or  a  thumb  to  be  introduced.  Dilated  bile- 
ducts  containing  mucus,  or  in  the  earh'  stages  bile,  may  project  as  eleva- 
tions on  the  surface  of  the  liver.  In  rare  instances  infective  cholangitis 
is  present. 


Fig.  90. — Microscopic  Drawing  of  Carcinoma  of  the  Common  Bile-duct. 
The  growth  is  columnar-celled  in  one  part,  but  has  the  appearance  of  a  squamous-celled 
growth  in  others.     The   latter  is  an  exceptional  appearance.     (From  a  specimen  lent  by  Dr. 
W.  C.  Bosanquet.) 


Condition  of  the  Gall-bladder. — AVlien  the  growth  is  in  the  common 
bile-duct,  the  gall-bladder  is  distended;  the  only  exception  to  this  is, 
when,  from  former  cholehthiasis,  the  gall-bladder  has  been  bound  down 
by  adhesions  and  retracted  on  itself. 

In  18  cases  where  the  growth  was  in  the  common  bile-duct  the  gall-bladder 
was  distended  in  17  (Devic  and  Gallavardin). 

^^Tien  the  growi^h  is  in  the  common  hepatic  duct,  the  gall-bladder 
is  nearly  always  small;  in  exceptional  in-stances  it  may  be  distended 
■with  mucus  from  concomitant  obstruction  of  the  cystic  duct,  or  may  be 
occupied  by  a  number  of  gall-stones.  When  the  growth  is  situated  at 
the  junction  of  the  cj'stic,  common  hepatic,  and  common  bile-ducts,  the 
gall-bladder  is,  as  a  rule,  not  enlarged,  but  from  irregularities  and 
44 


690  DISEASES    OF   THE    BILE-DUCTS. 

variations  in  the  degree  of  obstruction  to  the  different  ducts  correspond- 
ing differences  in  the  condition  of  the  gall-bladder  are  met  with. 

Secondary  growths  are  not  very  common,  probably  because  the 
primary  growth  proves  fatal  from  cholsemia  before  there  is  sufficient  time 
for  extensive  metastases.  They  are  most  often  found  in  the  liver.  In 
52  cases  the  Uver  was  affected  in  11.  Secondary  growths  may  also  arise 
in  the  adjacent  lymphatic  glands  and  in  the  peritoneum;  in  the  latter 
situation  they  may  produce  ascites.  Secondary  growths  very  seldom 
occur  when  the  primary  growth  is  in  the  common  hepatic  duct  or  in 
either  of  the  two  hepatic  ducts  (juxta-hepatic  form  of  carcinoma  of  the 
bile-ducts).  In  12  cases  of  juxta-hepatic  carcinoma  of  the  bile-ducts 
analysed  by  Lecene  and  Pagniez  *  there  was  no  instance  of  a  secondary 
growth. 

The  liver  shows  dilatation  of  the  bile-ducts,  first  with  bile,  but  later 
with  clear  mucoid  fluid.  The  organ  is  atrophi*ed  and  of  a  very  deep 
green  colour.  The  liver  cells  atro'phy,  and  there  are  areas  of  icteric 
necrosis. 

According  to  Futterer,t  this  icteric  necrosis  occurs  in  the  central  zone  of  the 
lobule,  the  intermediate  and  the  peripheral  zones  remaining  normal.  This  is  ex- 
plained on  the  theory  that  the  distension  of  the  interlobular  bile-ducts  compresses 
the  interlobular  channels  and  reverses  the  direction  of  the  flow  of  bile.  The  bile 
then  flows  into  the  periA^ascular  lymphatics  around  the  central  vein,  and  sets  up 
necrosis  of  the  neighbouring  liver  cells. 

The  hver  cells  contain  bile-pigment,  which  may  be  regarded  as  being 
in  the  radicles  of  the  bile  capillaries.  Around  the  necrosed  areas  small- 
cell  infiltration  and  the  formation  of  so-called  new  bile-ducts  are  some- 
times seen.  The  pseudocanalicular  formation,  which  is  by  no  means 
always  present,  is  an  attempt  at  compensation  on  the  part  of  liver  cells. 

In  the  majority  of  cases  there  is  no  cirrhosis  or  fibrosis  as  the  result 
of  biliary  obstruction.  The  atrophy  of  the  hver  cells  allows  the  existing 
fibrous  tissue  to  appear  more  prominent,  and  has  led  some  writers  to 
beheve  that  biliary  obstruction  produces  hepatic  fibrosis.  In  cases  where 
the  ducts  have  been  infected  there  may  be  pericholangitic  fibrosis.  It 
is  conceivable  that  hepatic  cirrhosis  may  have  existed  prior  to  the  devel- 
opment of  mahgnant  disease  of  the  bile-ducts,  or  that  some  fibrosis 
around  the  ducts  may  have  been  induced  by  cholangitis  due  to  gall- 
stones. 

Microbic  infection  of  the  ducts,  which  is  disposed  to  by  stagnation 
in  the  bile  channels,  may  give  rise  to  a  pericholangitic  cirrhosis,  or,  if 
more  acute,  to  suppurative  cholangitis,  empyema  of  the  gall-bladder, 
and  febrile  disturbance;  the  latter  events  are  more  likely  to  occur  when 
the  growth  is  situated  at  the  lower  end  of  the  common  bile-duct. 

CLINICAL  PICTURE. 

The  onset  is  usually  insidious,  and  generally  the  first  thing  noticed 
is  jaundice,  to  which  the  patient's  attention  may  be  called  by  his  friends. 

*  Lecene  and  Pagniez:  Archiv.  general,  de  M6d.,  1901,  p.  176. 
t  Fiitterer,  G. :  Chicago  Reporter,  vol.  xii,  April,  1897. 


MALIGNANT    DISEASE    OF   THE    LARGER    BILE-DUCTS.  691 

In  some  instances  there  may  be  an  acute  onset  of  gastro-intestinal  symp- 
toms, followed  by  jaundice  and  suggesting  ordinary  catarrhal  jaundice. 
Occasionally  somewhat  vague  dyspeptic  symptoms  exist  for  some  little 
time  before  the  appearance  of  jaundice.  In  a  few  cases  the  sudden  onset 
of  pain  followed  by  jaundice  imitates  the  impaction  of  a  gall-stone  in 
the  common  duct. 

Sjmiptonis. — Jaundice  is  necessarily  always  present;  it  steadily  pro- 
gresses, and  eventually  becomes  dark-green  or  black.  In  only  one  case, 
the  first  recorded,  has  jaundice  been  absent.  (Durand-Fardel.*)  There 
are  gastro-intestinal  symptoms,  furred  tongue,  foul  breath,  dyspep- 
sia, vomiting,  and  constipation,  which  may  alternate  with  diarrhoea. 
The  faeces  are  pale  and  devoid  of  bile-pigment.  There  may  be  distaste 
for  fatty,  or  indeed  for  all  food;  when  jaundice  is  advanced,  there  may 
be  small  gastro-intestinal  haemorrhages  from  cholsemia.  The  symptoms 
are  largely  those  of  jaundice  combined  with  progressive  loss  of  strength 
and  flesh.  Attacks  of  biliary  cohc,  which  may  be  due  to  cholelithiasis, 
but  are  usually  independent  of  the  presence  of  calculi,  are  met  with  occa- 
sionally; this  pseudo-gall-stone  colic  may  be  explained  as  due  to  spasm 
of  the  ducts  set  up  by  the  irritation  of  the  growth,  and  is  sometimes  seen 
in  malignant  disease  of  the  head  of  the  pancreas. 

Pain  of  a  dull  character  may  be  present  in  the  right  hypochondrium, 
but  is  occasionally  present  on  both  sides. 

Pain  is  sometimes  felt  in  the  epigastrium,  as  in  carcinoma  of  the 
head  of  the  pancreas,  and  may  then  be  due  to  invasion  of  the  head  of 
the  pancreas  by  a  growth  starting  in  the  lower  end  of  the  common  bile- 
duct.     This  form  of  pain  is  not,  as  a  rule,  a  marked  symptom. 

Itching  of  the  skin  usually  occiu's  when  jaundice  is  well  marked,  but 
occasionally  it  precedes  the  appearance  of  manifest  icterus,  though  it  is 
probably  then  the  earliest  result  of  the  bile  entering  the  circulation. 
Again,  in  some  instances,  there  may  he  little  or  no  itching,  even  when 
the  jaundice  is  very  deep. 

The  gall-bladder  tends  to  become  distended  as  a  result  of  backward 
pressure,  and  is  palpable  in  about  half  the  cases  as  a  uniform  smooth 
tumor.  The  smooth  surface  is  important  in  distinguishing  it  from 
primary  carcinoma  of  the  gall-bladder. 

The  gall-bladder  is  probably  always  enlarged,  except  when  the  growth 
involves  the  common  hepatic  or  hepatic  ducts,  but  it  is  not  necessarily 
palpable  during  hfe.  The  condition  of  the  liver  varies  considerably :  some- 
times it  is  enlarged  and  smooth  from  distension  with  bile ;  at  other  times, 
though  large,  it  is  concealed  by  tympanitic,  or  more  rarely  by  ascitic, 
distension,  while  it  may  ])e  of  the  normal  size.  Secondary  gro-wths  are 
very  seldom  felt  during  hfe;  in  fact,  there  is  hardly  time  for  generalisa- 
tion to  occur  -widely,  as  the  disease  kills  comparatively  rapidly  by  cho- 
lsemia. When  secondary  growths  are  present,  they  ma}'-  set  up  ascites 
by  pressing  on  the  portal  vein  or  by  irritating  the  peritoneum.  Ascites 
is  not  very  frequently  a  prominent  feature.  It  is,  however,  present  in 
*  Durand-Fardel:  Archiv.  gen.  de  Med.,  1S40,  p.  147. 


692  DISEASES   OF  THE    BILE-DUCTS. 

about  half  the  cases  examined  after  death  (Devic  and  Gallavardin  *), 
and  is  often  shght  in  amount  and  not  of  any  clinical  import. 

The  spleen  is  rarely  palpable.  In  Devic  and  Gallavardin's  55  cases 
it  was  noted  as  palpable  in  8. 

The  urine  is  diminished  in  quantity  and  deeply  bile-stained.  Occa- 
sionally albuminuria  is  recorded,  but,  as  a  rule,  there  is  no  albumin  or 
sugar.     Casts  are  present  without  albuminuria. 

The  progressive  jaundice  usually  lasts  about  five  or  six  months.  The 
patient's  condition  is  one  of  depression,  the  temperature  being  subnor- 
mal, unless  some  secondary  infection  occurs.  Xanthopsia,  when  every- 
thing the  patient  sees  has  a  yellow  tinge,  is  sometimes  present.  The 
usual  duration  of  jaundice — five  to  six  months — ^is  not  sufficiently  long 
to  allow  of  the  development  of  xanthelasma,  which  is  usually  associated 
with  jaundice  of  considerable  standing. t 

Pye  Smith, J  however,  has  briefly  recorded  xanthelasma  in  a  case  of 
primary  carcinoma  of  the  common  duct.  The  symptoms  of  biliary 
toxaemia  precede  death,  which  may  be  from  exhaustion,  coma,  or  de- 
lirium. The  biliary  toxsemia  is  due  to  two  factors :  (i)  a  general  poisoning 
of  the  blood  by  toxines  manufactured  in  the  alimentary  canal  and  nor- 
mally stopped,  and  either  destroyed  in  the  fiver  or  excreted  into  the  bile 
— ^this  is  due  to  a  failure  of  the  protective  or  detoxicating  function  of  the 
liver — and  (ii)  to  the  action  of  bilirubin  on  the  tissues.  Haemorrhages 
into  the  skin  and  severe  itcliing,  when  they  occur,  are  due  to  this  toxic 
condition  of  the  blood.  In  very  rare  instances  death  may  be  due  to 
peritonitis  set  up  by  perforation  of  the  gall-bladder.  In  a  case  recorded 
by  May  |  there  were  two  gall-stones  in  the  perforated  gall-bladder,  while 
in  Coats'  and  Finlayson's  ||  case  there  was  no  history  or  sign  of  chole- 
lithiasis. 

Death  may  in  very  rare  instances  be  due  to  haemorrhage  taking  place 
around  the  growth.  This  occurred  spontaneously  in  one  case  which  I 
examined  after  death,  and  is  a  source  of  danger  in  cases  where  any 
operative  measures — such  as  cholecystenterostomy — are  undertaken. 

Complications. — Besides  haemorrhage  around  the  growth  and  rupture 
of  the  gall-bladder,  suppurative  cholangitis  with  or  without  multiple 
miliary  abscesses  has  been  known  to  occur.  This  is  more  likely  to  super- 
vene when  the  growth  is  near  the  termination  of  the  common  bile-duct. 
As  in  cholelithiasis,  infective  endocarditis  has  been  known  to  develop, 
the  conditions  of  deep  jaundice  being  favourable  for  infection.  Throm- 
bosis of  the  portal  vein  was  found  in  Bourgeret  and  Cossy's  **  case. 

*  Devic  and  Gallavardin:  Rev.  de  M6d.,  Aug.,  1901,  p.  676. 
t  Vide  a  list  of  23  cases  of  xanthelasma  associated  with  jaundice  tabulated  in 
the  Transactions  of  the  Pathological  Society,  1882,  p.  381,  vol.  xxxiii. 
X  Pye  Smitli:  Trans.  Path.  Soc,  vol.  xxviii,  p.  243. 
§  May:  Munchen.  med,  Wochen.,  Bd.  xxxix,  S.  590,  1892. 
II  Coats  and  Finlayson:  Glasgow  Med.  Journ.,  vol.  xxxiv,  p.  84,  Aug.,  1890. 
**  Bourgeret  and  Cossy:  Bull.  Soc.  Anat.,  1873,  p.  347. 


MALIGNANT    DISEASE    OF    THE    LARGER    BILE-DUCTS.  693 


DIAGNOSIS. 

The  painless  onset,  the  steadily  progressive  character  of  the  obstructive 
jaundice,  eventually  becoming  dark  green,  the  age  of  the  patient, — ^viz., 
between  fifty  and  sixty, — and  the  absence  of  definite  proof  of  any  other 
cause  are  the  factors  which  suggest  malignant  disease  of  the  bile-ducts. 
But  as  it  imitates  persistent  obstructive  jaundice  due  to  other  conditions, 
it  will  be  advisable  to  consider  the  differential  diagnosis  between  them 
seriatim. 

Primary  carcinoma  of  the  head  of  the  pancreas,  though  it  does 
not  so  surely  compress  or  obstruct  the  common  bile-duct,  often  produces 
progressive  jaundice.  It  is  only  when  jaundice  is  present  that  the  ques- 
tion of  the  differential  diagnosis  from  primary  malignant  disease  of 
the  ducts  arises.  In  addition  to  jaundice,  both  these  conditions  may  or 
may  not  show  dilatation  of  the  gaU-bladder  during  hfe,  so  this  point 
is  of  no  use  in  the  diagnosis.  As  regards  pain,  that  of  pancreatic  car- 
cinoma is  epigastric,  but  from  extension  of  the  growth  to  the  bile-ducts 
it  may  trespass  into  the  hypogastric  region.  Enlargement  of  the  hver 
is  generally  absent  in  both,  though  it  has  been  thought  to  be  more  fre- 
quently seen  in  bile-duct  carcinoma,  and  secondary  growths  in  the  liver 
are  perhaps  more  often  present  in  pancreatic  cancer.  In  pancreatic 
disease  the  primary  tumor  is  seldom,  while  in  carcinoma  of  the  bile- 
ducts  it  is  almost  never,  palpable.  In  both  cases  the  cachexia  is  rapid, — 
perhaps  more  so  in  cancer  of  the  pancreas, — and  death  results  from 
cholsemia.  A  certain  amount  of  variation  with  regard  to  the  condition 
of  the  liver  and  gall-bladder,  and  in  the  site  of  pain,  may  occur  in  both. 
In  short,  a  diagnosis  between  the  two  cannot,  on  the  foregoing  grounds, 
be  made  with  any  approach  to  confidence,  and  since  pancreatic  car- 
cinoma is  the  commoner,  it  would,  on  the  score  of  probabihties,  be  diag- 
nosed whenever  their  common  symptoms  are  presented.  When  carci- 
noma of  the  lower  end  of  the  bile-duct  spreads  into  the  pancreas,  it  may 
compress  Wirsung's  duct  as  well,  and  so  lead  to  practically  the  same 
morbid  condition  as  primary  carcinoma  of  the  head  of  the  pancreas 
compressing  the  bile-duct. 

When,  however,  the  bile-duct  alone  is  compressed,  the  interference 
with  digestion  and  assimilation  theoretically  should  be  much  less  than 
when  both  it  and  the  pancreatic  duct  are  obstructed,  as  generally  must 
occur  in  pancreatic  carcinoma.  Attention  has  been  called  to  the  presence 
of  large  quantities  of  solid  fat  *  in  the  motions  in  obstruction  of  the 
jDancreatic  duct,  and  to  a  special  alteration  t  of  the  faeces,  depending  on 
the  absence  of  the  pancreatic  juice  from  the  intestine.  In  cases  of  ob- 
struction of  both  ducts  the  faeces  sometimes  show  a  great  excess  of  fat 
over  that  met  with  when  the  bile-duct  alone  is  obstructed,  but  whether 
those  features  are  sufficiently  constant  to  be  characteristic  remains  to 
be  proved  by  more  systematic  examinations  and  is  worth  investigation. 

At  present  it  must  be  admitted  that  a  certain  diagnosis  between 

*  Harley,  G. :  Path.  Trans.,  vol.  xiii,  p.  118.  Harley,  V.:  Path.  Journal,  vol. 
iii,  p.  246.   "  t  Walker,  T.  J. :  Medico-Chirurg.  Trans.,  vol.  Ixxii,  p.  257. 


694  DISEASES    OF   THE    BILE-DUCTS. 

primary  carcinoma  of  the  bile-ducts  and  that  of  the  head  of  the  pancreas 
cannot  be  made.  By  means  of  his  ''pancreatic  reaction"  Cammidge* 
is  able,  by  examination  of  the  urine,  to  distinguish  cases  in  which 
the  pancreas  is  the  site  of  growth,  etc.,  from  those  in  which  it  is 
unaffected.  In  a  recent  case  of  carcinoma  of  the  lower  end  of  the 
common  hepatic  duct  under  my  care  this  reaction  was  negative.  The 
same  is  probably  true  as  regards  differential  diagnosis  between  primary 
carcinoma  of  the  common  bile-duct  and  carcinoma  of  the  ampulla  of 
Yater.     This  point  is  considered  more  in  detail  on  page  701. 

Gall-stones,  impacted  or  lying  in  the  conunon  bile-duct,  should  be 
indicated  by  a  distinct  history  of  biliary  colic  immediately  preceding 
the  onset  of  jaundice.  But  in  a  patient  whose  cystic  and  common  bile- 
ducts  are  already  dilated  by  the  passage  of  gall-stones,  impaction  of  a 
calculus  may  occur,  especially  near  the  duodenum,  without  any  satisfac- 
tory history  of  its  occurrence.  In  about  a  third  of  the  cases  of  carcinoma 
of  the  bile-ducts  calculi  are  found  postmortem  in  the  gall-bladder,  and 
in  a  small  proportion  of  these  bihary  colic  has  occurred  in  life.  Con- 
versely, pseudo-gall-stone  colic  may  possibly  occur  in  cases  of  mahgnant 
disease  affecting  the  bile-ducts  in  the  absence  of  any  calcuh.  When 
bihary  colic  immediately  precedes  the  development  of  icterus,  the  diag- 
nosis of  cholehthiasis  is  more  probable,  but  since  impaction  of  the  gall- 
stones in  the  common  duct  may  take  place  without  a  characteristic  his- 
tory, it  is  desirable  to  consider  any  further  points  which  bear  on  the 
diagnosis  of  gall-stone  obstruction  from  that  due  to  bile-duct  carcinoma. 
The  duration  of  calculous  jaundice  is  very  much  longer  than  that  of 
carcinoma  of  the  bile-ducts,  and  death,  when  it  occurs,  is  usually  due 
to  some  complication,  such  as  suppurative  cholangitis,  rather  than  to 
cholsemia.  This  difference  in  the  course  of  the  two  affections  is  correlated 
with  a  difference  in  the  nature  of  the  obstruction  in  each  case.  In 
malignant  disease  the  obstruction  becomes  more  marked,  and  in  nearly 
all  cases  absolute  as  time  goes  on,  whereas  exactly  the  reverse  holds 
good  with  gall-stone  impaction;  the  obstruction  is  complete  at  first, 
but  subsequently,  from  the  constant  pressure  exerted  from  ■v^dthin  by 
the  calculus  on  the  wall  of  the  bile-duct,  from  inflammation,  and 
to  some  extent  from  extension  of  the  dilatation  of  the  ducts  above 
the  obstruction,  the  walls  of  the  duct  become  somewhat  separated  from 
the  calculus,  and  the  obstruction  becomes  partial  or  so  slight  that  eventu- 
ally the  jaundice  may  almost  disappear.  In  gall-stone  obstruction  of 
the  common  duct  periodic  attacks  of  intermittent  hepatic  fever  usually 
occur  {vide  p.  750)  which  are  Cjuite  characteristic  of  tliis  condition. 

The  course  and  duration  of  the  diseases,  if  uninterrupted  by  surgical 
treatment,  are  therefore  sufficiently  distinct  to  enal3le  a  differential  diag- 
nosis to  be  made,  though  this  may  not  be  possible  in  the  earher  stages. 

Coun^oisier's  law,  namely,  that  in  calculous  obstruction  of  the  common 

bile-duct  the  gall-bladder  is  not  enlarged,  while  in  obstruction  of  that 

duct  by  new-gro^\i:h  the  gall-bladder  forms  a  palpable  tumor,  should 

always  be  borne  in  mind.     But  the  gall-bladder  need  not  be  enlarged 

*  Cammidge,  P.  J.:  Lancet,  1904,  vol.  i. 


MALIGNANT    DISEASE    OF   THE    LARGER    BILE-DUCTS.  695 

in  all  cases  of  carcinoma  of  the  bile-ducts.  Thus  when  carcinoma  arises 
in  the  common  hepatic  or  in  either  of  the  hepatic  ducts,  the  gall-bladder 
is  not  enlarged,  and  there  may  be  difficulty  in  diagnosing  the  condition 
from  impacted  calculus  in  the  common  duct.  But  in  a  doubtful  case  en- 
largement of  the  gall-bladder  is  in  favour  of  the  obstruction  being  due 
to  mahgnant  disease  and  not  to  gall-stones  in  the  common  duct.  The 
following  points,  trhen,  w^oulcl  be  in  favour  of  cholelithiasis:  The  history 
of  colic  immediately  prececUng  the  onset  of  jaimdice;  intermittent  hepatic 
fever;  the  chronic  nature  of  the  illness;  the  absence  of  enlargement  of 
the  gall-bladder,  and  the  fact  that  although  of  considerable  duration, 
the  jaundice  is  not  very  deep  or  progressive. 

In  primary  malignant  disease  of  the  gall-bladder,  so  long  as 
the  groA^i:h  remains  limited  to  the  gall-bladder  and  there  is  no  pressure 
on  the  hepatic  or  common  ducts,  jaundice  is  absent,  and  there  is  little 
resemblance  between  this  disease  and  primary  carcinoma  of  the  ducts. 
The  jaundice  is,  therefore,  no  essential  part  of  the  cHsease,  and  is  due 
either  to  extension  of  the  primary  gro^\^h  or  to  pressure  exerted  by 
secondar}"  groMhs  on  the  bile-clucts.  It  occurs  in  the  course  of  more  than 
half  the  cases — according  to  Musser,  in  69  per  cent.,  which  is,  curiously 
enough,  also  the  proportion  in  wliich  gall-stones  were  present  in  his  100 
cases  of  carcinoma  of  the  gall-bladder.  When  jaundice,  due  to  obstruc- 
tion of  the  duct,  has  supervened,  the  case  is  for  all  practical  purposes 
one  of  malignant  disease  both  of  the  gall-bladder  and  of  the  bile-ducts. 
This  condition  is  even  less  amenable  to  palliative  operative  treatment 
than  mahgnant  disease  of  the  common  bile-duct;  for  in  the  latter  con- 
dition the  operation  of  cholecystenterostomy  can  be  resorted  to  for  the 
relief  of  cholsemia  with,  a  fair  prospect  of  success.  In  carcinoma  of  the 
gall-bladder  there  may  be  a  tumor  in  its  situation,  which  is  knobby  or 
irregular,  and  is  not  so  large  as  the  smooth,  dilated  gall-bladder  fre- 
quently met  with  in  carcinoma  of  the  bile-ducts  or  of  the  head  of  the 
pancreas.  In  addition  to  the  history,  the  ^'ery  frec{uent  association 
(80-95  per  cent.)  of  gall-stones  with  carcinoma  of  the  gall-bladder 
should  be  kept  in  mind. 

In  malignant  disease  of  the  liver,  whether  primary  or  secondary, 
with  jaundice,  the  histor}-  of  the  case  and  the  facts  that  the  liver  is 
considerably  enlarged  and  manifestly  infiltrated  with  gro\\i:h  and  that 
the  jaundice  is  not  so  extreme,  or,  as  a  rule,  of  such  long  duration,  will 
ser^^e  to  differentiate  it  from  ])rimary  carcinoma  of  the  ducts. 

From  hypertrophic  biliary  cirrhosis  there  vaW  seldom  be  an}^  real 
difficulty  in  diagnosis.  In  some  exceptional  cases  of  bile-duct  carcinoma 
the  spleen  is  enlarged,  ]:)ut  not  to  the  same  extent  as  in  biliars''  cirrhosis. 
The  latter  disease  occurs. in  younger  persons,  runs  a  chronic  course, 
measured  by  years  and  not  b}'  months,  and  presents  much  greater  enlarge- 
ment of  the  liver  and  spleen. 

Catarrhal  jaundice  is  usualh'  ushered  in  Ijy  vomiting  and  diarrhoea, 
while  the  onset  of  jaundice  due  to  malignant  stricture  of  the  bile-duct 
is  usually  unobtrusive  and  iniaccompanied  by  signs  of  gastro-intestinal 
catarrh.     But  the  course  of  the  two  is  so  diflferent — the  one  passing 


696  DISEASES   OF   THE    BILE-DUCTS. 

almost  spontaneously  away  in  a  few  weeks,  the  other  getting  progres- 
sively worse — ^that  even  if  at  first  there  be  difficulty  in  determining  which 
is  the  cause  at  work,  little  doubt  remains  after  a  few  weeks  have  gone  by. 

There  are  a  number  of  other  causes  which  may  sometimes  give  rise 
to  chronic  jaundice  of  varying  degree,  such  as  secondary  malignant 
disease  in  the  portal  fissure,  growths,  tumors,  or  hydatid  cysts  in  con- 
nexion with  the  liver,  inflammatory  adhesions,  or  even  possibly  gummata 
implicating  the  ducts,  aneurysms  of  the  hepatic  artery  or  of  the  ab- 
dominal aorta — in  short,  most  of  the  tumors  and  many  of  the  morbid 
conditions  to  be  met  with  in  the  abdominal  cavity  (vide  p.  541). 

But  the  question  of  diagnosis  will  seldom  arise  between  them  and 
primary  malignant  disease  of  the  ducts,  inasmuch  as  there  will  generally 
be,  either  in  the  history  or  in  the  physical  signs  and  symptoms,  a  clue 
to  the  nature  of  the  disease. 

TREATMENT. 

The  treatment  of  cases  thought  to  be  malignant  disease  of  the  bile- 
ducts  has  usually  been  confined  to  relieving  symptoms  and  alleviating 
pain  and  distress,  and  an  attempt  to  prevent  putrefactive  changes  in 
the  intestines  by  antiseptics  and  by  an  appropriate  diet.  The  palliative 
and  symptomatic  treatment  is  that  of  obstructive  jaundice  (vide  p.  535). 
Pain  may  require  morphia;  pruritus,  bathing  with  carbolic  acid  lotion 
(1  :40)  or  the  application  of  a  dusting-powder  of  starch  (1  oz.),  oxide 
of  zinc  (.5ss),  and  camphor  (.5iss)  (McCall  Anderson);  antipyrin  inter- 
nally, or  hypodermic  injections  of  pilocarpine.  Chloride  of  calcium  may 
be  given  both  for  pruritus  and  to  prevent  haemorrhages.  Intestinal 
putrefaction  may  be  combated  by  minute  doses  of  calomel  (^V^To" 
gr.)  and  by  preventing  constipation  by  blue  pill  and  salines.  Cholsemia 
may  be  obviated  temporarity  by  intravenous  or  better  by  subcutaneous 
transfusion  if  it  is  thought  to  be  worth  while. 

Surgical  interference  has  not  been  much  in  vogue,  presumably 
because  radical  measures  are  very  difficult  and  the  disease  is  necessarily 
fatal.  Though  it  cannot  be  more  than  paUiative,  the  operation  of  putting 
the  gall-bladder  into  communication  with  the  small  intestine — cholecyst- 
enterostomy — will,  in  favourable  cases, — i.  e.,  where  the  obstruction  is 
limited  to  the  common  bile-duct, — ^prevent  the  bile  being  dammed  up 
in  the  Hver  and  absorbed  by  the  lymphatics  into  the  general  circulation. 
Jaundice  and  cholsemia,  with  their  attendant  symptoms,  may  thus  be 
obviated,  and  the  patient's  general  condition  greatly  improved.  As 
already  mentioned,  death  is  likely  to  occur  in  complete  bihary  obstruction 
from  cholsemia,  and  if  this  is  prevented,  life  may  be  greatly  prolonged.* 

In  a  case  of  biliary  obstruction  due  to  what  turned  out  to  be  malignant  disease  of 
the  pancreas  Reclus  f  performed  cholecystenterostomy  with  the  remarkably  suc- 
cessful result  that  the  patient  experienced  great  relief  and  survived  the  operation 
for  twenty-one  months,  eventually  dying  with  numerous  secondary  growtlis. 

*  For  the  surgical  treatment  of  carcinoma  of  the  bile-ducts  see  Terrier  ain 
Auvray:  Chirurgie  du  foie  et  des  Voies  biliaires,  1900;  Schwartz:  Chirurgie  du  foie, 
1900:  Mayo  Robson:  Diseases  of  the  Gall-bladder,  1904. 

t  Reclus:  Sem   Med.,  1893,  p.  569. 


CARCINOMA    OF    THE    AMPULLA    OF    VATER.  697 

Curative  Surgical  Measures. — The  resection  of  a  growth  from  the 
bile-duct  with  union  of  the  two  divided  ends  is  the  ideal  operation,  but 
it  is  extremely  difficult.  In  the  only  recorded  case  of  this  kind — Kehr's  * 
— ^in  which  a  carcinoma  at  the  junction  of  the  common  hepatic,  cystic, 
and  common  bile-ducts  was  resected,  it  was  impossible  to  unite  the  cut 
ends  of  the  conmion  bile-duct  and  hepatic  duct,  so  the  latter  was  im- 
planted into  the  duodenum,  the  cut  end  of  the  common  bile-duct  being 
ligatured.  This  case  recovered  from  the  operation,  and  it  may,  therefore, 
be  expected  that  further  successes  will  be  obtained.  Reference  to  re- 
moval of  growths  in  the  region  of  the  diverticulum  of  Vater  is  made  on 
page  702. 

Mahgnant  disease  of  the  cystic  duct  has  been  removed  (Warren  |), 
but  this  operation  is  more  allied  to  excision  of  the  gall-bladder  and  is 
not  so  beset  with  difficulties  as  resection  of  part  of  the  hepatic  or  common 
bile-ducts. 


CARCINOMA  OF  THE  AMPULLA  OF  VATER. 

The  common  bile-duct,  before  opening  into  the  duodenum,  joins  with 
the  main  pancreatic  duct;  this  common  portion  is  called  the  ampulla 
or  diverticulum  of  Vater.  Normally  the  mucous  membrane  of  the 
ampulla  contains  glands  (Pilliet  J)  and  is  thro^vn  into  folds.  It  thus 
appears  rougher  than  the  inside  of  the  common  bile-duct,  but  it  is  not 
dilated  except  under  very  definite  pathological  conditions,  such  as 
impaction  of  a  gall-stone.  Carcinoma  may  start  in  the  mucous  mem- 
brane of  the  ampulla,  or  may  spread  to  it  from  the  lower  end  of  the 
bile-duct  or  from  the  termination  of  the  pancreatic  duct. 

Busson,§  in  1890,  collected  11  cases  of  carcinoma  of  the  diverticulum  Vateri, 
and  in  1896  Vincent  Georges,  |1  a  pupil  of  Hanot's,  collected  9  more.  Hanot  ** 
added  another  later  in  the  same  year.  Of  these  21  cases  only  about  half  a  dozen 
are  genuine  examples  of  carcinoma  of  the  ampulla  of  Vater,  the  others  being  either 
carcinoma  of  the  lower  end  of  the  bile-duct  or  carcinoma  of  the  duodenal  surface 
of  the  biliary  papilla. 

I  have  collected  16  cases,tf  14  of  them  since  the  beginning  of  1896, 

*  Kehr:  Miinchen.  med.  Wochen.,  1903,  S.  101. 

t  Warren:  Boston  Med.  and  Surg.  Journ.,  March  15,  1900,  p.  276. 

jPiUiet:  Compt.  rend.  Soc  Biolog.  Paris,  1894,  p.  549. 

§  Busson :  These  de  Paris,  1890. 

i!  Vincent  Georges :  These  de  Paris,  1896,  No.  404. 
**  Hanot:  Archiv.  general,  de  Med.,  vol.  clxxviii,  p.  547.     Previous  cases  re- 
corded by  Hanot  are  given  in  Vincent  Georges'  thesis. 

ft  Durand-Fardell :  La  Presse  Medical,  1896.  Vincent  Georges :  These  de  Paris, 
1896,  No.  404.  Rendu :  Soc.  M6d.  des  Hop.,  May  1,  1896.  Hanot :  Archiv.  g^n^ral. 
de  Med.,  t.  clxxviii,  p.  547.  Pilliet:  Bull.  Soc.  Anat.  Paris,  1889,  p.  509.  Dommici: 
Bull.  Soc.  Anat.  Paris,  1896,  p.  709.  Maury:  Soc.  Med.  des  Hop.,  May  9,  1902,  p. 
433.  Comil  and  Chevassu:  Bull.  Soc.  Anat.  Paris,  1903,  p.  151.  May:  Miinchen. 
med.  Wochen.,  Aug.  16,  1892.  Scheuer:  Berlin,  klin.  Wochen.,  Feb.  17,  1902. 
Halsted:  Johns  Hopkins  Hosp.  Bull,  No.  103,  Jan.,  1900.  Pratt  and  Fulton: 
Boston  Medical  and  Surgical  Journ.,  June,  1900,  p.  599.  De  Havilland  Hall: 
Lancet,  1902,  vol.  i,  p.  1102.  Klotz:  Montreal  Med.  Journ.,  vol.  xxxiii,  p.  477, 
1904.  RoUeston:  Lancet,  1901,  vol.  i,  and  one  from  St.  George's  Hospital,  vide 
p.  702. 


698 


DISEASES    OF   THE    BILE-DUCTS. 


which  appear  to  be  undoubted  examjoles  of  carcinoma  arising  in  the 
mucous  membrane  lining  the  diverticulum  Vateri. 

Hanot  *  regarded  carcinoma  of  the  ampulla  of  Vater  as  distinct  from 
carcinoma  of  the  lower  end  of  the  bile-duct,  or,  as  it  is  called,  juxta- 
ampullary  carcinoma  of  the  common  bile-duct.  He  laid  stress  on  the 
fact  that  the  gro\\i:h  is  limited  to  the  ampulla  of  Vater,  and  does  not 
arise  in  the  common  bile-duct  or  in  the  duodenum.  He  spoke  of  the 
condition  as  cancer  du  pylore  pancreatico-hiliaire.  The  diagram  repre- 
sents his  views.  It  must  be  admitted,  however,  that  the  parts  are  so 
small  that  it  may  be  very  difficult  or  even  impossiole  to  distinguish  the 
form  arising  in  the  terixdnation  of  the  bile-duct  (vide  1,  in  diagram), 

from  that  arising  from 
the  lining  of  the  am- 
pulla (vide  4,  in  dia- 
gram), away  from  the 
opening  of  the  com- 
mon bile-duct. 

Primary  carcinoma 
of  the  ampulla  Vateri, 
or,  as  it  might  more 
conveniently  be  called, 
the  choledochopancre- 
atic  duct,  must  be 
also  distinguished 
from  primary  carci- 
noma attacldng  the 
m  u  c  o  u  s  membrane 
covering  the  duodenal 
surface  of  the  bihary 
papilla.  Specimens  of 
this  form  of  duodenal 
carcinoma  are  to  be 
found  in  the  muse- 
ums of  St.  Bartholo- 
mew's, Guy's,  and 
St.  Thomas'  Hospitals. 
This  lesion  seems  to  be  especially  prone  to  lead  to  infective  cholangitis 
and  intra-hepatic  suppuration.  Carcinoma  of  the  ampulla  of  Vater  must 
thus  be  distinguished  from  carcinoma  (1)  of  the  termination  of  the  com- 
mon bile-duct;  (2)  of  the  terixdnation  of  Wirsung's  duct;  and  (3)  of  the 
duodenal  surface  of  the  biliary  papilla.  The  accompanying  diagram  il- 
lustrates these  distinctions.  Confusion  maj^  also  occur  between  carcinoma 
of  the  head  of  the  pancreas  and  primary  carcinoma  of  the  ampulla 
Vateri.  Histologically  they  differ ;  carcinoma  of  the  pancreas  is  spheroidal- 
celled,  while  carcinoma  of  the  diverticulum  Vateri  is  columnar-celled. 

*  Hanot:  Archiv.  gen.  de  Med.,  vol.  clxxviii,  Nov.,  1896,  p.  547. 
t  For  this  figure,  which  illustrated  a  paper  of  mine  in  the   Lancet  of  Feb.  17, 
1901,  I  am  indebted  to  the  proprietors  of  that  journal. 


Fig.  91. — Diagram  of    the    Ampulla  Vateri,   Showing  the 
Various  Situations  where    Carcinoma    mat  Arise    in 
Relation  with  it  and  in  its  Neighbourhood. 
A,  Common  bile-duct,     b,  Wirsung's  duct,     c.  Duodenum. 
D,  Biliary  papilla.      1,  Carcinoma    of    the  termination   of  the 
common  bile-duct.     2,  Carcinoma  of  the  termination  of  Wir- 
sung's duct.     3,  Carcinoma  of  the  duodenal  surface  of  the  biliary 
papilla.     4,  Carcinoma  of  the  ampulla  Vateri  itself. t 


CARCINOMA    OF    THE    AAIPULLA    OF    VATER.  699 

Pic  *  regarded  carcinoma  of  the  ampulla  as  an  aberrant  form  of  pancreatic 
carcinoma  corresponding  apparently  with  the  excretory  type  (columnar-celled)  of 
the  pancreatic  growth  described  by  Bard  and  Pic.f  Luzzato  j  has  described  two 
cases  of  carcinoma  of  the  Vaterian  region  arising  from  the  excretory  ducts  of  the 
pancreas.  This  is  tantamount  to  considering  it  to  be  carcinoma  of  the  end  of  the 
pancreatic  duct. 

Morbid  Anatomy. — The  gro\\i:h  begins  as  a  thickening  of  the  mucous 
membrane  of  the  ampulla  and  infiltrates  its  muscular  walls.  It  may 
form  a  villous  or  polypoid  growth,  and  may  then  project  through  the 
orifice  of  the  bihary  papilla,  which  is  dilated  or  ulcerated,  into  the  duo- 
denum. The  growth  is  white,  as  a  rule,  but  may  be  of  a  pinkish-white 
colour  when  projecting  into  the  duodenum.  It  is  alwa3's  comparatively 
small,  and  rarely  shows  any  naked-eye  evidence  of  ulceration.  It  is 
probable,  from  the  histological  accounts  given,  that  some  of  the  cases 
described  as  carcinoma  of  the  diverticulum  of  Vater  were  simple  papillo- 
matous, and  not  malignant,  growths.  A  growth  in  this  situation,  whether 
innocent  or  malignant,  would  rapidly  give  rise  to  jaundice  and  to 
cholseirda.  Secondary  growt.hs  are  seldom  found  in  the  recorded  cases; 
this  may  be  due  to  the  groT\i;h  being  an  innocent  papilloma,  or,  if  a  car- 
cinoma, to  its  killing  the  patient  from  cholaDmia  before  there  has  been 
time  for  secondar}^  growths  to  occur.  If  cholsemia  is  prevented  by  estab- 
lishing a  biliary  fistula,  as  in  case  on  p.  702,  life  may  be  prolonged  and 
secondary  gro^\i}hs  develop. 

Histologically  it  is,  like  primary  carcinoma  of  the  bile-ducts,  practi- 
cally alw^ays  a  columnar-celled  carcinoma.  But  from  its  i^osition  its 
pathological  effects  are  not  absolutely  identical  with  those  of  carcinoma 
of  the  bile-ducts.  A  growi-h  in  the  ami^ulla  of  Vater  tends  to  obstruct 
the  orifice  of  Wirsimg's  duct  and  thus  to  produce  dilatation  of  the  intra- 
pancreatic  ducts  and  chronic  interstitial  pancreatitis.  This  is  well  shown 
in  the  cases  described  on  pages  701  and  702.  It  is,  of  course,  possible,  how- 
ever, for  carcinoma  of  the  lower  end  of  the  common  bile-duct  to  extend 
into  the  ampulla  and  thus  obstruct  the  orifice  of  Wirsung's  duct.  When, 
from  obstruction  to  Wirsung's  duct  or  from  ascending  infection,  chronic 
interstitial  pancreatitis  results,  it  might  have  been  expected  that  diabetes 
would  occtir.  This,  however,  does  not  appear  to  have  been  met  with. 
The  explanation  of  this  has  been  given  by  Opie,§  who  has  shown  that 
obstruction  of  the  duct  is  very  seldom  followed  by  such  intimate  fibrosis 
of  the  pancreas  as  to  destroy  the  areas  of  cells  called  the  islands  of  Lan- 
gerhans.  These  structures  almost  certainly  provide  the  internal  secre- 
tion of  the  pancreas,  which  prevents  glycosuria.  Hence  so  long  as 
they  are  intact  diabetes  does  not  develop. 

If  carcinoma  arising  in  tlie  ampulla  of  A'ater  invohx-d  tlie  mucosa  and  walls 
of  the  orifice  of  the  biliary  papilla,  it  might,  provided  tlie  growth  did  not  involve 
the  orifice  of  Wirsung's  duct,  convert  tiie  common  bile-duct  and  Wirsung's  duct 
into  a  common  and  closed  channel.     The  entrance  of  ])'\le  into  the  pancreatic  duct 

*  Pic:  Rev.  de  M6d.,  1S95,  p.  71. 
t  Bard  and  Pic:  Rev.  de  Mod.,  1888,  p.  394. 
i  Luzzato:  La  Clinica  Medica  Italiana,  1902,  p.  282. 

§  Opie,  E.  L. :  Jour.  Exper.  Med.,  vol.  v,  p.  397,  1901.  Diseases  of  Pancreas, 
p.  178  1903. 


700 


DISEASES    OF   THE    BILE-DUCTS. 


might  then  occur  and  set  up  hasmorrhagic  pancreatitis.  This  production  of  hemor- 
rhagic pancreatitis  by  a  small  calculus  impacted  in  the  biliary  papilla  has  been  proved 
by  Halsted  and  Opie.* 

An  ascending  infection  of  the  bile-ducts  may  induce  suppurative 
cholangitis  and  multiple  hepatic  abscesses;  tliis  accident  is  more  likely  to 
occur  than  in  primarj'  carcinoma  of  the  bile-ducts. 

In  a  case  recorded  by  Pratt  and  Fulton  j  the  pus  from  multiple  abscesses  in 
the  liver  gave  a  pure  culture  of  the  Bacillus  aerogenes  capsulatus,  but  there  was  no 
gas-formation. 

Etiology. — The  male  sex  are  much  more  often  affected  than  the 
female  sex,  thus  differing  from  malignant  primary  disease  of  the  gall- 


FiG.  92.- 


-Carcinoma  op  the    Ampulla  of  Vater   Ixvadixg  the   Mtjscular  Walls  of  the 
Duct  axd  Duodenum.     It  is  a  Columnar-celled  Carcinoma. 


bladder  and  resembhng  the  sex  incidence  in  primary  mahgnant  disease 
of  the  larger  bile-ducts.     In  16  cases  13  were  males  and  3  females. 

It  is  a  disease  of  advanced  life.  In  16  cases  the  average  age  was 
55.6  years,  being  55.6  years  in  the  12  males,  and  55.6  years  in  the  3 
females.     The  extremes  were  34  and  81  years. 

There  is  no  relation  between  gall-stones  and  this  form  of  mahgnant 
disease  of  the  bihary  system;  in  only  2  out  of  16  cases  were  calculi  present. 
This  is  rather  remarkable,  since  gall-stones  are  not  infrequently  found 
in  the  diverticulum  Vateri,  and  may  remain  there  for  very  considerable 

*  Halsted  and  Opie:  Johns  Hopkins  Hospital  BuUetm,  vol.  xii,  Xos.  121,  122, 
123.     April,  May,  June,  1901. 

t  Pratt  and  Fulton:  Boston  Med.  and  Surg.  Jour.,  June  7,  1900,  p.  599. 


CAECINOMA    OF    THE    AMPULLA    OF    VATER.  701 

periods,  so  that  it  might  naturally  have  been  assumed,  on  the  analogy 
of  the  gall-bladder,  that  their  irritation  would  give  rise  to  carcinoma. 

The  symptoms,  signs,  and  diagnosis  of  carcinoma  of  the  ampulla  are, 
in  the  main,  the  same  as  those  in  cancer  of  the  common  bile-duct  (the 
reader  is  referred  to  p.  691).  There  are  only  a  few  points  of  difference 
requiring  attention  as  bearing  on  the  diagnosis  between  the  two  condi- 
tions, which  must  be  regarded  as  a  very  difficult  or  even  impossible 
problem : 

(i)  Jaundice  is  said  to  be  often  intermittent,  the  fgeces  becoming  bile- 
stained  and  the  icteric  tint  of  the  skin  diininishing  or  even  passing  off 
in  the  earher  stages  when  the  obstruction  is  possibly  valvular,  or  partly 
due  to  spasm  of  the  duct  set  up  by  the  irritation  of  the  groAvth.  In  this 
connexion  it  may  again  be  pointed  out  that  confusion  is  apt  to  arise 
in  recorded  cases  between  carcinoma  of  the  ampulla  and  of  carcinoma  of 
the  duodenal  surface  of  the  papilla,  in  which  jaundice  is  by  no  means 
constant,  (ii)  Intermittent  hepatic  fever  and  suppurative  cholangitis 
are  apt  to  occur,  (iii)  Diarrhoea  is  more  often  seen  than  in  carcinoma  of 
the  ducts,  where  constipation  is  the  rule.  Attacks  of  diarrhoea  may 
alternate  with  periods  of  obstinate  constipation.  The  clinical  mani- 
festations of  the  disease  are  illustrated  by  the  following  cases : 

Carcinoma  of  the  Ampulla  of  Vater.  Dilated  Bile  and  Pancreatic  Ducts. 
Haemorrhage  into  Pancreatic  Duct. — A  man  aged  sixty-six  was  admitted  into 
St.  George's  Hospital  under  my  care  on  July  22,  1900,  with  jaundice,  pruritus, 
weakness,  and  wasting.  He  had  never  had  any  severe  iUness,  denied  alcoholic 
excess  and  syphilis.  Ten  weeks  previously  he  had  been  quite  well;  jaundice  then 
appeared  quite  painlessly.  A  month  later  he  began  to  waste,  got  weaker,  and 
became  drowsy,  and  two  weeks  later  the  skin  began  to  itch.  When  exarnined  on 
admission  he  was  deeply  jaundiced,  the  skin  showing  the  effects  of  scratching;  the 
liver  was  enlarged,  reaching  to  fourth  rib  aboA^e  and  two  and  one-half  fingerbreadths 
below  in  the  right  nipple  line.  It  was  quite  smooth;  the  gall-bladder  could  be 
indistinctly  felt;  the  spleen  could  not  be  made  out.  The  abdomen  was  somewhat 
distended,  but  there  was  no  evidence  of  ascites.  There  was  tenderness  at  a  spot 
over  the  eleventh  and  twelfth  ribs  in  the  right  hypochondrium.  Per  rectum  nothing 
abnormal,  except  an  hypertrophied  prostate,  could  be  felt.  The  urine  contained 
albumin,  bile-pigments,  and  bile  acids,  but  no  sugar.  A  tentative  diagnosis  of 
malignant  disease  of  the  head  of  the  pancreas  was  made.  On  July  25th  he  had 
diarrhoea,  on  July  26th  he  vomited,  had  a  rigor,  and  the  temperature  fell  to  96° ; 
pulse  96,  small.  Respirations  were  36  and  the  abdomen  moved  well.  The  liver 
seemed  larger  than  on  admission.  The  freedom  with  which  the  abdomen  moved 
made  it  appear  unlikely  that  perforation  into  the  peritoneum  had  taken  place; 
suppuration  around  the  gall-bladder  Avas  thought  of,  but  his  condition  was  so  bad 
that  ^  grain  of  morphia  was  given  hypodermically  to  relieve  his  pain  and  distress. 
He  died  eighteen  hours  after  the  onset  of  acute  symptoms. 

The  autopsy  showed  a  small,  hard  growth  arising  from  the  mucous  membrane 
of  the  cavity  common  to  the  openings  of  the  common  bile-duct  and  the  pancreatic 
duct,  entirely  inside  the  biliary  papilla,  and  not  visible  from  the  duodenum.  The 
growth  blocked  the  pancreatic  and  common  bile-ducts.  The  common  bile-duct 
was  as  big  as  one's  thumb  and  contained  dark  bile  and  mucus;  when  opened  and 
the  finger  introduced  in  a  downward  direction,  it  was  found  to  end  blindly,  like  a 
test-tube.  The  hepatic  ducts  and  the  ducts  in  the  left  lobe  of  the  liver  were  widely 
dilated;  except  the  main  right  hepatic  duct,  the  bile-ducts  in  the  right  lobe  were 
but  little  dilated.  The  cystic  duct  and  gall-bladder  were  greatly  dilated;  no  calculi 
were  found  in  the  gall-bladder  or  in  the  bile-ducts.  The  liver  (4  pounds)  was  smooth 
and  of  a  deep  green  colour.  Wirsung's  duct  was  tortuous,  dilated  throughout  its 
entire  length,  while  near  the  head  of  the  pancreas  it  formed  a  cyst  into  which  recent 
haemorrhage  had  taken  place.  It  is  probable  that  the  terminal  acute  symptoms 
depended  on  this  hsem.orrhage.     Towards  the  tail  of  the  pancreas  the  duct  con- 


702  DISEASES    OF   THE    BILE-DUCTS. 

tained  dark  fluid,  probably  altered  blood  of  older  date.  The  pancreas  was  adlaerent 
to  the  posterior  wall  of  the  stomach  by  old  adhesions,  evidently  the  result  of  former 
inflammation.  No  calculi  were  found  in  the  ducts  of  the  pancreas.  The  pancreas 
itself  was  greatly  fibrosed  and  hard.  No  secondary  growths  were  found  in  any  part 
of  the  body.  The  abdomen  contained  two  pints  of  bile-stained  fluid.  The  stom- 
ach and  intestines  showed  signs  of  recent  catarrhal  inflammation.  Kidneys  (6 
ounces  each)  showed  senile  change  and  a  few  cysts.  Heart  (11  ounces)  was  normal 
for  the  time  of  life.  The  lungs  were  emphysematous  and  showed  hypostatic  con- 
gestion. 

Microscopically  the  growth  was  a  columnar-celled  carcinoma  and  invaded  the 
muscular  coat,  lying  under  the  floor  of  the  ampulla  of  Vater  {vide  Fig.  92).  The 
pancreas  showed  extensive  fibrosis,  some  recent  small-cell  infiltration,  dilatation 
of  the  ducts,  which  contained  minute  calculous  masses,  and  widespread  atrophy 
of  the  glandular  tissue  of  the  pancreas.  The  islands  of  Langerhans  were,  however, 
intact;  this  may  be  correlated  with  the  absence  of  glycosuria.* 

Carcinoma  of  the  Ampulla  Vateri  Imitating  Cholelithiasis. — A  woman 
aged  fifty-two  was  attacked  six  and  a  half  months  before  death  with  colic,  shiver- 
ing, diarrhoea,  vomiting,  and  distension  of  the  abdomen.  The  pain  lasted  for  two 
weeks  and  was  succeeded  by  jaundice.  She  had  several  similar  attacks  resembling 
biliary  colic,  and  when  admitted  to  St.  George's  Hospital,  under  the  care  of  Dr. 
Cavafy,  on  March  30,  1892,  had  lost  three  stone  in  weight.  She  was  deeply  jaun- 
diced and  complained  of  abdominal  tenderness,  itchmg  of  the  skin,  and  wealcness. 
Grating  was  felt  in  the  region  of  the  gall-bladder.  Cholecystotomy  was  performed, 
but  no  calculi  were  found.  At  the  operation  there  was  ascites.  Before  death 
nodules  of  growth  appeared  in  the  skin  around  the  fistula  leading  into  the  gall- 
bladder. 

At  the  autopsy,  which  I  performed,  a  growth  was  foimd  projectmg  from  the 
gaping  lips  of  the  biliary  papilla;  it  arose  inside  the  ampulla  of  Vater  and  com- 
pletely blocked  the  common  bile-duct;  the  duct  of  Wirsung  was  obstructed  and 
presented  a  cystic  dilatation  as  large  as  a  hen's  egg  near  the  tail  of  the  pancreas, 
which  was  adlaerent  to  the  fundus  of  the  stomach. 

There  were  a  number  of  secondary  growths  in  the  liver,  which  Avas  small  and 
deeply  bile-stained.  There  was  no  cirrhosis  microscopically,  but  numerous  masses 
of  inspissated  bile  in  the  minute  bile-ducts.  Microscopically  the  growth  was  a 
columnar-celled  carcinoma. 

The  treatment  of  carcinoma  of  the  ampulla  has  so  far,  "with  the 
exception  of  Halsted's  f  and  Mayo's  cases,  been  palhative  and  confined 
to  relief  of  the  symptoms  and  on  the  same  lines  as  in  carcinoma  of  the 
bile-cliicts. 

Halsted  successfully  performed  a  radical  operation  consisting  in  the 
wide  removal  of  a  primary  carcinoma  of  the  duodenal  papilla  and  diver- 
ticulum Vateri  in  a  woman  aged  sixty.  The  common  bile-duct  and 
pancreatic  ducts  were  engrafted  into  the  duodenum;  three  months  later 
the  cystic  duct  was  engrafted  into  the  duodenum  to  relieve  the  biliar}'' 
obstruction  which  had  persisted.  Death  occurred  within  a  year  of  the 
first  operation  from  recurrent  carcinoma  in  the  head  of  the  pancreas 
and  rhiodenum,  which  had  obstructed  the  openings  of  the  common  and 
cystic  ducts  into  the  duodenum.  In  a  somewhat  similar  case  Mayo  % 
removed  a  carcinoma  of  the  terminal  part  of  the  common  bile-duct  by 
the  duodenal  route;  it  recurred  in  eighteen  months'  time.  The  result 
of  this  brilliant  and  formidable  surgical  procedure  is  disappointing. 

*  This  case  was  reported  in  the  Lancet,  1901,  vol.  i,  p.  467. 

t  Halsted:  Johns  Hopkins  Hospital  Buhetin,  No.  103,  Jan.,  1900. 

t  Mayo:  Boston  Medical  and  Surgical  Journ.,  vol.  cxlviii,  p.  545,  1903. 


CHOLELITHIASIS. 

CAUSES  OF  CHOLELITHIASIS. 

The  formation  of  gall-stones,  whether  in  the  -ducts  or  in  the  gall- 
bladder, may  be  considered  under  the  following  two  heads — (i)  Immedi- 
ate or  exciting  causes,     (ii)  Disposing  factors. 

IMMEDIATE  OR  EXCITING  FACTORS. 

The  immediate  cause  of  the  production  of  calculi  is  a  mild  form  of 
catarrhal  inflammation  of  the  mucous  membrane  hning  the  ducts  and 
gaU-bladcler.  Catarrhal  inflammation  of  the  bile-ducts  leads  to  an  albu- 
minous exudation  which,  as  shown  by  experimental  addition  of  egg- 
albumin  to  bile,  precipitates  bilirubin  in  chemical  combination  with 
calcium  *  as  bilirubin-calcium  calcuh.  This  is  the  only  form  of  calculus 
actually  produced  in  the  bile-ducts,  though  under  conditions  such  as 
impaction  of  a  gall-stone  in  the  common  duct  the  formation  of  additional 
calculous  material  containing  cholesterin,  as  well  as  bilirubin-calcium, 
takes  place. 

Simple  stagnation  and  inspissation  of  bile  do  not  lead  to  the  pre- 
cipitation of  bilirubin-calcium  or  to  the  formation  of  bihhumin,  which 
is  constantly  found  in  these  bilirubin-calcium  calculi.  Something  more 
than  inspissation — viz.,  catarrhal  inflammation — is  necessary  for  the 
formation  of  these  calculi. 

In  catarrhal  inflammation  of  the  mucous  membrane  of  the  gall-bladder 
there  is  an  abnormal  formation  and  secretion  of  cholesterin  by  the  mucous 
cells  and  glands  in  its  walls.  Tliis  excessive  and  pathological  production 
of  cholesterin  is  responsible  for  the  formation  of  cholesterin  calculi. 
This  differs  from  the  ancient  conception  that  cholelithiasis  was  due  to 
a  mere  precipitation  of  the  cholesterin  normally  j^resent  in  bile,  brought 
about  by  a  change  in  the  characters  of  the  bile,  such  as  concentration 
or  alteration  in  its  chemical  properties  or  reaction. 

Inflammation  of  the  gall-bladder  leads  to  a  perverted  metabolism 
inside  the  mucus-secreting  cells  in  its  walls,  resulting  in  the  formation 
of  cholesterin  inside  these  cells.  Evidence  of  this  can  be  seen  micro- 
scopically in  the  presence  of  myelin  l:)odies  inside  the  cells.  It  was 
formerly  thought  that  the  cholesterin  formed  elsewhere,  and  especialh^ 
in  the  central  nervous  system,  was  picked  up  from  the  blood  and  excreted 
into  the  gall-l^ladder,  but  there  is  no  evidence  to  support  this,  since 
administration  of  cholesterin  to  animals  under  the  skin  or  1)y  the  mouth 
does  not  increase  the  amount  of  cholesterin  in  the  bile. 

It  wall  be  noticed  that  the  results  of  catarrh  in  the  small  bile-ducts 

*  Naunyn:  Cholelithiasis,  p.  20.     Translated  by  New  Sydenham  Soc.,  1896. 

703 


704  DISEASES    OF   THE    BILE-DUCTS. 

and  in  the  gall-bladder  differ  both  in  the  mechanism  and  in  the  nature 
of  the  calcuh  produced.  As  the  result  of  catarrh  of  the  small  intra-hepatic 
ducts  there  is  a  precipitation  of  biUrubin-calcium,  while  catarrh  of  the 
gall-bladder  leads,  by  a  perverted  metabohsm  of  the  mucous  membrane, 
to  a  pathological  formation  of  cholesterin  analogous  to  that  seen  in  cer- 
tain cysts,  such  as  l\vclroceles,  ovarian,  etc. 

The  catarrh  of  the  ducts  and  gall-bladder  may  be  spoken  of  as  htho- 
genic.  If  the  catarrh  starts  in  the  ducts,  the  small  calcuh  of  bihrubinate 
of  calcium  may  possibly  find  their  way  into  the  gall-bladder  and  there 
form  the  nucleus  of  cholesterin  calculi  formed  as  the  result  of  an  ex- 
tension of  the  inflammation  to  the  gall-bladder.  Acute  suppurative 
inflammations  of  the  ducts  and  gall-bladder  do  not  lead  to  the  formation 
of  calculi.  This  would  appear  to  depend  on  the  fact  that  destruction 
of  the  mucous  cells  necessarily  prevents  the  formation  of  cholesterin. 
As  catarrhal  inflammation  is  the  essential  antecedent  of  cholehthiasis, 
it  will  be  necessary  to  consider  what  are  the  exciting  and  disposing 
causes  of  catarrhal  cholecystitis  and  cholangitis. 

The  exciting  causes  are  infection  with  micro-organisms  and  possibly 
,the  action  of  poisons  excreted  into  the  ducts. 

The  microbic  origin  of  gall-stones  has  attracted  very  considerable 
attention  since  it  was  first  suggested  by  Gahppe"^  in  1886.  Experiment- 
ally it  has  been  shown  that  the  production  of  cholecystitis  by  the  bacillus 
of  typhoid  fever  and  the  colon  bacillus  is  followed  by  cholehthiasis. 
Non-virulent  cultures  of  streptococci  and  staphylococci  may  also  give 
rise  to  calculus  formation;  virulent  cultures,  however,  set  up  intense 
cholecystitis  mthout  any  production  of  calcuh.  (Mignot.)  From  Itaha's  t 
researches  it  appears  that  pure  cultures  of  streptococci  or  staphylococci 
may  lead  to  the  formation  of  calcuh  which  are  composed  only  of  hme 
salts;  cholesterin  may  be  found  when  there  is  an  admixture  with  cultures 
of  the  BaciUus  coh.  Thus  experimental  work,  hke  chnical  observation, 
shows  that  cholehthiasis  is  due  to  a  comparatively  mild  form  of  chole- 
cystitis, or,  expressed  in  other  words,  is  produced  by  an  attenuated 
infection ;  this  depends  on  the  preser\^ation  of  the  cholesterin-producing 
epithehum  in  the  shghter  forms  of  cholecystitis  and  its  destruction  in 
more  acute  inflammations  of  the  gall-bladder. 

The  important  micro-organisms  in  the  production  of  cholehthiasis  are : 
(1)  The  colon  bacillus.     (2)  The  typhoid  bacillus. 

(1)  The  most  important  part  in  the  microbic  origin  of  biliary  calculi 
is  usuaUy  ascribed  to  bacilh  belonging  to  the  colon  group.  Experimentally 
Mignot  J  produced  calcuh  in  a  guinea-pig  as  a  result  of  the  action  of 
Bacillus  coh  in  the  gall-bladder  in  1897.  The  colon  bacillus  has  often 
been  demonstrated  inside  bihary  calculi  (Gilbert  and  Dominici,§  Mignot, 
etc.);  recent  calcuh  especiaUy  show  the  presence  of  baciUi,  wliile  old 
calculi  usually  do  not,  or  at  best  show  only  the  faintly  staining  shadows 
of  micro-organisms. 

*  Galippe:  Comp.  Rend,  de  la  Soc.  biolog  Paris,  1886,  p.  116. 

t  Italia:  La  Riforma  Medica,  1901,  ii,  830. 

t  Mignot:  Soc.  de  Chinirg.,  May  19,  1897. 

§  Gilbert  and  Dominici:  Soc.  de  biolog.,  June  16,  1894,  p.  485. 


CHOLELITHIASIS.  705 

Chauffard,*  who  rather  opposes  the  bacterial  origin  of  cholelithiasis, 
has  pointed  out  that  the  presence  of  micro-organisms  in  a  calculus  does 
not  necessarily  prove  that  they  had  any  part  in  its  formation,  since 
micro-organisms  may  invade  a  calculus  from  the  outside. 

It  is  generally  beheved  that  the  colon  bacillus  reaches  the  gall-bladder 
by  an  ascending  infection  of  the  common  bile-duct  from  the  duodenum. 
It  appears,  from  bacteriological  examination  of  the  duodenum  in  health, 
that  during  fasting  the  mucous  membrane  may  be  sterile  and  that  when 
micro-organisms  are  found,  they  are,  so  to  speak,  accidental  and  derived 
from  the  ingesta.  (Gushing  and  Livingood.f)  It  is,  therefore,  probable 
that  a  catarrhal  condition  of  the  duodenum  would  be  necessary  to  enable 
an  ascending  infection  to  occur.  A  factor  of  importance  in  the  production 
of  an  ascending  infection  is  more  or  less  stagnation  of  the  bile;  otherwise 
the  micro-organisnxs  woidd  be  washed  out  of  the  ducts  by  the  bile.  On 
the  other  hand,  it  is  highly  probable  that  the  colon  reaches  the  liver  by 
the  portal  vein  and  is  excreted  into  the  ducts. 

(2)  Bacillus  Typhosus. — The  causal  relationship  between  typhoid 
fever  and  gall-stones  was  suggested  by  Bernheim,{  of  Nancy,  in  1889, 
on  chnical  groimds,  viz.,  the  occurrence  of  biliary  colic  in  patients  with 
typhoid  fever  who  had  not  previously  had  any  signs  of  gall-stones. 
Calculi  have  often  been  found  in  the  gall-bladder  shortly  after  typhoid 
fever  in  patients  who  had  not  previously  exhibited  any  signs  of  chole- 
lithiasis (Gilbert  et  Girode,§  Hanot,  |1  and  others).  Dufourt**  found 
a  history  of  enteric  in  19  cases  of  cholelithiasis  in  which  no  symptoms 
of  gall-stones  had  appeared  previous  to  the  fever.  In  12  of  these  cases 
symptoms  of  gall-stones  appeared  within  six  months  of  the  attack  of 
enteric  fever. 

In  42  cases  of  gall-stones  13  had  had  typhoid  fever  and  had  not  had 
any  signs  of  cholelithiasis  before  the  fever  (Curschmann  |f ). 

In  typhoid  fever  the  Bacilli  typhosi  are  almost  constantly  found  in 
the  gall-bladder  after  death,  and,  as  a  rule,  without  any  calculus  formation. 
It  is,  therefore,  probable  that  the  production  of  calculi  depends  on 
cholecystitis  and  not  on  the  presence  of  inicro-organisms  alone.  Ty- 
phoidal  cholecystitis  is  described  elsewhere  (vide  p.  593).  The  agglutina- 
tion of  typhoid  bacilli  in  the  bile  has  been  suggested  as  a  nucleus  or 
starting-point  for  the  formation  of  calculi  (Richardson  J  J),  but  this  is 
not  supported  by  experiments  outside  the  body;  Gushing §§. added  tjqihoid 
bacilli  to  bile  and  then  precipitated  them  by  adding  serum  from  a  typhoid 
patient,  but  failed  to  obtain  any  precipitation  of  material  from  the  bile. 

*  Chauffard:  Rev.  de  Med.,  Feb.,  1897,  p.  81. 

t  Gushing  and  Livingood:  Johns  Hopkins  Hosp.  Eeports,  vol.  ix,  p.  543. 
j  Bernheim :  Diet.  Encyclop.  de  Dachambre,  Article  latere,  1889. 
§  Gilbert  and  Girode:  C.  R.  Soc.  biolog.,  1893,  p.  958. 
II  Hanot:  Bullet.  Med.,  Jan.  22,  1896. 
**  Dufourt:  Rev.  de  Med.,  1893,  p.  274. 
tt  Curschmann:  Die  Unterleibstyphus,  Wien,  1898,  p.  355. 
j  j  Richardson,  M.  W. :  Tlie  Jour,  of  Boston  Soc.  of  Med.  Science,  vol.  iii,  p.  79, 
Jan.,  1899.     Quoted  by  Cusliing. 

§§  Gushing,  H. :    Remarks  on   Dr.  Hunner's  Case  of  Typhoi(hil  Cholecystitis, 
Johns  Hopkins  Hosp.  Bull.,  Nos.  101,  102,  Aug.-Sept.,  1899,  p.  I(i3. 
45 


706  DISEASES   OF  THE    BILE-DUCTS. 

Gilbert  and  Dominici,*  in  1893,  in  experimental  typhoidal  cholecystitis 
in  a  rabbit,  produced  greenish  concretions.  This  was  confirmed  by 
Gilbert  and  Fournier  f  in  1897.  The  question  whether  typhoid  bacilli 
reach  the  gall-bladder  by  means  of  the  portal  vein  or  directly  up  the 
common  bile-  and  cystic  ducts  has  been  discussed  in  the  section  on  the 
Causation  of  Cholecystitis  {vide  p.  595).  Here  it  may  be  said  that  it 
is  more  probable  that  the  bacilli  are  carried  to  the  liver  by  the  portal 
vein  and  then  excreted  into  the  bile-ducts  and  so  reach  the  gall-bladder, 
than  that  there  is  an  ascending  infection  from  the  duodenum. 

Leptothricial  Cholelithiasis. — Pearce  |  has  described  a  case  of  cholelithiasis  in 
a  man  aged  fifty-nine  years  which  seemed  to  depend  on  leptothricial  infection. 
The  threads  of  leptothrix  were  found  in  the  calculi. 

Question  of  the  Production  of  Cholelithiasis  by  Toxaemia. — ^The 

theoretical  production  of  cholecystitis  by  toxines,  such  as  abrin,  and 
by  bacterial  poisons  has  been  referred  to  elsewhere.  It  was  there  stated 
that  Claude's  §  experiments  make  it  probable  that  cholecystitis  may  be 
produced  by  toxines,  but  though  it  might  reasonably  be  expected  (Gil- 
bert II),  I  am  not  aware  that  a  toxic  lithogenic  catarrh  of  the  gall-bladder 
has  been  produced  experimentally.  It  may,  therefore,  be  concluded  that 
although  the  production  of  gall-stones  from  catarrhal  inflammation  of 
the  gall-bladder  set  up  by  the  irritating  effects  of  poisons,  without  any 
microbic  intervention,  is  logically  possible,  it  has  not  been  shown  to 
occur  in  man. 

DISPOSING  CAUSES. 

Factors  which  Favour  the  Production  of  Catarrh  of  the  Gall-bladder  and 
Bile-ducts,  and  so  Dispose  to  Cholelithiasis. — -1.  Stagnation  of  bile  in  the 
gall-bladder  does  not  of  itself  lead  to  the  formation  of  calculi,  but  it 
renders  infection  more  easy,  since  if  any  micro-organisms  get  into  the 
bile,  they  are  not  removed,  but  allowed  to  multiply  there  and  may 
subsequently  set  up  cholecystitis.  Further,  in  the  absence  of  stagnation, 
micro-organisms  present  in  the  gall-bladder  need  not  set  up  cholecystitis ; 
this  has  been  shown  experimentally  by  Ehret  and  Stolz,**  and  is  sup- 
ported by  the  frequency  with  which  cultures  of  tjq^hoid  bacilli  are  found 
in  the  gall-bladder  without  any  evidence  of  cholecystitis  in  fatal  cases 
of  typhoid  fever. 

Experimentally  Mignot  ft  showed  that  stagnation  of  bile  in  an  aseptic  gall- 
})ladder  does  not  lead  to  crystallisation  of  cholesterin  out  of  the  bile,  and  he 
believes  that  absolute  stagnation  of  bile  prevents  the  formation  of  stratified  cal- 
culi and  is  less  favourable  to  cholelithiasis  than  relative  inertia  of  the  gall- 
bladder. 

Sedentary  habits,  want  of  exercise,  obesity,  and  diseases  which  neces- 

*  Gilbert  and  Dominici:  Compt.  rend.  Soc.  biolog.,  1893,  p.  1033. 

t  Gilbert  and  Fournier:  Ibid.,  1897,  p.  936. 

i  Pearce,  R.  M. :  University  of  Pennsylvania  Med.  Bull.,  Aug.,  1901,  p.  217.' 

§  Claude :  Bull.  Soc.  Anat.  Paris,  June-July,  1896. 

II  Gilbert:  Archiv.  general,  de  MM.,  Sept.,  1898. 
**  Ehret  and  Stolz:  Berlin,  klin.  Wochen.,  1902,  S.  13. 
tt  Mignot:  Archiv.  general,  de  Med.,  Aug.-Sept.,  1898. 


CHOLELITHIASIS.  707 

sitate  a  quiet  and  restful  life  dispose  to  cholelitliiasis.  Want  of  exercise 
carries  with  it  feeble  contractions  of  the  abdominal  muscles,  and  as  a 
result  bile  is  not  expelled  so  frequently  or  efficiently  from  the  gall-bladder. 
This  explains  why  gall-stones  are  rare  in  outdoor  labourers  and  common 
in  women.  The  influence  of  a  sedentary  life  is  shown  by  the  occurrence 
of  biliary  calcuh  in  pet  dogs  and  by  their  absence  in  wild  animals.  Sitting 
upright  and  leaning  forwards  over  a  desk  keep  the  fundus  of  the  gall- 
bladder in  a  dependent  position  and  prevent,  or  at  any  rate  interfere, 
vnth  its  being  properly  emptied.  It  has,  therefore,  been  considered  a 
disease  of  literary  men,  but  has  also  been  noticed  to  develop  in  prisoners 
confined  in  gaol.  The  recumbent  posture  in  an  easy  chair,  however,  is 
favourable  to  the  flow  of  bile  out  of  the  gall-bladder. 

Tight  lacing  frequently  leads  to  dilatation  of  the  gall-bladder  from 
the  downward  displacement  of  the  duodenum  straining  and  kinldng 
the  cystic  duct,  which  even  under  normal  conditions  requires  a  spiral 
valve  to  keep  it  open.  (Keith.*)  Further,  downward  displacement 
of  the  right  lobe  of  the  liver  makes  the  fundus  of  the  gall-bladder  more 
dependent  than  in  health,  and,  since  the  cystic  duct  is  more  fixed  at  the 
transverse  fissure  of  the  liver,  tends  to  produce  kinking  of  the  duct.  A 
wandering  liver  has  much  the  same  effect.  Nephroptosis,  or  a  floating 
kidney,  on  the  right  side  may,  by  traction  on  the  peritoneum  covering 
the  common  bile-duct  in  the  lesser  omentum,  obstruct  the  outflow  of  bile 
from  the  gall-bladder. 

Any  cause  that  interferes  vdih  diaphragmatic  respiration  and  there- 
fore with  the  emptying  of  the  gall-bladder  tends  to  produce  stagnation 
of  bile  in  the  gall-bladder.  Among  the  factors  exerting  this  influence 
are  tight  lacing,  abdominal  distension  from  pregnancy,  ascites,  abdominal 
tumors,  etc.,  cardiac  and  pulmonary  disease. 

2.  Foreign  bodies  are,  of  course,  only  exceptionally  found  in  the 
gall-bladder.  Aseptic  foreign  bodies  do  not  give  rise  to  the  formation  of 
gall-stones;  this  has  been  shown  experimentally  by  Mignot.  If,  however, 
cotton-wool  impregnated  with  colon  bacilli  is  introduced  into  the  gall- 
bladder, calculi  are  formed.  Calculi  have  been  found  to  contain  pins 
(Nauche,t  Carless  J),  pieces  of  hydatid  membrane,  the  ova  of  bilharzia 
(Gautrelet  §),  and  round  worms  (Lobstein).  Round  worms  may  invade 
the  bile-ducts  and  infect  the  ducts  with  micro-organisms  from  the  duo- 
denum, and  in  very  rare  instances  may  get  into  the  gall-l)ladder.  In 
Mertens'  ||  48  cases  of  round  worms  in  the  bile-ducts  five  were  compli- 
cated by  calculi.  Hanot  **  considered  the  worms  the  cause  of  the 
calculi,  but  Mertens  thought  the  calculi  dilated  the  bile-passages  and 
facilitated  the  entrance  of  the  worms. 

*  Keith,  A. :  Lancet,  1903,  vol.  i,  p.  6S9. 

fNauche;  Lobstein:  Quoted  by  Trousseau:  Clinical  Med.,  vol.  iv,  p.  230. 
Translated  bj''  New  Sydenham  Soc. 

%  Carless,  A. :  Kings  College  Hospital  Reports,  vol.  iii,  p.  101. 

§  Gautrelet:  L'Union  Medicale,  1885,  No.  138.  Quoted  by  Scheube:  Diseases 
of  Warm  Countries. 

II  Mertens:  Deutsche  med.  Wochen.,  Bd.  xxiv,  S.  358,  1898. 
**  Hanot:  Archiv.  general,  dc  Med.,  tome  cl.Kxvii,  p.  74. 


708  DISEASES    OF   THE    BILE-DUCTS. 

Homans  *  records  an  interesting  case  in  which  he  removed  97  calcuh  from  the 
gall-bladder  of  a  woman;  twenty  months  later  he  again  opened  the  gall-bladder 
for  similar  symptoms,  and  found  7  calculi  crystallised  on  the  sutures  which  lay 
free  in  the  gall-bladder.  In  3  patients  operated  on  by  Kehr  f  recurrent  colic 
was  found  to  depend  on  calculous  formation  around  sutures  introduced  at  the  first 
operation. 

Foreign  bodies  tend  to  produce  stagnation  and  so  favour  the  pro- 
duction of  catarrh  if  microbes  are  present;  microbes  introduced  alone 
may  be  removed  with  the  bile,  but  if  introduced  together  with  a  foreign 
body,  they  are  enabled,  as  shown  by  Mignot's  experiments,  to  induce 
cholelithiasis. 

Catarrhal  inflammation  of  the  duodenum  and  intestinal  tract  is 
of  great  importance  in  providing  micro-organisms  to  induce  similar 
changes  in  the  gall-bladder. 

Excessive  eating  or  drinking,  especially  alcoholism,  tends  to  induce 
gastro-intestinal  catarrh,  and  hence  cholecystitis  and  gall-stones  are 
likely  to  occur  in  gross  feeders,  especially  when  of  sedentary  habits. 
Chronic  venous  engorgement  of  the  portal  system,  whether  from  the 
backward  pressure  of  heart  disease,  from  cirrhosis  of  the  liver  or  other 
causes,  disposes  to  catarrh  of  the  gastro-intestinal  tract  and  so  to  chole- 
lithiasis. 

Appendicitis  has  been  thought  to  give  rise  to  cholecystitis  with  cal- 
culous formation  by  acting  as  a  primary  focus  from  which  virulent  coli 
bacilli  may  travel  to  the  gall-bladder. 

In  18  cases  of  cholelithiasis  operated  upon  by  Ochsner  %  appendicitis  was  found 
in  6.  Becker  §  has  collected  34  cases  in  which  appendicitis  and  cholecystitis  were 
associated,  and  in  720  laparotomies  for  diseases  of  the  biliary  tract  Kehr  ||  observed 
appendicitis  in  18,  or  2.5  per  cent. 

On  the  other  hand,  the  association  of  appendicitis  and  cholecystitis 
has  been  interpreted  in  the  opposite  sense,  viz.,  that  infection  spreads 
from  the  gall-bladder  to  the  appendix.     (Dieulafoy.**) 

Relation  of  Various  Factors  and  Diseases  to  Cholelithiasis. — 
Diet. — A  vegetable  diet,  by  leading  to  fermentation,  is  more  likely  than 
a  mixed  or  proteid  regimen  to  be  followed  by  gall-stones.  It  has  been 
thought  that  a  carbohydrate  diet  disposed  to  cholecystitis  by  producing 
a  smaller  amount  of  bile  acids,  which  dissolve  cholesterin,  than  a  purely 
or  largely  proteid  diet. 

German  soldiers  are  more  often  affected  with  cholelithiasis  than 
English  soldiers;  this  has  been  correlated  with  the  fact  that  their  daily 
allowance  of  meat  is  6  ounces  as  against  12  ounces  in  the  English  army. 
On  the  other  hand,  gall-stones  are  very  rare  among  the  natives  of  India 
who  largely  subsist  on  rice. 

The  production  of  gall-stones  has  been  put  down  to  a  deficiency  in 

*  Homans:  Boston  Med.  and  Surg.  Journ.,  July  1,  1897.  Annals  of  Surgerv, 
vol.  xxvi,  p.  114,  1897  [Plate]. 

t  Kehr:  Gall-stone  Disease,  p.  105.     American  transl.,  1901. 
X  Ochsner:  Philadelphia  Medical  Journal,  1900,  p.  652. 
§  Becker:  Deutsche  Zeitschrift  f.  Chirurg.,  Bd.  Ixvi,  S.  246. 
II  Kehr:  Die  Therapie  der  Gallenwege,  Bd.  iv,  S.  456,  1902. 
**  Dieulafoy:  La  Presse  Medicale,  June  17,  1903,  p.  445. 


CHOLELITHIASIS.  709 

the  solvents  of  cholesterin,  but  this  is  not  in  accord  with  Kausch's  ob- 
servation that  the  solvents  of  cholesterin  are  always  present  in  sufficient 
amounts  to  dissolve  the  normal  amount  of  cholesterin.  Diet  probably 
disposes  to  cholelithiasis  by  setting  up  dyspepsia  and  gastro-intestinal 
catarrh.  A  saccharine  or  fatty  diet  has  long  been  thought  to  be  favour- 
able to  the  production  of  gall-stones. 

Restriction  in  the  amount  of  liquid  taken  by  the  mouth  would  tend 
to  diminish  the  amount  of  bile  and  so  to  impair  the  freedom  with  which 
the  ducts  are  flushed.  It  is,  therefore,  reasonable  to  treat  cases  of  chole- 
lithiasis with  free  draughts  of  water,  and  to  believe  that  an  insufficient 
intake  of  liquid  may  act  injuriously.  On  the  other  hand,  in  diabetes 
mellitus,  where  the  polyuria  would  naturally  be  expected  to  diminish 
the  biliary  secretion,  cholelithiasis  is  rare.  {Vide  p.  711.)  Inasmuch  as 
the  amount  of  calcium  in  the  bile  is  not  affected  by  that  taken  by  the 
mouth,  it  is  very  improbable  that  hard  water  induces  cholelithiasis. 

Long  intervals  between  meals  lead  to  stagnation  of  bile  in  the  gall- 
bladder and  so  favour  infection.  Kehr  *  suggests  that  the  greater  fre- 
quency of  gall-stones  among  German  women  as  compared  with  men  may 
depend  on  their  going  to  bed  early  and  therefore  fasting  for  a  number 
of  hours,  while  late  suppers  taken  by  men  empty  the  gall-bladder. 

Anxiety  and  worry  have  often  been  regarded  as  a  cause  of  gall-stones, 
and  possibly  act  by  inducing  dyspepsia  and  constipation  and  so  reducing 
the  resistance  of  the  body  as  a  whole,  or  possibly  of  the  gall-bladder  in 
particular,  and  so  disposing  to  infection. 

Indigestion  is  a  frequent  result  of  gall-stones;  so-called  irregular 
biliary  colic  not  infrequently  manifests  itself  as  dyspepsia,  and  may  be 
due  to  adhesions  between  the  gall-bladder  and  stomach.  While  fully 
recognising  that  dyspepsia  may  be  a  manifestation  of  cholelithiasis,  there 
is  no  doubt  that  gastro-intestinal  catarrh  is  a  very  important  cause  of 
gall-stones.  Abnormal  bodies  manufactured  in  the  intestinal  tract  will 
tend  to  set  up  catarrh  of  the  biliary  tract,  wliile  direct  infection  via  the 
ducts  may  also  be  set  up.  Continued  indigestion  should  be  regarded  as 
an  important  factor  in  the  production  of  gall-stones. 

Constipation  may  increase  intestinal  catarrh  and  so  dispose  to  infec- 
tion of  the  gall-bladder;  it  may  also,  by  leading  to  faecal  accumulation 
in  the  hepatic  flexure  of  the  colon,  interfere  with  the  flow  of  bile  through 
the  cystic  duct  and  thus  produce  stagnation  in  the  gall-bladder.  Further, 
intestinal  catarrh  may  be  partly  due  to  vigourous  purgatives  taken  in 
order  to  get  the  bowels  open. 

Kraus  f  found  that  80  per  cent,  of  his  patients  with  gall-stones  at  Carlsbad 
had  constipation. 

Pregnancy. — Gall-stones  often  develop  during  or  shortly  after  preg.- 
nancy.  Naunyn  {  estimated  that  90  per  cent,  of  women  with  chole- 
lithiasis had  borne  children.  Pregnancy  in  many  women  necessitates  a 
very  sedentary  life,  and  is  frequently  accompanied  by  considerable  con- 

*  Kehr:  Gall-stone  Disease,  p.  70.     American  transl.,  1901. 

t  Kraus:  On  Gall-stones,  p.  20.  J  Naunyn:  On  Cholelithiasis,  p,  40. 


710  DISEASES    OF    THE    BILE-DUCTS. 

stipation.  It  has  naturally  been  thought  that  the  pregnant  uterus  im- 
pedes the  descent  of  the  cUaphragm  and  so  leads  to  failure  in  the  expul- 
sion of  bile  from  the  gall-bladder.  Mosher,*  however,  finds  that  preg- 
nancy interferes  less  ^\^th  the  descent  of  the  diaphragm  than  has  been 
generally  thought,  and  that  respirator}'  movements  tend  to  become 
equalised  so  that  diaphragmatic  respiration  persists  as  late  as  the  eighth 
month. 

It  has  been  thought  that  the  enlarged  uterus  may  induce  compression 
of  the  bile-ducts  and  so  favour  catarrh  of  the  ducts  and  cholelitliiasis. 
(Korte,  Heddseus.t) 

Repeated  pregnancies  lead  to  a  relaxed  condition  of  the  muscular 
abdominal  waUs  and  so  to  failure  in  the  exiDulsion  of  the  contents  of  the 
gall-bladder,  and  may  be  followed  by  enteroptosis  which  may  show 
itself  as  a  floating  kidney  or  unduly  movable  liver,  both  of  which  con- 
chtions  may  interfere  with  the  exit  of  bile  from  the  gall-bladder. 

Glenard's  disease  or  visceroptosis  may  dispose  to  cholelithiasis  in 
several  ways.  The  liver  usually  shares  in  the  general  prolapse  of  the 
abdominal  organs,  and  kinking  of  or  traction  on  the  cystic  duct  may 
result  and  obstruct  the  exit  of  bile.  "^Vhile  nephroptosis  on  the  right  side 
may  also  lead  to  obstruction  of  the  cystic  duct,  and  so  favour  inflamma- 
tion of  the  gall-bladder  and  the  production  of  gall-stones.  From  passive 
engorgement  of  the  intestines  catarrhal  inflammation  may  result,  and 
thus  tend  to  lead  to  the  same  change  in  the  gall-bladder.  Keith  J  states 
that  gall-stones  are  almost  invariabty  present  in  Glenard's  disease. 

Cardiac  disease  disposes  to  choleUthiasis  in  the  first  place  by  rendering 
life  more  sedentary  and  thus  leading  to  stagnation  of  bile  in  the  gall- 
bladder, which  favours  catarrhal  inflammation  of  the  gall-bladder.  Heart 
disease,  in  fact,  makes  the  life  of  a  male  much  the  same  as  regards  its 
sedentary  character  as  that  of  women. 

In  cases  of  mitral  disease  with  backward  pressure  gastric  and  duo- 
denal catarrh  are  readily  set  up  and  thus  an  ascending  inflammation  is 
rendered  available.  The  walls  of  the  gall-bladder  may  be  swollen  and 
chronically  engorged,  and  so  more  liable  to  become  inflamed  should 
infection  be  conveyed  from  the  duodenum.  The  influence  of  cardiac 
disease  is  shown  by  statistics  from  the  postmortem  room. 

In  1347  successive  autopsies  at  the  Manchester  Royal  Infirmary  gall-stones 
T\-ere  found  bj'  Brockbank  §  in  101,  or  in  7.4  per  cent.  Of  these,  504  showed  gross 
cardiac  lesions,  and  in  this  category  calculi  were  present  in  55,  or  10.9  per  cent. 
— males,  5.2  per  cent. ;  females,  22.6  per  cent. ;  while  in  84.3  without  cardiac  dis- 
ease calculi  were  met  with  in  46,  or  5.4  per  cent., — males,  3.2,  females,  10.2, — so 
that  a  gross  cardiac  lesion  seemed  to  double  the  incidence  of  cholelithiasis.  This 
appeared  to  be  ahnost  equaU}'  true  both  for  the  males  and  females. 

In  200  cases  of  cardiac  disease  collected  from  the  postmortem  records  of  St. 
George's  Ho-spital  Dr.  F.  A.  Mills  ||  found  that  the  incidence  of  cholelithiasis  in  119 
males  was  14,  or  11.7  per  cent.,  while  in  81  females  there  were  16,  or  19.5  per  cent. 

*Mo.sher:  Johns  Hopkins  Bull,  Aug.,  1901. 
t  Heddteus:  Beitrage  z.  klin.  Chirurg.,  1894,  Bd.  xii,  S.  439. 
$  Keith,  A.:  The  Anatom)-  of  Glenard's  Disease,  London  Hospital  Gaz.,  Oct., 
1902,  p.  60;  and  Lancet,  1903,  vol.  i,  p.  639. 

§  Brockbank,  E.  M. :  Edin.  Med.  Jour.,  vol.  iii,  p.  51,  1898. 

II  Mills,  F.  A. :  Unpublished  Thesis  for  M.  B.  Degree,  Cambridge. 


CHOLELITHIASIS.  711 

From  ]\IiUs'  statistics  it  appears  that  the  influence  of  heart  disease 
increases  the  incidence  of  calcuH  relatively  more  in  males  than  in  females, 
for  normally  calculi  are  three  times  more  frequent  in  females,  while  in 
these  cases  of  cardiac  disease  they  are  less  than  twice  as  common.  Mills' 
statistics  also  showed  that  cardiac  disease  seems  to  affect  the  incidence 
of  cholelithiasis  by  making  it  occur  rather  earlier  in  life  than  under 
ordinary  conditions. 

In  Brockbank's  statistics  mitral  stenosis  Avas  much  the  most  effective 
form  of  heart  disease  in  inducing  cholelithiasis;  thus  in  87  cases  gall- 
stones were  present  in  19,  or  21.8  per  cent.,  this  being  twice  as  high  as 
in  any  other  form  of  cardiac  disease.  In  Mills'  200  cases  of  cardiac  disease 
the  percentage  of  gall-stones,  however,  was  liighest  in  the  aortic  cases, 
21.6  per  cent.,  and  next  in  mitral  disease,  18.75  per  cent. 

In  20  cases  of  thoracic  aneur3^sm  collected  by  Mills  (18  males,  2  females) 
there  were  no  calculi;  this  tends  to  show  that  the  causes  of  arterial 
disease  and  aneurysm,  such  as  strain,  high  tension,  hard  work,  syphilis. 
do  not  dispose  to  cholelithiasis.  In  fact,  some  of  them,  almost  certainly 
hard  work  and  exercise,  tend  to  prevent  it.  The  increased  incidence  of 
cholelithiasis  in  cardiac  cases  is,  therefore,  due  to  the  effects  of  the 
heart  lesion  and  not  to  causes  of  cardiac  disease,  such  as  strain,  high 
pressure,  and  so  forth. 

Pulmonary  diseases,  such  as  emphysema,  which  interfere  with  the 
movements  of  the  diaphragm,  or  conditions  such  as  chronic  interstitial 
pneumonia,  advanced  emphysema,  pneumoconiosis,  which  lead  to 
failure  of  the  right  side  of  the  heart  and  so  to  backward  pressure,  will 
dispose  to  gall-stones. 

Diabetes. — It  might  naturally  be  thought  that,  owing  to  the  profuse 
diuresis,  the  bile  would  be  concentrated  and  that  this  would  dispose  to 
cholangitis,  since  the  ducts  would  not  be  so  perfectly  flushed.  Ascending 
infection  from  the  duodenum  would  thus  be  rendered  easier.  Most  sta- 
tistics, however,  show  that  biliary  calculi  are  rare  in  the  bodies  of  patients 
dying  with  ordinary  diabetes  mellitus,  and  it  may,  therefore,  be  assumed 
that  diabetes  has  no  tendency  to  produce  cholelithiasis. 

In  220  cases  of  diabetes  collected  by  Windle  *  there  was  only  one  calculus,  or 
0.45  per  cent.  In  142  cases  of  diabetes  (including  122  recorded  by  Seegen)  there 
was  only  one  where  a  biliary  calculus  was  mentioned. t  This  scarcity  Brockbank 
refers  to  the  nitrogenous  diet  providing  plenty  of  bile  acids  which  keep  the  choles- 
terin  in  solution. 

In  27  consecutive  cases  of  diabetes  examined  at  St.  George's  Hospital  calculi 
were  found  in  4.  These  small  figures  are  in  antagonism  to  those  quoted  above, 
and  are  possibly  explained  by  the  fact,  referred  to  below,  that  in  two  of  the  four 
cases  the  diabetes  was  really  secondary  to  chronic  interstitial  pancreatitis  set  up 
by  gall-stones  in  the  common  bile-duct. 

But  although  dialoetes  docs  not  lead  to  tlie  production  of  gall-stones, 
the  converse  does  not  hold  good.  Thus,  if  a  calculus  becomes  lodged 
near  the  lower  end  of  the  common  bile-duct,  it  may  lead  to  infection 
and  chronic  interstitial  pancreatitis,  which  may  eventually  become  so 

*  Windle:  Quoted  by  Brockbank,  On  Cliolelithiasis,  189G. 
t  Williamson:  Diabetes,  p.  119. 


712  DISEASES    OF    THE   BILE-DUCTS. 

extensive  as  to  destroy  the  islands  of  Langerhans  and  set  up  diabetes 
mellitus.  I  have  seen  at  least  2  such  cases,  which  are  included  among 
the  4  cases  of  diabetes  at  St.  George's  Hospital  which  showed  chole- 
hthiasis.  The  occurrence  of  transient  glycosuria  during  biliary  cohc  is 
quite  another  question  and  is  referred  to  on  page  728. 

To  sum  up,  diabetes  does  not  favour  the  production  of  gall-stones, 
but  cholehthiasis  may  indirectly  produce  pancreatic  diabetes. 

In  100  cases  of  Bright' s  disease  Brockbank  found  6  cases  of  gall-stones. 
Inasmuch  as  arteriosclerosis  and  gall-stones  both  occur  about  the  same 
jDeriod  of  life,  it  would  be  natural  to  find  them  often  combined. 

In  115  cases  of  cholelithiasis  Mosher  *  found  that  50,  or  43  per  cent.,  had  arterio- 
sclerosis. 

Myxoedema. — ^Many  of  the  concUtions  favourable  to  the  formation  of 
gall-stones  are  present  in  this  disease,  such  as  the  age  (middle  hfe),  sex 
(female),  and  sedentarj"  habits. f 

Both  in  portal  cirrhosis  and  in  biliary  cirrhosis  it  is  rather  surprising 
that  biHary  calculi  are  not  commoner.  In  biliarj^  cirrhosis  there  is  catarrh 
of  the  small  bile-ducts,  and  microscopic  calcuh  or  plugs  of  il^spissated 
bile  are  often  seen  in  the  minute  bile-ducts  and  capillaries.  In  portal 
cirrhosis  a  secondary  catarrh  of  the  bile-ducts  is  not  infrequent,  and  is 
certainly  favoured  by  the  condition  of  the  liver. 

In  136  cases  of  cirrhosis  examined  after  death  at  St.  George's  Hospital  calculi 
were  present  in  21,  or  15.4  per  cent.,  but  in  some  of  these  21  cases  there  were  only 
small  bilirubin-calciimi  calculi. 

Minute  bihrubinate  of  calcium  calcuh  are  probably  more  frequent 
than  is  at  present  known  in  cases  of  common  or  portal  cirrhosis;  they 
are  smaU,  and  may  easily  escape  observation  unless  carefully  sought 
for. 

Malignant  Disease. — It  was  suggested  by  Musser  J  that  the  presence 
of  malignant  disease  anywhere  in  the  body  had  a  tendenc}"  to  lead  to 
the  formation  of  calculi  in  the  gall-bladder.  It  would  indeed  be  natural 
to  expect  that  gall-stones  would  be  found  more  frequently  in  the  subjects 
of  mahgnant  disease  than  in  ordinary  routine  postmortem  wprk;  for 
carcinoma,  which  is  the  most  frequent  form  of  malignant  disease,  occurs, 
hke  gall-stones,  most  often  in  middle  and  later  Ufe,  and  its  victims  are 
often  obhged  to  lead  a  quiet,  sedentary  hfe  which  tends  to  biharv'  stagna- 
tion and  so  favours  cholecystitis.  It  is,  therefore,  remarkable  that  the 
follo-^dng  statistics  do  not  show  any  increased  incidence  of  gall-stones 
in  patients  dying  mth  carcinoma. 

In  thirteen  and  one-half  years  4236  patients  were  examined  after  death  at  St. 
George's  Hospital.  Of  these,  242,  or  5.7  per  cent.,  had  gall-stones.  Among  the 
4236  cases  276  had  carcinoma  of  some  part  of  the  body  other  than  the  gall-bladder; 
of  these,  16,  or  5.7  per  cent.,  had  gall-stones  (176  males,  5  cases  of  cholelithiasis, 
or  2.8  per  cent.;  102  females,  11  calculi,  or  10.7  per  cent.).  This  incidence  of 
cholelithiasis  was  highest  in  primary  carcinoma  of  the  liver,  uterus,  and  mamma. 

*  Mosher:  Johns  Hopkins  Hosp.  BuU.,  Aug.,  1901. 

t  Vide  Hertoghe:  La  Nouvelle  Iconographie  de  la  Salpotriere,  1.S99. 

t  Musser,  J.  H. :  Boston  Med.  and  Surg.  Joum.,  vol.  cxxi. 


CHOLELITHIASIS.  713 

(J.  G.  Cooper.*)     In  96  cases  of  malignant  disease  of  various  parts  of  the  body 
collected  by  Beadles  f  there  was  no  case  of  cholelithiasis. 

Possibly  some  statistics  of  malignant  disease  may  show  a  high  inci- 
dence of  cholelithiasis,  but  it  must  be  borne  in  mind  that  malignant 
disease  generally  is  commoner  in  women  than  in  men,  and  the  influence 
of  sex  must  not  be  regarded  as  the  effect  of  malignant  disease.  Thus 
in  44  cases  of  carcinoma  of  the  mamma  gall-stones  were  present  in  16 
per  cent.  (Williams.  J)  Though  this  percentage  would  be  high  for  ordin- 
ary routine  work,  it  can  easily  be  explained  by  the  influence  of  sex  and 
age,  the  subjects  of  mammary  carcinoma  being  practically  always  women 
and  usually  over  thirty-five  years  of  age. 

As  is  well  known,  gall-stones  are  present  in  from  80  to  95  per  cent,  of 
cases  of  primary  carcinoma  of  the  gall-bladder,  but  there  can  be  no 
doubt  that  the  carcinoma  is  subsequent  to  and  disposed  to  by  the  presence 
of  calcuh.     (Videp.Q27.) 

In  13  cases  where  secondary  growths  were  present  in  the  gall-bladder  Siegert§ 
found  2  cases  with  calculi,  and  in  13  similar  cases,  most  of  which  I  have  exam- 
ined myself,  only  one  had  a  calculus.  This  shows  that  the  local  action  of  a  new- 
growth  in  the  gall-bladder  does  not  favour  cholelithiasis. 

Uterine  fibromyomata  are  not  uncommonly  associated  with  gall-stones. 

In  58  cases  of  gall-stones  in  women  13,  or  22.4  per  cent.,  had  fibromyo- 
mata.    (Mosher.  !|) 

Among  the  insane  the  percentage  of  gall-stones  in  routine  postmortem 
work  is  much  above  the  average ;  thus  at  Colney  Hatch  Beadles  **  finds 
that  27  per  cent,  of  females  and  5  per  cent,  of  males  have  them,  and  he 
quotes  Warnock's  tt  fignres  of  50  per  cent,  females  and  11  per  cent,  males 
dying  in  Peckham  House  Asylum  to  show  that  this  is  by  no  means  con- 
fined to  pauper  lunatics. 

Cholelithiasis  is  much  commoner  in  chronic  melancholiacs  than  in 
acute  maniacs;  Keay,tJ  who  quotes  figures  supporting  this  statement, 
believes  that  the  stooping  position  of  melancholiacs  may  play  some  part 
in  determining  the  production  of  gall-stones. 

Hereditary  Influences. — The  idea  that  cholelithiasis  is  an  hereditary 
condition  depending  on  an  underlying  constitutional  disposition  is  a  very 
old  one;  Morgagni,  indeed,  insisted  on  the  association  of  renal  and  biliary 
lithiasis,  and  has  been  followed  by  Bouchard,  Chauffard,§§  and  others 
who  believed  that  cholelithiasis  was  a  manifestation  of  the  "arthritic" 
diathesis,  which  included  rheumatism,  gout,  and  "uric  acid."  Lan- 
cereaux||||  in  117  cases  of  much  the  same  condition,  which,  however,  he 

*  Cooper,  J.  G. :  Unpublished  Thesis  for  M.  B.,  Cambritlge,  1903. 

t  Beadles:  Trans.  Path.  Soc,  vol.  xlvii,  p.  77. 

t  WiUiams,  R. :  Brit.  Med.  .Journ.,  1893,  vol.  ii,  p.  490. 

§Siegert:  Virchow's  Arohiv,  Bd.  cxxxiii,  S.  3.53. 

II  Mosher:  Johns  Hopkins  Hosp.  Bull.,  Aug.,  1901. 
**  Beadles:  Trans.  Path.  Soc,  vol.  xlvii,  p.  82. 
tt  Warnock:  Med.  Times  and  Hosp.  Gaz.,  Oct.  13,  1894. 
XX  Keav:  Medical  Treatment  of  Ciall-.stones,  p.  34. 
§§  Chauffard:  Rev.  de  Mod.,  1897. 
II II  Lancereaux:  Traito  dos  Maladies  du  foio  ct  du  iiancrcas,  p.  (iSli,  IS,'.)'.). 


714  DISEASES    OF   THE    BILE-DUCTS. 

calls  ''herpetism/'  found  cholelithiasis  in  47.  No  doubt  sedentary  habits, 
overeating,  and  dyspepsia  favour  the  development  of  both  gout  and 
gall-stones,  and,  as  Senac  has  shown,  the  two  conditions  may  occur  in 
the  same  person;  in  166  cases  of  gall-stones  collected  by  him  gout  was 
present  in  95.  The  view  that  any  diathesis  plays  an  important  part  has 
not  met  with  so  much  support  since  it  became  clear  that  local  inflamma- 
tion of  the  gall-bladder  is  the  immediate  cause  of  gall-stones ;  Frerichs  * 
and  Naunyn,t  in  particular,  have  thrown  the  weight  of  their  influence 
against  the  constitutional  factor  in  cholelithiasis.  Quite  recently  Gilbert 
and  Lereboullet  +  have  laid  stress  on  a  family  tendency  to  catarrh  of 
the  biliary  system  (simple  family  cholsemia)  which  renders  its  subjects 
specially  prone  to  various  forms  of  jaundice,  liver  disorder,  and  lithogenic 
cholecystitis.  It  is,  indeed,  probable  that  this  diathesis,  though  not 
the  sole  or  most  essential  factor,  is  yet  of  importance  in  the  production 
of  cholelithiasis,  while  it  must  not  be  forgotten  that  conditions  of  life 
and  disposing  factors,  such  as  obesity,  may  be  transmitted  from  one 
generation  to  another.  Some  statistics  show  that  gall-stones  are  heredi- 
tary in  a  large  proportion  of  cases;  this  was  so  in  62  per  cent,  of 
Kraus'  Carlsbad  patients. 

Occupation. — As  already  pointed  out,  sedentary  occupations  dis- 
pose to  cholecystitis  and  gall-stones;  it  therefore  occurs  more  frequently 
among  the  rich  who  are  lazy,  hard-working  literary  men,  clerks,  and 
devoted  men  of  business,  shoemakers,  and  in  the  poor  in  workhouses 
and  asylums  than  in  active  persons  whether  well-to-do  or  tramps.  Davy  § 
found  that  it  was  rare  among  soldiers,  but  possibly  this  is  less  true  in  j 

these  days  of  short  service  than  when  he  wrote,  viz.,  in  the  first  half  of_^y 
the  last  century.     Among  472  patients  at  Carlsbad  more  than  50  per  cent, 
were  professors,  teachers,  officials,  or  clergymen.     (Kraus.  |]) 

INCIDENCE. 

The  incidence  of  gall-stones  in  routine  postmortem  work  varies  some- 
what in  different  countries  between  10  and  6  per  cent. 

In  10,866  cases  obtained  by  combining  the  figures  of  Roth,  Schloth,  and  Schroe- 
der  there  were  1029  in  which  gall-stones  were  present,  or  9.4  per  cent.**  This 
agrees  with  Kehr's  ft  estimate  that  one-tentla  of  tlie  adult  German  population  are 
the  subjects  of  cholelithiasis.  In  America  and  England  tlie  percentage  is  lower. 
In  1655  American  cases  there  were  115,  or  6.9  per  cent.,  with  gall-stones  (MosherJJ). 
Voelcker,§§  at  the  Middlesex  Hospital,  found  gall-stones  in  8.5  per  cent.  Brock- 
bank,  nil  at  Manchester,  found  101  cases  of  gall-stones  in  1347  autopsies,  oi:  7.4  per 
cent.,  while  at  St.  George's  Hospital  there  were  242  in  4236,  or  5.7  per  cent.*** 

*  Frerichs:  Diseases  of  the  Liver,  vol.  ii,  p.  511,  New  Sydenham  Soc,  1861. 

t  Naunynr  Cholelithiasis,  p.  43,  New  Sydenham  Soc,  1896. 

%  Gilbert  and  Lereboullet:  Gaz.  hebdomen.  de  Med.  et  de  Chirurg.,  Sept.  21, 
1902. 

§  Davy,  J. :  Diseases  of  the  Army,  p.  421.  ||  Kraus:  On  Gall-stones,  p.  19. 

**  Naunyn:  Cholelithiasis,  p.  144.     Transl.  New  Sydenham  Soc. 
tt  Kehr :  On  Gall-stone  Disease,  p.  99.     American  transl. 
+t  Mosher:  Johns  Hopkins  Hospital  Bulletin,  Aug.,  1901. 
§§  Voelcker,  A.  F. :  Brit.  Med.  Journ.,  1898,  vol.  u,  p.  1555. 
nil  Brockbank:  Edinburgh  Medical  Journ.,  vol.  iii,  p.  51,  1898. 
***For  these  figures  I  am  indebted  to  Mr.  T.  C.  English. 


CHOLELITHIASIS.  715 

The  percentage  found  in  bodies  examined  after  death  is  fairl}*  repre- 
sented by  the  statistics  of  a  general  hospital.  The  niniibers  would,  of 
course,  be  extremely  small  in  a  children's  hospital  and  disproportionately 
high  in  a  workhouse  infirmary. 

Race  and  Geographical  Distribution. — Gall-stones  are  rare  in 
warm  and  tropical  countries  and  are  common  in  cold  and  damp  cities, 
probably  because  these  conditions  tend  to  induce  catarrh  of  the  biliary 
tract. 

Cholelithiasis  is  common  in  Germany,  Austria,  SAveden,  Hungary, 
Russia,  and  is  said  to  be  infrequent  in  Holland,  Finland,  Denmark,  and 
Italy.  England  probably  comes  about  midway  between  these  two 
groups.  In  America  the  percentage  incidence  is  about  the  same  as  in 
England;  thus  Mosher  found  it  to  be  7  per  cent.*  The  natives  of  India 
are  remarkably  free  from  gall-stones.  Gall-stones  are-  ver\^  rare  in 
negroes,  probably  from  their  more  active  life  and  possibly  from  the  good 
state  of  their  teeth,  in  virtue  of  which  they  would  not  be  exposed  to 
infection  of  the  alimentary  canal  from  pyorrhoea  alveolaris. 

In  America  cholelithiasis  is  less  common  in  coloured  than  in  white  patients ; 
in  106  cases  of  gall-stones  operated  upon  in  Louisville  only  one  was  coloured.! 
In  routine  postmortem  examination  at  the  Johns  Hopkins  Hospital,  Baltimore, 
however,  the  percentage  incidence  of  gall-stones  among  blacks  was  5.5  as  against 
7.9  among  whites. 

In  England  a  large  number  of  cases  come  from  the  east  coast,  espe- 
cially Lincolnshire.  Ralfe  J  says  that  the  bleak  country  between  Staf- 
ford and  Wolverhampton  furnishes  a  high  percentage  of  cases,  and  that 
the  damp  valleys  in  Wales  are  responsible  for  many  cases.  Kea3^§  con- 
siders that  it  is  commoner  in  Lancashire  than  in  London. 

Age. — The  incidence  of  gall-stones  increases  as  age  advances.  The 
majority  of  patients  with  cholelithiasis  are  over  forty  years  of  age,  and 
it  is  rare  before  thirty. 

Harley  ||  gives  the  following  estimate :  75  per  cent,  of  cases  occur  in  persons 
over  forty;  20  per  cent,  between  thirty  and  forty;  4  per  cent,  between  twenty 
and  thirty;   1  per  cent,  under  twenty. 

In  Brockbank's  **  101  cases  of  cholelithiasis  79  were  over  and  22  under  forty 
years  of  age.  In  242  cases  in  which  gall-stones  were  found  at  St.  George's  Hospital 
199,  or  82  per  cent.,  Avere  forty  or  over.  The  largest  number  were  between  the 
ages  of  fifty  and  sixty;   of  tlie  242  cases,  89,  or  37  per  cent.,  were  in  this  decade. 

The  frequency  of  biliary  calculi  in  the  gall-bladder  of  old  people  may 
possibly  be  due  to  senile  atrophy  of  the  smooth  muse  alar  tissue  in  the 
walls  of  the  gall-bladder  and  bile-ducts  (Charcot  and  Pitresft).  which,  by 
leading  to  some  degree  of  stagnation,  favours  infection  and  at  the  same 
time  interferes  with  the  expulsion  of  any  calculi  that  are  formed.  Thus, 
while  calculi  are  very  frequent  in  the  l-)odios  of  old  persons,  especially  in 

*  Mosher:  Jolms  Hopkins  Hos|).  BuU.,  -Vug.,  1901. 

t  International  Text-book  of  Surgery,  Gould  and  Warren,  vol.  ii,  p.  741. 

i  Ralfe:  Clin.  .Journ.,  Sept.  4,  189.5. 

§  Keay:  Medical  Treatment  of  Gall-stones,  p.  27. 

1!  Harley,  G. :  Diseases  of  the  Liver,  1883,  p.  577. 
**  Brockbank,  E.  M. :  F.dinburgli  Medical  Journal,  1898,  vol.  iii,  p.  51. 
tt  Charcot  and  Pitres :  Quoted  by  Waring :  Diseases  of  Liver,  p.  218. 


716  DISEASES    OF   THE    BILE-DUCTS. 

asylums  and  workhouses,  symptoms  of  biliary  colic  are  comparatively 
rare. 

Cholelithiasis  in  Early  Life.— Calculi  are  rare  under  twenty  years 
of  age.  Wlien  cholelithiasis  does  occur  in  early  life,  the  cases  may  be 
divided  into  two  classes : 

(i)  Those  in  which  the  processes  begins  in  intra-uterine  Hfe.  A 
striking  example  of  tliis  category  is  Wendel's  *  case  of  a  child  eleven 
days  old  in  whose  gall-bladder  there  were  90  small  cholesterin  calcuh. 
Thomson  f  has  collected  7  cases  of  jaundice  in  infants  either  still-born 
or  dying  within  the  first  month,  in  which  gall-stones  were  present  in  the 
ducts.  He  makes  the  very  probable  suggestion  that  gall-stone  formation 
in  infants  and  congenital  obliteration  of  the  ducts  are  dependent  on  the 
same  inflammatory  process.  Still  J  has  collected  10  cases,  including 
Thomson's  7,  in  which  small  calculi  were  present  in  infants  dying  within 
a  month  of  their  birth. 

(ii)  Calculi  found  in  children.  It  is  hard  to  draw  a  hard-and-fast 
line  between  these  two  categories,  and  very  possibly  in  cases  where  the 
cHnical  manifestations  are  first  noticed  months  or  years  after  birth  the 
process  began  in  intra-uterine  life  or  depended,  as  Albu  §  has  suggested, 
on  some  change  in  the  ducts  allied  to  congenital  obliteration  of  the  ducts. 
Cholecystitis  from  typhoidal  or  colon  infection  may  occur  in  early 
life ;  it  is,  indeed,  rather  surprising,  in  the  face  of  the  frequency  of  vari- 
ous forms  of  gastro-intestinal  infection  in  early  Hfe,  that  cholecystitis  is 
so  rare.  It  has  been  suggested  that  the  appHcation  of  a  tight  binder  to 
a  child's  abdomen  should,  by  inducing  biliary  stasis,  dispose  to  the 
formation  of  calculi.  (Wendel.)  Small  bilirubin-calcium  calculi  may  be 
found  in  cases  of  bihary  cirrhosis,  and  are  then  due  to  inflammation 
spreading  from  the  smallest  bile-ducts — a  descending  cholangitis. 

A  number  of  cases  between  three  and  fifteen  years  have  been  collected  by 
Gourdm  Serveniere  ||  and  Mercat.**  Trousseau  tt  had  previously  described  one  in 
a  girl  aged  nine  years. 

Sex. — Gall-stones  are  more  frequent  in  the  female  than  in  the  male 
sex;  the  ratio  has  been  variously  estimated  at  from  five  to  one  to  four 
to  three.  Schroederf  |  found  gall-stones  five  times  in  females  to  once  in 
males ;  Brockbank,  §  §  four  times  in  females  to  once  in  males ;  Harley  H  ||  and 
Kraus,***  twice  in  females  to  once  in  males;  Mosher,|ft  three  times  in 
females  to  twice  in  males.  In  242  cases  in  which  gall-stones  were  found 
after  death  at  St.  George's  Hospital  the  number  of  women  (136)  was 
in  excess  of  the  males  (106)  in  the  ratio  of  4  to  3. 

*  Wendel:  Medical  Record  (N.  Y.),  July  9,  1898,  p.  41. 

t  Thomson,  J. :  Edinburgh  Hosp.  Reports,  vol.  v. 

t  Still,  G.  F. :  Trans.  Path.  Soc,  vol.  1,  p.  154. 

§  Albu:  Deutsche  med.  Wochen..  March  31,  1898,  S.  201. 

I!  Serveniere:  These  Paris,  1889.  **  Mercat:  These  Paris,  1884. 

tt  Trousseau:  Chnical  Medicine,  vol.  iv,  p.  224.     Transl.  New  Sydenham  Soc. 
tj  Schroeder:  Quoted  by  Naunyn,  Cholelithiasis,  p.  40. 

§§  Brockbank:  Loc.  cit.  ||  ||  Harley:  Diseases  of  Liver,  p.  575,  1883. 

***  Kraus:  On  Gall-stones,  English  translation,  p.  2,  1896. 
ttt  Mosher:  Johns  Hopkins  Hospital  Bulletin,  Aug.,  1901. 


CHOLELITHIASIS.  717 

The  factors  determining  the  greater  incidence  of  gall-stones  in  women 
are: 

(i)  A  lax  condition  of  the  abdominal  walls,  wliich  favours  ^dscerop- 
tosis  and  may  even  produce  hepatoptosis.  As  a  result,  stagnation  of 
bile  in  the  gall-bladder,  a  condition  disposing  to  infection,  is  brought 
about,  (ii)  Abdominal  tumors,  such  as  uterine  myomata,  ovarian  cysts, 
and  the  pregnant  uterus  produce  relaxation  of  the  abdominal  wall  and 
interfere  vdih  diaphragmatic  respiration,  (iii)  Tight  lacing  may  act  in 
several  ways :  by  displacing  the  liver  it  may  kink  the  common  or  cystic 
ducts  and  mechanically  obstruct  the  outflow  of  bile  from  the  gall-bladder. 
It  also  tends  to  diminish  diaphragmatic  breathing  and  to  increase  costal 
respiration.  The  movements  of  the  diaphragm  are  of  importance  in 
empt}dng  the  gall-bladder,  and  hence  if  they  are  cUminished,  stagnation 
of  bile  follows,  (iv)  The  more  sedentary  life  led  by  most  women,  (v) 
Constipation  is  commoner  in  women  and  is  favourable  to  infection  of  the 
bile-ducts  and  gall-bladder.  (\d)  Pregnancy.  (Vide  p.  709.)  (vii)  The 
frequency  of  inflammatory  pehdc  conditions  in  women  has  been  urged 
by  Mosher  *  as  a  cause  of  the  greater  incidence  of  gall-stones  among 
women.  The  resulting  peritoneal  adhesions  may  indirectly  exert  some 
mechanical  difficulties  to  the  free  exit  of  bile  from  the  gall-bladder,  while 
at  the  outset  infection  may  be  carried  to  the  gall-bladder. 


CLASSIFICATION  OF  GALL-STONES. 

The  foUo'^dng  classification  of  gall-stones,  according  to  their  chemical 
composition,  is  given  by  Naunyn: 

I.  Pure  cholesterin  calculi  are  comparatively  uncommon.  They  are 
white,  yellow,  or  more  rarely  brown  or  greenish,  and  have  a  translucent 
appearance.  The  surface  is  nodular,  crystalline,  or  smooth,  but  hardly 
ever  facetted.     On  section  they  are  crystalline,  but  not  stratified. 

II.  Laminated  cliolesterin  calculi  contain  90  per  cent,  of  cholesterin, 
with  calcium  carbonate  and  traces  of  bilirubin  and  bilivercUn  in  com- 
bination with  calcium.  Externally  they  resemble  pure  cholesterin  cal- 
culi, but  are  often  facetted.  On  section,  there  are  alternating  laminse — 
white  and  brown,  yellow  or  green.  The  coloured  layers  contain  bilirubin- 
calcium  when  brown,  and  biliverdin-calcium  and  calcium  carbonate  when 
green. 

III.  The  Common  Gall-stones  (Mixed Cholesterin  Calculi). — They  vary 
in  size  and  colour.  They  are  usually  facetted,  are  seldom  larger  than 
a  cherry,  and  may  be  very  small  and  numerous.  They  are  usually  3'ellow, 
but  may  be  brown  or  white.  When  fresh,  they  are  greasy  and  soft,  but 
when  dried,  they  become  hard  externalh'.  There  may  be  a  central  ca^'ity 
inside. 

IV.  Mixed  hilirvhin  ayul  cholesterin  calculi  contain  as  much  as  25 
per  cent,  of  cholesterin,  the  remainder  being  bilirubin-calcium.jfeThey 
occur  in  the  gall-bladder  or  large  bile-ducts,  and  consist^of  a  nucleus  of 

*  Mosher:  .Johns  Hopkins  Hosp.  Bull.,  Aug.,  1001. 


718  ■    DISEASES    OF   THE    BILE-DUCTS. 

cholesterin  covered  by  thick  lavers  ot  dark-brown  material  which  readily 
chips  off. 

V.  Pure  Bilirubin-calcium  Calculi. — They  vary  from  the  size  of  a 
pea  to  a  grain  of  sand.  There  are  two  types:  one  is  solid,  brown  in 
colour,  rough  on  the  surface,  and  with  a  tendency  to  become  welded 
together.  The  second  type  is  harder,  smooth,  black,  has  a  metallic  lustre, 
and  internally  a  spongy  structure. 

VI.  Rarer  Forms. — (a)  Amorphous  and  incompletely  crystalline  choles- 
terin gravel:  these  small  calculi  may  look  like  pearls ;  the  nucleus  is  of 
different  composition— of  ten  of  bilirubin  cholesterin.  (5)  Calcium  car- 
bonate calculi  are  very  infrequently  seen,  (c)  Calculi  containing  foreign 
bodies,  such  as  fragments  of  worms,  ligatures  {vide  p.  709).  {d)  Cori- 
glomerate  calculi,  which  are  composed  of  two  or  more  small  calculi  united 
under  a  common  sheath,  (e)  Casts  of  bile-ducts  are  very  rare  in  man; 
bilirubin-calcium  casts  are  found  in  cattle. 


MODE  OF  FORMATION  OF  CALCULI  IN  THE  GALL-BLADDER. 

The  cholesterin  from  which  the  calculi  are,  in  the  first  instance, 
largely  formed,  is  not  derived  from  the  bile  itself,  but  from  the  disinte- 
gration of  the  cells  lining  the  gall-bladder,  and  is  the  outcome  of  per- 
verted metabolism  induced  by  catarrh.  Inside  the  cells  of  an  inflamed 
gall-bladder  myelin  bodies — ^the  precursors  of  cholesterin — can  be  seen. 
Cholesterin  is  formed  by  other  mucous  surfaces,  but  calculus  formation 
does  not  result,  since  there  is  an  absence  of  the  necessary  cementing  sub- 
stance. According  to  Naunyn,  the  cementing  substance  is  present  in  the 
gall-bladder  in  the  form  of  bilirubin-calcium.  Masses  of  cholesterin 
inixed  with  bilirubin-calcium  form  the  earliest  stage  of  a  calculus.  The 
further  development,  according  to  Naunyn,  may  proceed  in  different 
ways :  The  mass  may  become  surrounded  with  a  firm  crust  of  bilirubin- 
calcium,  while  the  cholesterin  and  bilirubin-calcium  crystallise  out  on  the 
inner  surface  of  the  outer  crust,  thus  leaving  a  central  cavity.  Or  the 
firm  outer  layer  may  be  produced  by  drying,  starting  in  the  outer  layer 
of  the  mass  of  bilirubin-calcium  and  cholesterin,  after  which  crystalli- 
sation takes  place  inside  the  shell  with  the  production  of  a  central 
cavity  as  before.  So  far  as  the  formation  of  an  immature  calculus  has 
been  traced,  the  further  changes  leading  to  the  growth  and  formation  of 
a  stratified  and  more  solid  calculus  are  as  follows : 

The  growth  of  a  calculus  is  chiefly  the  result  of  deposition;  on  its 
surface,  of  concentric  layers  of  cholesterin  and  of  bilirubin-calciimi  or 
biliverdin-calciura.  The  cholesterin  forms  white  laminro,  and  is  de- 
posited, not  as  crystals,  but  as  a  pultaceous  mass  of  myelin  bodies  sup- 
plied by  the  cells  of  the  gall-bladder.  In  the  formation  of  pure  choles- 
terin calculi  the  gall-bladder  contents  must  be  free  from  any  bile,  as  in 
cases  of  obstruction  of  the  cystic  duct.  Bilirubin-calcium  forms  brown 
strata,  while  biliverdin  produces  green  strata;  their  deposition  occurs 
when  the  gall-bladder  contains  bile. 

An  important  change  by  which  the  calculus  becomes  affected  is  the 


CHOLELITHIASIS.  719 

infiltration  of  its  substance  from  without  by  cholesterin,  exactly  in  the 
same  way  as  a  calculus  in  the  urinary  bladder  is  invaded  by  phosphates 
and  other  salts.  The  secondary  infiltration  of  a  gall-stone  with  choles- 
terin  ma}''  be  derived  from  the  epithelial  walls  of  the  gall-bladder  if  in 
contact  with  it,  or  from  the  cholesterin  in  the  bile.  The  cholesterin 
tracks  along  small  fissures  and  canals  in  the  calculus,  and  penetrates  into 
its  interior;  it  then  crystallises,  and  these  crystals  increase  in  size.  This 
process  begins  at  the  centre,  and  spreads  outwards  towards  the  periphery. 
While  this  permeation  with  cholesterin  is  proceeding  the  bilirubin-calcium 
is  dissolved  out,  and  the  percentage  of  cholesterin  increases;  in  this  way 
a  pure  cholesterin  calculus  may  be  produced. 

Time  Required  for  the  Formation  of  Calculi. — From  his  experi- 
mental researches  Mignot  *  believes  that  it  takes  five  or  six  months  to 
form  a  stratified,  well-formed  biliary  calculus.  For  this  it  is  necessary 
that  there  should  be  comparative  stagnation  of  bile,  othermse  the  soft, 
immature  calculus  would  be  expelled  with  the  bile  from  the  gall-bladder. 
Calculi  found  in  the  gall-bladder  may  be  all  of  the  same  age  and  due  to 
one  and  the  same  attack  of  cholecystitis,  which  is  a  transitory  event. 
If  recurrent  attacks  occur, — and  this  readily  may  take  place  in  a  damaged 
gall-bladder, — fresh  calculi  may  be  formed. 

The  formation  of  calculi  in  the  ducts  is  described  under  the  immediate 
causes  of  cholelithiasis. 

Size  and  Number. — There  may  be  one  or  almost  any  number  of 
calculi  in  the  gall-bladder.  A  single  calculus  may  be  very  large  and 
cause  great  distension  of  the  gall-bladder. 

Meckel  recorded  a  calculus  6^^  inches  long  and  6  inches  thick.  A  large  single 
calculus  is  usually  a  laminated  or  a  pure  cholesterin  stone. 

In  Fiedler's  t  case  a  calculus  weighed  46  grammes  (li  ounces)  and  consisted 
of  three  pieces  which  fitted  together  to  form  a  cast  of  the  elongated  gall-bladder 
and  was  at  least  12  inches  long.  Richter  J  in  1793  recorded  an  enormous  calculus 
weighing  3  ounces  5  drachms,  which  is  the  largest  ever  described.     (Mayo  Robson.§) 

Occasionally  very  large  numbers  of  small  calculi  are  found  in  the 
gall-bladder. 

Naunyn  |1  counted  5000  in  a  gall-bladder,  V)ut  this  is  surpassed  by  7802  in 
Otto's  **  case. 

The  small  calculi  found  in  sued  large  number  are  curiously  alike  in 
appearance,  and  are  generally  of  the  mixed  cholesterin  form. 

Shape. — There  is  a  great  deal  of  \-ariation  in  the  sliape  of  biliary 
calculi,  which  largely  depends  on  tlieir  sun-oundings.  A]:)art  from  ex- 
ternal influences,  calculi  probably  tend  to  l)e  roimd. 

The  large  single  stone  filling  up  the  gall-bladder  is  usually  somcwliat 
elongated  and  pear-shaped,  and  may  l)e  conglomerate  from  the  union 

*  Mignot,  R. :  Tliese  Paris,  1S97,  and  .\rchiv.  general,  de  Mod.,  .Vug.,  1S98. 
t  Fiedler:  .Iahrcsl)cricht  d.  ( iesellschaft  f.  Nat.  u.  Heilk.,  Dresden,  1879. 
%  Vide  Hutchinson's  Archives  of  Surgery,  vol.  iii,  p.  6,  1892. 
§  Diseases  of  Gall-bladder,  p.  21.5,  ed.  iii. 

II  Naunyn :  On  Cholelithiasis,  ]).  6.     Translat.  New  Sydenham  Soc. 
**  Otto:  Quoted  by  G.  Harley,  Diseases  of- the  Liver,  p.  583,  1883. 


720 


DISEASES    OF   THE    BILE-DUCTS. 


and  welding  together  of  previously  separate  calculi.     A  single  loose 

calculus,  when  composed  of  pure  cholesterin, 
is  often  bossed  like  a  mulberry  calculus  in 
the  kidney.  Multiple  gall-stones  in  the 
gall-bladder  are  sometimes  round,  but  are 
more  often  irregidarly  square,  mth  facets 
separated  by  rounded  edges.  When  im- 
pacted in  the  commencement  of  the  cys- 
tic duct,  a  calculus  may  be  somewhat 
elongated. 

Crumbling  calcuh  in  the  common  bile- 
duct  become  elongated  and  moulded  to  the 
duct.  The  small  bilirubin-calcium  calculi 
formed  in  the  intra-hepatic  ducts  are  elong- 
ated and  represent  the  lumen  of  the  duct 
in  which  they  were  formed.  Occasionally 
branching  calcuh  resembhng  coral  are  found 
in  the  larger  intra-hepatic  ducts. 

Situation. — Calculi  in  the  gall-bladder 
are  usually  loose  in  the  bile,  or,  when  the 
cystic  duct  has  been  permanently  blocked 
for  some  time,  in  the  mucus.  In  some  cases 
the  gall-bladder  is  firmly  contracted  on  the 
calculus.  In  some  instances  the  gall-bladder 
may  contain  a  large  number  of  calculi  closely 
packed  and  facetted  on  each  other,  there 
being  no  bile  or  jnucus  in  the  gall- 
bladder. 

In  cases  where  the  gall-bladder  is 
thus  distended  with  calcuh  a  crackhng 
sensation  may  sometimes  be  felt  on 
palpation. 

A  large  gall-stone  may  be  adherent 
to  the  mucous  membrane  of  the  gall- 
bladder. In  an  hour-glass  gall-bladder 
calcuh  contained  in  the  distal  com- 
partment may  be  closely  united  to  the 
mucous  membrane.  It  is  compara- 
tively common  to  find  a  calculus  im- 
pacted in  the  neck  of  the  gall-bladder 
and  thus  obstructing  the  orifice  of  the 
cystic  duct. 

Calculi,  or  masses  of  cholesterin 
which  hardly  deserve  the  name  of 
calculi,  are  sometimes  found  embedded 
in  the  wall  of  the  gall-bladder.  This 
has  a  direct  relation  to  the  manufacture 

of  cholesterin  by  the  mucous  membrane  of  the  gall-liladdcr  and  of  its 
mucous  glands. 


Fig.  93. — Dhawixg  of  a  Gall- 
bladder IN  St.  George's 
Hospital  Museum,  Dis- 
tended WITH  A  Number  of 
Facetted  Gall-stones. 
(Drawn  by  Dr.  E.  A.  Wilson.) 


Fig.  94. — A  Calculus  Impacted  in 
THE  Neck  of  the  Gall-bladder. 
(Drawn  by  Dr.  E.  A.  Wilson.) 


CHOLELITHIASIS. 


721 


In  a  case  of  parietal  calculi  recorded  by  Peraire  *  there  were  a  series  of  gall- 
stones embedded  in  the  wall  of  the  gall-bladder,  and  27  calculi  the  size  of  peas  in 
the  lumen  of  the  cystic  duct,  but  none  in  the  cavity  of  the  gaU-bladder. 

A  gall-stone  may  set  up  ulceration  and  weakening  of  the  gall-bladder, 
and  may  thus  form  for  itself  a  Idnd  of  diverticulum  in  which  it  becomes 
encysted.  This  is  a  rare  event,  and  is  more  often  seen  near  the  fundus 
or  at  the  neck  of  the  gall-bladder.  Under  ordinary  conditions  the  calculi 
are  naturally  usually  found  lying  in  the  fundus  of  the  gall-bladder. 

The  occurrence  of  calcuh  in  the  cystic  and  common  bile-duct  is 
referred  to  elsewhere.  {Vide  pp.  737  and  739.)  In  rare  instances  a  cal- 
culus derived  from  the  gall-bladder  passes  backwards  from  the  cystic 
duct  into  the  common  hepatic  duct. 

An  olive-shaped  calculus  the  size  of  a  small  pigeon's-egg  M^as  removed  from 
the  common  hepatic  duct  of  a  woman  aged  sixty-seven  years  by  Le  Filliatre.t 


.^- 


Fig.  95. — Laege  Intea-hepatic  Calculi  Distending  the  Right  and  Left  Hepatic  Ducts. 
(Drawn  by  Dr.  E.  A.  Wilson.) 


Intra-hepatic  Calculi. — Large  intra-hepatic  calculi  occupying  the 
hepatic  ducts  and  distending  them  are  very  rare.  I  met  with  one  such 
case  in  a  man  who  died  with  diabetes  from  secondary  chronic  pancrea- 
titis. J     (Vide  Fig.  95.) 

Murchison§  refers  to  a  plate  of  Cruveilhier's  (livraison  xii,  Plate  V), 
showing  large  branching  intra-hepatic  calculi  like  coral.  There  is  a  good 
specimen  of  multiple  intra-hepatic  calculi  in  the  Westminster  Hospital 
Museum  (No.  581).  These  calcuh  almost  necessarily  set  up  jaundice 
and  a  good  deal  of  pericholangitis,  wliich  may  be  suppurative.  The 
calcuh  are  chiefly  composed  of  bilirubin-calcium.  Small  black  bihrubin- 
calcium  calculi  are  not  uncommon. 

*  Peraire:  Bull.  Soc.  Anat.  Paris,  1902,  p.  707. 
t  Le  Filliatre :  Bull.  Soc.  Anat.  Paris,  1900,  p.  626. 
j  Rolleston:  Trans.  Path.  Soc,  vol.  xlix,  p.  133. 
§  Murchison :  Diseases  of  Liver,  2d  ed.,  p.  545. 
46 


722  DISEASES    OF   THE    BILE-DUCTS. 

Occasionally  masses  of  calculous  material  are  found  embedded  in 
the  substance  of  the  liver  in  dilated,  ampulla-like  terminations  of  bile- 
ducts  which  have  lost  their  continuity  with  the  bile-ducts. 

Small  facets  on  the -surface  of  gall-stones  show  that  there  either  are 
or  have  been  more  than  one  calculus  in  the  gall-bladder  or  ducts.  Two 
or  more  facets  on  one  calculus  are  in  favour  of  the  number  of  stones 
being  more  than  two.  Facetting  generally  indicates  that  the  calculi 
have  been  closely  packed. 

Facetting  is  commoner  on  medium-sized  stones,  but  may  be  seen  on 
comparatively  large  calculi.  In  small  bilirubin-calcium  calculi  which 
are  freely  movable  on  each  other  there  are  no  facets  as  a  rule. 

Spontaneous  Fracture  of  Gall-stones  in  the  Gall-bladder. — Cases 
in  which  a  gall-stone  has"  been  found  to  have  broken  up  within  the  gall- 
bladder have  been  reported  by  Pearce  Gould,*  Hadden,t  Calvert, |  and 
myself. §  Traumatism  during  life  or  in  the  course  of  the  postmortem 
examination  appears  to  have  been  excluded,  and,  though  conceivable, 
it  does  not  seem  very  likely  that  vigourous  contraction  of  the  gall-bladder 
would  fracture  even  a  friable  calculus.  It  is  more  probable  that  the 
fracture  is  brought  about  in  much  the  same  way  as  spontaneous  fracture 
of  vesical  calculi  in  the  urinary  bladder,  as  explained  by  W.  M.  Ord,  1| 
and  Plo Wright.**  It  is  known  that  under  ordinary  conditions  cholesterin 
works  its  way  in,  while  bilirubin-calcium  passes  out,  of  biliary  calculi. 
Chauffard  ft  and  others  have  shown  that  micro-organisms  of  the  colon 
group  may  also  pass  in.  By  forming  a  deposit  between  the  layers  of 
the  calculus  this  microbic  invasion  would  tend  to  loosen  and  split  off 
the  more  superficial  layers  of  the  calculus. 

It  was  suggested  by  Calvert  that  fracture  might  depend  on  drying 
of  a  calculus.  It  is  conceivable  that  in  some  instances  the  union  and  sub- 
sequent disruption  of  a  number  of  calculi  might  imitate  spontaneous 
fracture.  Care  must  also  be  taken  not  to  regard  as  examples  of  spon- 
taneous fracture  marked  facetting  of  the  surfaces  of  adjacent  calculi. 

CLINICAL  PICTURE. 

Gall-stones  are  frequently  present  in  the  gall-bladder  without  giving 
rise  to  any  symiDtoms.  Kehr  J  J  states  that  symptoms  occur  in  only  5 
per  cent,  of  persons  whose  gall-bladders  contain  calculi.  This  latency  is 
especially  common  in  old  people,  in  whom  the  muscular  tissue  of  the 
gall-bladder  and  ducts  is  atrophied,  and  it  has  been  thought'  that  for 
this  reason  the  passage  of  a  calculus  out  of  the  gall-bladder  into  the  ducts 
is  less  likely  to  occur. 

The  symptoms  produced  by  gall-stones  are  extremely  numerous  anil 

*  Pearce  Gould:  Trans.  Clinic.  Soc,  vol.  xxi,  p.  193. 

t  Hadden,  W.  B. :  Trans.  Path.  Soc,  vol.  xli,  p.  160. 

X  Calvert,  .1.:  Trans.  Path.  Soc,  vol.  xlix,  p.  139. 

§  Rolleston,  H.  D. :  Trans.  Path.  Soc,  vol.  xlix,  p.  135. 

II  Ord,  W.  M. :  Trails.  Path.  Soc,  vol.  xxviii,  p.  170;  vol.  xxxii,  p.  304. 
**  Plowriaiht:  Trans.  Path.  Soc,  vol.  xlvii,  p.  132. 
ft  Chauffard:  Rev.  de  Med.,  Feb.,  1S97. 
XX  Kelir,  H.:  Diagnosis  of  Gall-stone  Disease,  p.  25,  .Vnierican  translat. 


Plate  6. 


j^^^ 

^t^ 


Gall-stones  from  a  Case  in  which  Fractukf.  was  Spontaneous. 

The   largest  calculus    sbows   surface    wliei'e   spoutaneous    fi'acture    h;is    occurred.  The    calculus 

below  and  to  the  left   fitted  into  it.     The  oilier  calculi  were  in  the  same  gall-bladder.  I'roiu    a  case 

of  primary  carcinnnni  of  the  gall-bladdiu'  in  which  spontaneous  fracture  of  the  calculi  bad  occurred. 
I'aiMled  by  Dr.  K.  A.  Wilson. 


CHOLELITHIASIS.  723 

variable.  It  mil  be  most  satisfactory  to  divide  their  description  into 
that  of — (i)  Biliary  colic;  (ii)  the  purely  mechanical  or  aseptic  effects 
of  gall-stones;  and  (iii)  the  inflammatory  and  infective  changes  set 
up  by  cholelithiasis;  special  descriptions  will  be  given  of  intestinal  ob- 
struction and  of  fistulte  produced  by  gall-stones,  under  the  headings 
of  (ii)  and  (iii)  respectively. 

BILIARY  COLIC. 

Typical  biliary  colic  is  generally  regarded  as  the  result  of  spasm  set 
up  by  the  passage  of  a  calculus  down  the  cystic  and  common  bile-ducts. 
Attacks  of  pain  of  less  severity  may  possibly  be  due  to  spasm  set  up  by 
a  stone  in  the  gall-bladder  which  has  not  actually  entered  the  cystic  duct. 
Inspissated  bile  and  precipitated  masses  of  cholesterin  and  bile-pigments 
in  the  ducts  may  also  induce  modified  attacks  of  biliary  colic.  Inflamma- 
tion and  spasm  extending  to  the  ducts  from  cholecystitis  must  also  be 
reckoned  with  as  a  cause  of  biliary  colic.  In  other  words,  bihary  colic 
may,  like  the  pain  of  appendicitis,  be  independent  of  calculi.  Chole- 
cystitis with  closure  of  the  cystic  duct  from  any  cause  will  give  rise 
to  painful  contractions  of  the  gall-bladder;  in  many  cases  the  factor 
responsible  for  closure  of  the  cystic  duct  is  a  calculus. 

In  recent  times  some  writers,  such  as  Riedel*  and  Kehr,  have  mini- 
mised the  purely  mechanical  role  of  calculi  in  the  production  of  biliarv 
colic,  and  have  insisted  on  the  importance  of  cholecystitis  and  on  the  ex- 
tension of  inflammation  to  the  ducts  as  the  cause  of  pain  and  jaundice. 
But  while  inflammatory  obstruction  of  the  cystic  duct  is  quite  enough  to 
set  up  painful  contractions  of  an  inflamed  gall-bladder,  there  is  no  reason 
to  doubt  that  the  mechanical  irritation  of  a  calculus  in  the  ducts  sets 
up  spasm  and  colic  in  the  same  Avay  that  a  calculus  in  the  ureter  causes 
renal  colic.  In  other  words,  biliary  cohc  may  be  due  to  inflammatory 
or  to  mechanical  obstruction,  or  to  both  combined. 

Cause  of  the  Passage  of  Calculi  out  of  the  Gall-bladder. — Gall- 
stones are  very  commonly  latent  in  the  gall-bladder;  it  has,  indeed,  as 
mentioned  above,  been  estimated  that  only  .5  per  cent,  of  persons  with 
gall-stones  in  the  gall-bladder  suffer  from  them.t  It  is,  therefore,  clear 
that  some  conditions  other  than  those  of  ordinary  life  must  be  responsible 
for  the  passage  of  calculi  into  the  cystic  duct,  and  that  something  more 
is  required  than  the  ordinary  muscular  contractions  of  the  gall-bladder 
which  suffice  to  drive  out  the  bile.  It  has  been  thought  that  unusually 
vigourous  contractions  of  the  gall-bladder,  such  as  might  be  induced  by 
violent  emotion,  may  determine  the  passage  of  gall-stones  into  the  cystic 
duct.  The  onset  of  colic  at  the  menstmal  periods  has  been  referred  to 
spasmodic  contraction  of  the  gall-bladder  set  up  by  nervous  perturbation. 
Occasionally  jolting,  such  as  riding  in  a  cart  without  springs,  a  railway 
journey,  riding  a  bicycle,  etc.,  has  been  thought  to  determine  the  passage 
of  calculi  into  the  cystic    duct.      Koay  J  l)('lio\'os  that  ]):iin   following 

*  Riedel:  Berlin,  med.  Woclion.,  Bd.  xxxviii,  S.  i,  1901. 

t  Kehr,  H. :  Diagnosis  of  (!all-stono  Disease,  ]).  25.     American  translation. 

t  Keay:  Mediral  Treatment  of  (iall-stones,  p.  37. 


724  DISEASES   OF  THE    BILE-DUCTS. 

jolting  is  due  to  stretching  of  adhesions  rather  than  to  the  passage  of 
gall-stones,  and  that  a  stooping  posture  favours  the  migration  of  a  cal- 
culus out  of  the  gall-bladder.  Von  Noorden  *  has  pointed  out  that  biUary 
coHc  may  occur  in  patients  immediately  after  treatment  for  obesity,  and 
suggests  that  the  removal  of  fat  allows  the  pressure  of  corsets  to  interfere 
with  the  flow  of  bile  out  of  the  gall-bladder. 

Clinical  palpation  of  the  gall-bladder  is  certainly  sometimes  followed 
by  cohc,  but  it  can  be  very  rarely  that  the  stone  is  directly  forced  into 
the  cystic  duct.  Traumatism,  such  as  a  fall  or  blow,  may,  by  reducing 
the  resistance  of  the  gall-bladder,  allow  micro-organisms  to  set  up  chole- 
cystitis and  so  lead  to  the  expulsion  of  a  calculus  into  the  ducts. 

Wliile  not  denjdng  the  possibility  that  the  contractions  of  the  gall- 
bladder maj^  drive  calculi  into  the  cystic  and  common  bile-duct,  Kehr  f 
beUeves  that  the  important  factor  in  determining  the  migration  of  calcuH 
from  the  gall-bladder  into  the  ducts  is  inflammation  of  the  gall-bladder. 
The  mechanism  is  as  follows :  Cholecystitis  gives  rise  to  an  inflammatory 
exudation  which  distends  the  gall-bladder  and  drives  the  calculus  into 
the  cystic  duct.  Enlargement  of  the  gall-bladder,  tenderness,  and  fever 
during  bihary  colic  are  in  favour  of  the  view  that  cholecystitis  plays  an 
important  part  in  its  production.  When  the  calculus  is  impacted  in  the 
duct,  it  will  mechanically  set  up  painful  spasm  of  the  ducts  and  gall- 
bladder. Acute  cholecystitis  may  be  set  up  by  ixdcrobic  infection  de- 
rived either  from  the  intestine  or  from  the  general  circulation.  Diarrhoea, 
typhoid  fever,  influenza,  may  thus  be  antecedent  conditions  to  an  attack 
of  bihary  colic. 

Onset. — The  extremely  violent  pain  of  bihary  colic  may  come  on 
quite  suddenly,  or  may  be  preceded  by  symptoms,  such  as  shivering, 
nausea,  and  vomiting,  compatible  with  the  view  that  cholecystitis  is 
in  progress.  Formerly  the  entrance  of  a  gall-stone  into  the  cystic  duct 
was  thought  to  be  the  outcome  of  contractions  of  the  gall-bladder  set  up 
reflexly  by  the  passage  of  food  into  the  duodenum,  and  three  to  four 
hours  after  food  was  thought  to  be  a  specially  probable  time  for  the  onset 
of  biliary  cohc.     Biliary  colic  more  commonly  commences  at  night. 

The  onset  of  the  menstrual  period  has  been  thought,  by  inducing 
nervous  disturbance  and  general  engorgement  of  the  abdominal  viscera, 
to  determine  an  attack  of  biliary  colic. |  During  pregnancy  and  lactation 
biliary  colic  is  either  less  frequent  or  absent,  but  after  weaning  the  child 
severe  attacks  may  occur.  As  has  already  been  pointed  out,  pregnancy 
favours  the  production  of  gall-stones.  {Vide  p.  709.)  After  delivery 
conditions  leading  to  infection  of  the  gall-bladder  are  not  uncommon,  and 
thus  the  onset  of  colic  may  be  determined. 

Signs  and  Symptoms. — The  pain  in  bihary  colic  is  due  to  two  factors 
— ^in  the  first  instance,  there  is  probably  nearly  always  acute  inflammation 
of  the  gall-bladder,  which  precedes  and  may  be  the  determining  factor  in 
the  expulsion  of  calculi  into  the  cystic  duct.  The  pain  of  acute  cholecystitis 

*  Von  Noorden,  C. :  Diseases  of  the  Metabolism  and  Nutrition,  Part  I,  Obesity, 
p.  31,  1903.     E.  B.  Treat  and  Co.,  New  York. 

t  Kehr:  Loc.  cit.,  p.  26.  J  Cornillon:  Le  progr6s  Med.,  April  24,  1897. 


CHOLELITHIASIS.  725 

is  felt  in  the  right  h^iDochondrium  and  epigastrium.  When  the  calculi 
pass  into  the  cystic  duct,  severe  muscular  spasm  is  set  up,  which  mani- 
fests itself  by  pain  in  the  right  loin  and  back.  Keay,*  from  personal 
experience  and  from  observation  of  patients,  believes  that  pain  depending 
on  the  presence  of  a  calculus  in  the  cystic  duct  begins  to  the  right  of  the 
region  between  the  eighth  and  eleventh  dorsal  vertebrae.  In  this 
view  Keay  differs  from  most  authorities,  such  as  Naunyn,  who  state 
that  the  pain  begins  in  the  epigastrium  or  right  hypochondrium.  Tliis 
pain  is  extremely  severe,  as  if  the  back  was  being  broken.  It  passes  to 
the  right  hypochondrium  and  radiates  from  this  spot  in  all  directions — 
to  the  left  hypochondrium,  the  umbilical  and  hypogastric  regions,  to 
the  thighs,  and  even  to  the  arms  and  neck.  The  pain  is  usually  stated 
to  radiate  to  the  right  shoulder,  but  this  is  less  frequent  in  biliary  colic 
than  in  hepatic  abscess. 

The  pain,  which  is  usually  paroxysmal,  is  probably  one  of  the  most 
agonising  forms  humanity  is  subject  to;  women  speak  of  it  as  being 
much  worse  than  the  pains  of  labour.  The  intensity  of  the  pain  may 
give  rise  to  hysterical  or  epileptiform  attacks,  and  in  very  rare  cases  the 
patients  have  died  apparently  simply  from  the  shock  of  the  pain.  (All- 
butt,!  Mayo  Robson.J) 

The  pain  is  so  excruciating  that  the  patient  throws  himself  into  various 
positions  to  obtain  relief,  but  without  any  success.  He  may  roll  in  agony 
on  the  floor  and  scream,  cry,  or  groan  in  a  very  distressing  manner.  The 
intense  pain  gradually  diminishes,  and  the  patient  experiences  a  constant 
duU  aching  which  is  interrupted  by  paroxysms  of  intense  pain.  It  is 
supposed  that  alleviation  of  the  pain  may  coincide  with  the  passage  of 
the  calculus  out  of  the  small  cystic  duct  into  the  larger  common  bile-duct. 

The  first  attack  is  nearly  always  much  more  severe  than  subsequent 
seizures,  and  it  is  believed  that  a  small  calculus  in  a  first  attack  may 
give  rise  to  far  more  pain  than  larger  gall-stones  on  subsequent  occasions. 
There  is  thus  no  absolute  relationship  between  the  size  of  the  calculi  and 
the  severity  of  the  pain.  The  ducts  become  dilated  by  the  passage  of 
successive  calculi,  and  eventually  a  large  one  may  pass  almost  unnoticed. 

Pain  may  suddenly  disappear  as  if  by  magic,  and  may  be  due  to  the 
escape  of  the  calculus  into  the  duodenum.  Keay  believes  that  at  the 
moment  when  the  stones  pass  into  the  duodenum  there  is  a  peculiar  ghd- 
ing  sensation  to  the  right  of  the  tenth  and  twelfth  dorsal  vertebrae. 

The  violent  pain  usually  lasts  for  some  hours — ^three  to  twelve — if 
unrelieved  by  moiphia.  In  rare  instances  it  may  only  last  for  a  few 
minutes. 

The  pain  is  sometimes  described  as  lasting  for  days,  but  this  is  proba- 
bly due  to  a  succession  of  attacks  supervening  rapidly,  with  pain  of  a 
less  severe  character,  due  to  the  inflamed  or  distended  and  inflamed  gall- 
bladder, in  the  intervals  between  the  more  severe  paroxysms. 

It  has  been  estimated  that  the  temperature  is  raised  in  60  per  cent. 

*Keay:  Brit.  Med.  Journ.,  1900,  vol.  i,  p.  901.     Medical  Treatment  of  Gall- 
stones, p.  75.  t  Allbutt:  In  his  System  of  Medicine,  vol.  iii,  471. 
t  Mayo  Robson:  Allbutt's  System  of  Med.,  vol.  iv,  p.  238, 


726  DISEASES    OF    THE    BILE-DUCTS. 

of  the  cases.  The  fever  is  well  explained  on  the  ground  that  there  is 
concomitant  cholecystitis  or  cholangitis,  and  in  some  instances  there  is 
palpable  and  tender  enlargement  of  the  gall-bladder  and  may  be  splenic 
enlargement  and  albuminuria  to  lend  support  to  the  theory  of  infection. 
The  mechanism  is  much  the  same  as  in  intermittent  hepatic  fever  {vide 
p.  751)  from  which,  however,  it  differs  in  being  acute. 

The  fever  was  formerly  thought  to  be  reflex  in  origin,  and  due  to 
the  violent  nervous  stimuli  accompanying  the  colic.  Such  a  view  is  to 
some  extent  supported  by  cases  in  which  at  operation  there  is  no  manifest 
inflammation  of  the  gall-bladder  or  ducts.  Nevertheless  even  in  such 
cases  it  is  not  unreasonable  to  believe  that  there  is  some  degree  of  infection 
sufficient  to  induce  fever,  though  not  to  produce  naked-eye  changes. 

Boix  *  has  suggested  that  during  an  attack  of  biliary  cohc  the  detoxicating 
function  of  tlie  liver  is  suspended  and  that  poisonous  bodies  absorbed  from  the 
intestinal  tract,  and  usually  stopped  or  rendered  harmless  by  the  liver,  thus  pass 
into  the  general  circulation  and  give  rise  to  pyrexia. 

Reflex  vomiting  accompanies  the  intense  pain,  and  is  often  followed 
by  some  relief.  The  contents  of  the  stomach  are  first  brought  up,  and 
subsequently  those  of  the  duodenum;  in  very  rare  instances  a  calculus 
has  been  vomited.  There  is  usually  bile  in  the  vomit,  which  suggests  that 
at  this  period  the  common  duct  is  not  completely  occluded.  Dyspepsia 
and  flatulence  may  accompany  or  follow  the  attack.  There  is  naturally 
distaste  for  food,  though  thirst  may  be  urgent.  Constipation  is  usually 
present.  Where  jaundice  is  already  marked,  the  fseces  may  be  devoid 
of  bile,  but  this  is  far  from  invariable. 

The  abdomen  is  usually  somewhat  retracted  from  vigourous  contraction 
of  the  abdominal  muscles.  Occasionally  there  is  considerable  tympanitic 
distension,  but,  according  to  Naunyn,  this  is  seen  otily  in  persons  habitu- 
ally subject  to  flatulence.  Transient  dilatation  of  the  stomach  has  been 
described.  There  is  tenderness  over  the  situation  of  the  gall-bladder 
and  sometimes  over  the  liver. 

Enlargement  of  the  liver  is  present  in  some  instances,  but  very  fre- 
quently its  presence  or  absence  is  difficult  to  determine,  as  the  hypo- 
chondrium  is  extremely  tender  and  the  patient,  being  in  great  pain,  is 
naturally  far  from  tolerant  of  examination,  while  the  recti  are  rigid  and 
interfere  with  accurate  palpation.  The  swelling  of  the  liver  may  be 
explained  as  partly  due  to  inflammation  of  the  bile-ducts  and  partly  to 
retention  in  the  liver  of  bile  from  the  obstruction.  Tenderness  of  the 
liver  is  often  present  without  any  manifest  enlargement.  The  gall- 
bladder is  probably  frequently  enlarged  from  accompanying  cholecystitis, 
but  its  examination  is  far  from  easy,  as  there  are  usually  considerable 
tenderness  over  the  gall-bladder  and  rigidity  of  the  abdominal  muscles. 

Naunyn  estimates  that  the  gall-bladder  is  only  palpable  in  one-third  of  the 
cases  of  biliary  colic. 

The  spleen  is  only  enlarged  in  cases  where  there  are  severe  infective 
processes  at  work. 

*  Boix,  E. :  Archiv.  genc^ral.  de  Med.,  1901,  t.  clxxxviii,  p.  466. 


CHOLELITHIASIS.  727 

During  a  paroxysm  the  skin  is  hot  and  moist  or  bathed  in  perspiration, 
and  there  may  be  rigors  or  shivering. 

From  the  intense  pain  there  is  considerable  ):)rostration,  which  remains 
for  a  time  after  the  paroxysm  has  passed  off. 

Nervous  symptoms  occasionally  accompany  biliary  colic  and  are  due 
to  the  intense  visceral  pain.  Various  hysterical  manifestations  *  or 
epileptiform  convulsions  may  occur.  Sudden  death  during  a  paroxysm 
of  pain,  due  to  cardiac  inhibition  brought  on  reflexly  through  the  vagus, 
has  been  recorded  in  rare  instances. 

Naunyn  f  refers  to  nine  cases  in  which  death  took  place  during  severe  attacks 
of  biUary  cohc;  CUfford  Allbutt,t  Mayo  Robson,§  and  Calvert  ||  have  also  referred 
to  similar  cases. 

In  exceptional  instances  temporary  hemiplegia,  paraplegia,  or  even 
tetany  have  been  observed  in  biliary  colic.  Sleepiness  and  drowsiness 
may  naturally  follow  attacks  of  biliary  colic  and  be  due  to  nervous 
exhaustion,  to  the  presence  of  bile  in  the  circulation,  or  in  some  degree 
to  the  effects  of  morphia  given  for  the  relief  of  the  paroxysmal  pain. 

Extreme  drowsiness  was  a  striking  feature  in  a  woman  aged  thirty  who  had 
suffered  from  gall-stone  colic  for  six  years.     (Levi.**) 

Kehr  ft  states  that  patients  subject  to  gall-stone  colic  frequently 
suffer  from  attacks  of  migraine,  which,  however,  disappear  when  the 
calculi  are  removed  by  operation.  During  biliary  colic  hiccough  may 
occur. 

There  may  be  a  dry  cough  due  to  reflex  irritation.  Reflex  con- 
striction of  the  vessels  in  the  lungs  with  rise  of  blood-pressure  in  the 
pulmonary  artery,  as  shown  by  accentuation  of  the  second  sound  over 
the  pulmonary  artery,  has  been  described  and  is  supported  by  the  ex- 
perimental observation  that  irritation  of  the  bile-duct  induces  a  reflex 
constriction  of  the  pulmonary  vessels.  (Francois-Franck  and  Arloing.) 
Signs  of  congestion  of  the  base  of  the  right  lung,  and,  in  very  exceptional 
instances,  haemoptysis  (Cassouti  J|),  have  been  observed.  Dilatation  of 
the  right  side  of  the  heart  has  been  described  and  has  been  referred  by 
Potain  to  the  rise  of  pulmonary  blood-pressure.  It  may  also  be  due  in 
some  measure  to  the  action  of  poisons  absorbed  from  the  bile-ducts  or 
in  some  cases  from  the  effect  of  bile  salts  in  the  blood.  Temporary 
dilatation  of  the  left  ventricle  with  a  systolic  apical  murmur  may  also  be 
met  with. 

There  may  be  palpitation,  disturbed  cardiac  rhythm,  with  rapid 
action,  irregularity,  or  even  slowing  of  the  heart.  The  pulse  during  a 
paroxysm  becomes  small,  feeble,  and  is  generalh^  of  about  the  normal 

*  Jeanselme  et  Rabe:  Soc.  Med.  des  Hop.,  July  15,  1898. 

t  Naunyn :  Cholelithiasis,  p.  89.     Transl.  New  Sydenham  Soc. 

j  AUbutt,  in  Svstem  of  Medicine,  vol.  iii,  p.  471. 

§  Mayo  Robson :  Gall-stones,  1892. 

!|  Calvert,  J.  T.:  Indian  Med.  (Jaz.,  vol.  xxxviii,  p.  413. 
**  Levi:  Archiv.  general,  de  Med.,  t.  clxxvii,  p.  63,  1896. 
tt  Kehr:  Diagnosis  of  Gall-stone  Disease,  American  transl.,  p.  56. 
+  J  Cassouti:  Bulletin  Med.,  No.  70,  1897. 


728  DISEASES   OF  THE    BILE-DUCTS. 

rate;  in  some  cases  it  is  even  slower  than  normal.  Kraus*  observed  a 
pulse  of  42  in  one  case. 

Examination  of  the  blood  shows  that  there  may  be  no  leucocytosis 
in  severe  bihary  cohc,  while  in  other  cases  it  may  be  present  in  a  moderate 
degree.  The  factors  determining  the  presence  or  absence  of  leucocytosis 
are  probably  the  extent  and  character  of  the  cholecystitis;  if  there  is 
catarrhal  inflammation,  there  is  no  increase  in  the  number  of  leuco- 
cytes, while  in  suppurative  cholecystitis  there  may  be  considerable 
leucocytosis.  (Ewing.f)  Albuminuria  is  not  infrequent,  and  transient 
glycosuria  is  occasionally  observed  during  a  paroxysm.  There  is  some 
difference  of  opinion  as  to  the  frequency  with  which  glycosuria  occurs. 
It  has  been  referred  to  the  widespread  nervous  disturbance,  but  it  is 
conceivable  that  it  is  toxic. 

True  diabetes  may  be  the  result  of  chronic  pancreatitis  set  up  by  a 
calculus  in  the  lower  part  of  the  common  bile-duct,  but  these  cases  are 
not  often  the  subject  of  typical  severe  attacks  of  biliary  cohc.  Con- 
versely in  two  well-marked  cases  of  diabetes  meUitus  Gilbert  and  E. 
Weil  I  observed  that  during  intercurrent  attacks  of  hepatic  colic  the 
glycosuria  diminished. 

Bile-pigment  occurs  in  the  urine  before  there  is  any  manifest  jaundice; 
the  presence  of  bile  in  the  urine  may  be  quite  transient  and  may  be 
succeeded  by  an  excessive  amount  of  urobihn. 

Indican  does  not  occur  in  uncomplicated  cases;  this  is  a  point  of 
importance  in  distinguishing  biliary  from  appendicular  and  intestinal 
colic  where  indican  may  be  present. 

Jaundice  is  not  an  invariable  accompaniment  of  biliary  colic.  Its 
incidence  has  been  variously  estimated  at  one-half  to  three-quarters  of 
all  the  cases.  In  the  higher  estimate  cases  of  very  slight  and  transient 
icterus  are  included.  Naunyn  §  considers  that  definite  jaundice  is  present 
in  half  the  cases.  It  comes  on  a  varying  time  after  the  onset  of  the  pain, 
and  no  constant  interval  can  be  given.  It  may  vary  between  a  few 
hours  to  two  or  even  three  days.  The  occurrence  of  jaundice  after 
biliary  colic  is  the  result  of  obstruction  to  the  flow  of  bile  through  the 
common  bile-duct.  The  obstruction  is  generally  assumed  to  be  due  to 
the  presence  of  the  calculus  in  the  duct,  but  it  may  be  due  to  the  spread 
of  inflammation  and  spasm  from  the  gall-bladder  to  the  ducts,  and  may 
occur  when  the  calculus  is  still  in  the  gall-bladder  or  in  the  cystic  duct. 
Riedel  beheves  that  two-fifths  of  the  cases  of  jaundice  in  choleUthiasis 
are  due  to  this  cause. 

As  in  other  forms  of  jaundice,  the  urine  contains  bile-pigment  before 
the  conjunctivae  become  stained,  and  the  latter  become  yellow  before 
the  skin; 

During  an  attack  of  gall-stone  colic  not  only  is  no  food  taken,  but 
the  vomiting  and  fever  lead  to  temporary  loss  of  flesh  and  weight.  When 
attacks  are  repeated,  nutrition  may  become  very  seriously  affected. 

*  Kraus :  On  Gall-stones,  p.  36,  English  translation,  1896. 

t  Ewing :  Clinical  Pathology  of  the  Blood,  p.  340. 

t  Gilbert  and  Weil:  Soc.  Med.  des  Hop    July  22,  189S. 

§  Naunyn :  Cholelithiasis,  p.  76.     Transl.  New  Sydenham  Soc. 


CHOLELITHIASIS.  729 

Complications. — ^The  extremely  forcible  peristaltic  contractions  of 
the  intestines,  set  up  refiexly  during  the  height  of  bihary  colic,  may  lead 
to  volvulus  of  the  small  intestine  and  so  to  acute  intestinal  obstruction. 
Mayo  Robson  *  has  drawn  special  attention  to  this  complication  of  acute 
biliary  colic.  Intestinal  obstruction  produced  by  gall-stones  in  other 
ways,  viz.,  by  mechanical  obstruction  of  the  lumen  of  the  bowel  by  a 
large  calculus;  as  the  result  of  local  peritonitis  around  the  gall-bladder, 
and  by  adhesions,  is  referred  to  elsewhere.     (Vide  pp.  742,  747,  749.) 

Rupture  of  the  gall-bladder  or  ducts  during  an  attack  is  fortunately 
a  very  rare  accident;  when  it  occvirs,  infection  of  the  peritoneum  with 
fatal  results  is  very  prone  to  occur. 

Pauly  t  describes  a  case  in  which,  after  an  attack  of  bihary  cohc,  coUapse, 
abdominal  distension,  and  death  occurred.  Blood  clot  was  found  in  the  abdomen. 
There  was  rupture  of  the  capsule  of  the  liver  leading  into  a  cavity  containing  blood. 
There  Avere  calculi  in  the  gall-bladder  and  a  calculus  obstructing  the  common  duct. 

The  cholecystitis  which  probably  always  precedes  and  gives  rise  to 
biliary  colic  may  infect  the  peritoneum  and  set  up  peritonitis. 

Termination. — An  attack  of  biliary  colic  may  terminate  suddenly, 
the  pain  disappearing  in  a  moment,  probably  from  the  calculus  escaping 
into  the  duodenum.  In  other  cases  the  pain  may  recur  at  frequent 
intervals,  the  calculus,  or  possibly  a  succession  of  calculi,  being  finally 
discharged  into  the  duodenum.  There  does  not  appear  to  be  any  con- 
vincing evidence  that  recurrent  attacks  of  colic  without  jaundice  are 
due  to  a  calculus  which  has  once  passed  into  the  cystic  duct,  returning 
to  the  gall-bladder  and  entering  the  cystic  duct  again  and  again.  Some 
of  these  cases  are  probably  cholecystitis  alone,  while  others  may  be  due 
to  pancreatic  lithiasis. 

In  other  instances  the  calculus  may  become  impacted  close  to  the 
biliary  papilla  and  produce  chronic  jaundice  and  the  symptoms  of  inter- 
mittent hepatic  fever.     {Vide  p.  751.) 

In  rare  instances  death  may  occur  from  various  causes.  As  has 
already  been  pointed  out,  the  pain  may  be  so  intense  that  death  results 
from  reflex  cardiac  inhibition.  Death  from  peritonitis  due  to  rupture 
or  ulceration  of  the  ducts  or  gall-bladder  is  also  described. 

Diagnosis. — The  extremely  severe  character  of  the  pain  in  the  right 
hypochondrium  and  back,  the  tenderness  over  the  gall-bladder  between 
the  ninth  costal  cartilage  and  the  umbilicus  (Mayo  Robson),  vomiting, 
the  subsequent  development  of  jaundice,  though  this  is  not  essential, 
and  the  recognition  of  gall-stones  in  the  stools  are  the  chief  points  on 
which  a  diagnosis  of  gall-stone  colic  rests.  The  presence  of  calculi  in 
the  faeces  of  course  clinches  the  diagnosis,  but  calculi  are  by  no  means 
always  found.  To  search  for  them  the  motions  should  be  passed  into 
a  solution  of  carbolic  acid  1  :  60,  and  broken  up  with  the  aid  of  a  piece 
of  stick  and  passed  through  a  sieve. 

The  patient  may  be  in  such  agony  that  it  may  l)e  very  difficult,  espe- 
cially in  a  first  attack  or  when  seen  for  the  first  time,  to  make  (wt  what 

*  Mavo  Robson:  Mcdico-Chirurg.  Trans.,  vol.  Ixxviii,  p.  117. 
t  Pauly:  Lyon  Medical,  t.  Ixx,  p.  4,30,  July  24,  1892. 


730  DISEASES    OF    THE    BILE-DUCTS. 

is  the  matter.  In  such  cases  a  hypodermic  injection  of  morphia  will 
relieve  the  patient  to  some  extent  and  enable  an  investigation  and  a 
diagnosis  to  be  made.  A  few  whiffs  of  chloroform  remove  the  mdely 
spread  pains  and  leave  a  subdued  pain  in  the  region  of  the  gall-bladder. 

Differential  Diagnosis  from  Cholecystitis. — In  acute  inflammation  of 
the  gall-bladder  occurring  in  the  absence  of  gall-stones  the  pain  is  less 
excruciating  than  when  a  calculus  is  impacted  in  the  ducts.  But,  as 
already  pointed  out,  Kehr  *  believes  that  cholecystitis  is  antecedent  to 
every  attack  of  biliary  colic,  and  Naunyn  f  has  shown  how  frequently 
cholecystitis  accompanies  biliary  colic  and  how  difficult  it  may  be  to 
distinguish  between  simple  cholecystitis  and  biliary  colic. 

Renal  Colic. — Since  the  pain  due  to  a  calculus  in  the  cystic  duct  is 
felt  to  the  right  of  the  spine  opposite  the  eighth  to  eleventh  dorsal  ver- 
tebrae, it  is  not  surprising  that  cases  of  biliary  colic  are  from  time  to  time 
diagnosed  as  renal  colic  due  to  a  calculus  in  the  right  kidney.  In  renal 
cohc  the  pain  tends  to  radiate  down  the  ureter  instead  of  for^^ards 
towards  the  epigastric  and  hypochondriac  regions,  while  -the  kidney  is 
tender  on  palpation  in  the  loin,  and  the  urine  may  contain  blood,  pus, 
or  albumin,  and  is  free  from  bile. 

The  diagnosis  of  cholelithiasis  in  early  life  is  difficult,  as  it  is  hardly 
likely  to  be  thought  of  unless  there  is  jaundice.  The  abdominal  pain 
will  probably  be  referred  to  intestinal  disturbance.  In  this  respect 
cholelithiasis  resembles  renal  colic  in  infants,  which,  as  Gibbons  %  has 
shown,  is  very  likely  to  be  overlooked. 

Floating  Kidney. — As  described  elsewhere  (p.  546),  a  floating  kidney 
on  the  right  side  may  produce  both  biliarv^  colic  and  jaundice.  The 
diagnosis  depends  on  the  detection  of  a  floating  kidney  and  on  disap- 
pearance of  the  symptoms  when  nephroptosis  has  been  efficiently  treated 
either  by  a  belt  and  pad  or  by  the  operation  of  fixing  the  kidney  in  the 
loin  (nephropexy).  If  attacks  of  jaundice  and  colic  still  continue,  it  is 
probable  that  there  is  cholelithiasis  in  addition,  which  is  by  no  means 
infrec{uently  the  case. 

Gastric  and  Duodenal  Ulcer. — The  pain  due  to  biliary  colic  is  often 
regarded  not  only  by  the  sufferers,  but  also  by  their  medical  advisers, 
as  clue  to  disease  of  the  stomach,  such  as  ulcer,  or  as  a  duodenal  ulcer. 
In  some  cases  of  biliary  colic  the  pyloric  end  of  the  stomach  ma}^  be 
involved  in  adhesions  due  to  past  attacks  of  local  peritonitis  originally 
set  up  by  cholecystitis.  In  making  a  differential  diagnosis  it  must  be 
remembered  that  the  pain  of  gastric  ulcer  has  a  direct  relationship,  to  food, 
while  gall-stone  pain  frequently  begins  at  night,  hours  after  a  meal  has 
been  taken,  and  when  the  stomach  is  empty.  The  pain  of  gall-stone 
colic  is  more  to  the  right  of  the  abdomen  than  that  of  gastric  ulcer,  and 
may  be  absent  for  long  periods,  while  that  of  ulcer  constantly  recurs 
after  food.  In  gastric  ulcer  the  pain  is  chiefly  in  the  epigastrium,  and 
the  vomited  matters  show  excess  of  hydrochloric  acid,  while  in  bihary 

*  Kehr:  Gall-stone  Disease,  p.  26,  American  transl. 

t  Naunyn:  On  Cholelithiasis,  pp.  113-125.     Transl.  New  Sydenliam  Soc. 

X  Gibbons,  R.  A.:  Med.-Chirurg.  Trans.,  vol.  Lxxix,  p.  41. 


CHOLELITHIASIS.  731 

colic  the  amount  of  hydrochloric  acid  is  either  iiorinal  or  diminished. 
Fever,  sweating,  rigors,  and  prostration  are  in  favour  of  l^iliary  colic. 

Acute  Dyspepsia. — In  acute  gastritis  with  flatulent  distension  of  the 
stomach  the  symptoms  are  less  urgent  than  in  biliary  colic,  and  there 
is  tenderness  over  the  stomach  rather  than  over  the  gall-bladder. 

Hyperchlorhydria. — In  some  cases  of  nervous  dyspepsia  with  hyper- 
acidity of  the  gastric  juice  attacks  of  pain,  which  may  wake  the  pa- 
tient up  at  3  in  the  morning,  occur  and  may  be  regarded  as  due  to 
biliary  colic.  Dr.  T.  McCrae  has  told  me  of  such  cases  which,  though 
very  rare  in  England,  are  not  so  in  America.  Examination  of  the 
gastric  juice  and  the  relief  obtained  from  bicarbonate  of  soda  should 
enable  the  medical  men  to  recognise  the  true  nature  of  these  cases. 

Duodenal  ulcer  is  very  rare  in  women,  and  is  often  quite  latent  until 
it  perforates  into  the  peritoneal  cavity,  when  it  gives  rise  to  symptoms. 
Pain  comes  on  two  hours  after  food,  tenderness  is  to  the  right  and  much 
in  the  same  position  as  the  gall-bladder,  and  hsematemesis  may  occur 
or  there  may  be  melsena  without  hsematemesis. 

Appendicitis. — In  some  cases  the  pain  is  referred  to  the  right  iliac 
fossa  and  the  condition  resembles  appendicitis.  A  possible  explanation 
of  this  is  that  local  peritonitis  has  spread  from  the  gall-bladder  and  in- 
volved the  serous  coat  of  the  appendix  (Tripier  and  Paviot  *).  In  other 
words,  it  is  the  coexistence  of  pericholecystitis  with  biliary  colic  which 
gives  rise  to  the  pain  resembling  that  of  appendicitis.  Confusion  is  more 
likely  to  occur  between  ordinary  cholecystitis  and  appendicitis  than  in 
typical  biliary  colic  in  which  the  pain  is  much  more  severe  and  higher 
up  in  the  abdomen.  It  must  also  be  remembered  that  in  rare  cases, 
of  which  Becker  f  has  collected  34,  appendicitis  and  cholelithiasis  may 
coexist. 

Mucous  Colic  {or  Colitis). — Occasionally  the  attacks  of  abdoiTiinal pain 
in  mucous  colitis  are  sufficiently  severe  to  suggest  the  existence  of  biliary 
colic.  Examination  of  the  stools  should  lead  to  the  detection  of  the 
characteristic  casts,  and  so  to  a  recognition  of  the  real  nature  of  the 
disease.  It  is  worth  while  pointing  out  that  membranous  cholecystitis 
with  attacks  of  biliary  colic  have  been  reported  in  patients  with  mucous 
colitis.  {Vide  p.  603.)  Mucous  colic  may  be  associated  with  the  passage 
of  intestinal  sand  and  with  abdominal  pain. 

From  Intestinal  Lithiasis. — There  are  two  forms  of  intestinal  sand: 
(i)  The  false — or  food  residues,  such  as  the  sclerenchyma  of  fruits,  espe- 
cially the  pips  of  pears,  the  vertebrae  of  sardines,  or  salts  or  drugs,  such 
as  magnesia  or  salol  taken  medicinally.  It  is  important  to  be  aware 
of  the  fact  that  olive  oil  taken  by  the  mouth  to  relieve  cholelithiasis 
may  be  passed  as  saponified  masses,  which,  from  a  superficial  or  careless 
examination,  may  be  regarded  as  softened  calculi. |  When  colic  from 
other  causes,  such  as  constipation,  is  followed  by  the  passage  of  these 
food  residues,  a  diagnosis  of  biliary  sand  might  easily  be  made  unless  the 

*  Tripier  and  Paviot:  La  Semaine  Medicale,  1903,  p.  29. 
t  Becker:  Deutsch.  Zcitschrift  f.  Chirurg.,  Bd.  Ixvi,  S.  246. 
X  Compare  Del^'^pine,  S. :  Trans.  Path.  Soc,  vol.  xli,  p.  111. 


732  DISEASES    OF    THE    BILE-DUCTS. 

masses  are  chemically  or  microscopically  examined,  (ii)  True  intestinal 
sand  is  composed  of  calcium  phosphate,  and  is  probably  the  result  of 
a  "lithogenic  catarrh"  of  the  intestine.  It  may  also  contain  urobihn. 
The  presence  of  true  intestinal  sand  is  often  associated  with  mucous 
colitis.  In  some,  but  not  in  all,  cases  of  true  intestinal  sand  there  are 
severe  attacks  of  abdominal  pain.  A  careful  examination  of  the  chemical 
nature  of  the  sand  is  necessarj^  to  distinguish  the  condition  from  biUary 
coHc  due  to  minute  calcuh. 

In  acute  'pancreatitis  there  is  more  profound  collapse;  the  pain  is  more 
in  the  epigastrium,  and  is  more  intense  and  constant  than  in  biliary  colic. 
Acute  pancreatitis  may  follow  on  biliar}^  cohc  (Thayer  *),  and  the  hsemor- 
rhagic  form  may,  as  Opie  f  has  shown,  be  due  to  bile  passing  into  the 
pancreatic  duct  when  the  orifice  of  the  bihar\'  papilla  is  blocked  by  a 
smaU  calculus. 

Hepatic  Crises  in  Tabes,  ete.— Crises  resembhng  bihary  cohc  are  very 
rare  in  tabes,  but  the  resemblance  may  be  very  close,  as  is  shown  by  the 
following  case: 

Krauss  J  records  a  case  of  a  womaii  aged  forty-four  who  was  the  subject  of 
tabes  and  had  recurrmg  attacks  of  colic  and  jaundice.  The  autopsy  showed  that 
the  gall-bladder  and  ducts  were  healthy  and  free  from  calculi.  The  liver  showed 
chronic  venous  engorgement  without  any  heart  or  lung  disease  to  account  for  it. 
The  condition  was  regarded  as  being  analogous  to  gastric,  renal,  and  other  crises. 

The  obscure  condition,  hepatalgia,  or  neuralgia  of  the  hver,  has  been 
described  b}^  Chfford  Allbutt  §  and  Pariser,  ||  the  latter  of  whom  has 
reported  seven  cases  of  ner^^ous  hepatic  cohc.  The  patients  are  neurotic 
or  neurasthenic,  but  these  conditions  of  course  in  no  way  protect  against 
cholehthiasis.  Osier  **  speaks  of  pseudobiliar}^  colic  as  not  uncommon 
in  nerv^ous  women,  and  as  being  periodic  and  often  excited  by  emotion, 
but  not  accompanied  by  jaundice.  It  may  be  difficult  to  exclude  chole- 
hthiasis completely,  but  the  absence  of  jaundice  is  significant. 

From  enteralgia,  or  neuralgia  of  the  abdominal  sympathetic,  the  diag- 
nosis is  not  always  easy.  According  to  Chfford  Allbutt,tt  the  pain  of 
enteralgia  often  begins  at  the  navel  and  is  more  stabbing  than  in  biUarj^ 
colic. 

Pseudo-gall-stone  cohc  may  occur  in  malignant  cUsease  involving  the 
ducts  and  in  malignant  disease  of  the  head  of  the  pancreas,  but  there  is 
such  deep  jaundice  and  the  conchtion  of  the  patient  is  so  grave  that  httle 
or  no  difficulty  in  ehminating  ordinary  bihary  cohc  is  hkely  to  arise. 

Lead  Colic. — In  severe  lead  cohc  there  is  a  superficial  resemblance  to 
gall-stone  cohc  in  that  there  are  great  abdominal  pain  and  difficulty  in 
making  a  thorough  examination  of  the  patient.  The  blue  fine  on  the 
gums,  the  anaemia,  and  the  absence  of  any  localisation  of  tenderness 

*  Thayer,  W.  S. :  American  Medicine,  March  1,  1902. 
t  Opie,  E.  L. :  Johns  Hopkins  Hosp.  Bull.,  1901,  vol.  xii,  p.  179. 
t  Krauss:  Journal  of  Nervous  and  Mental  Diseases,  vol.  xxvi,  p.  107,  1899. 
§  Clifford  Allbutt :  Visceral  Neuroses,  1884,  and  his  Sj^stem  of  Medicme,  vol.  iii, 
p.  481.  II  Pariser:  Centralblatt  f.  mn.  Med.,  1896,  Bd.  xvii,  S.  467. 

**  Osier,  W. :  Practice  of  Med.,  p.  564,  4th  ed.,  1901. 
tt  Clifford  Allbutt :  AUbutt's  System  of  Medicine,  vol.  iii,  p.  482. 


CHOLELITHIASIS.  733 

near  the  gall-bladder  point  to  lead  colic.  I  have  seen  recurrent  attacks 
of  colic  mth  slight  jaundice  in  a  worker  in  lead,  and  the  question  arises 
whether  spasmodic  contraction  of  the  bile-ducts  may  be  set  up  by  lead 
and  be  analogous  to  intestinal  colic. 

Angina  Pectoris. — The  severity  of  the  pain  may,  when  it  is  referred 
to  the  cardiac  region,  lead  to  an  erroneous  diagnosis  of  angina  pectoris; 
such  cases,  however,  are  very  rare. 

In  a  case  of  de  Havilland  Hall's  *  there  were  attacks  of  pain  in  the  cardiac 
region,  followed  by  faintness  which  resembled  angina,  but  were  not  relieved  by 
nitrites.  Subsequently  unmistakable  biliary  colic,  followed  by  a  broncho-biliary 
fistula,  developed  and  the  aberrant  pain  disappeared. 

Lumbago. — The  pain  in  the  back  with  which  biliary  colic  may  begin 
may,  in  some  cases,  lead  to  an  erroneous  diagnosis  of  lumbago  or  of 
spinal  disease  unless  a  careful  and  complete  examination  is  made. 

Prognosis.— Under  tliis  heading  recovery  from  the  actual  attack 
and  the  prospect  as  regards  the  future  rec[uire  consideration. 

It  is  only  in  the  rarest  cases  that  death  results  during  an  attack  of 
biliary  coUc.  It  may  be  due  to  the  intensity  of  the  pain  giving  rise  to 
cardiac  failure. 

Naimyn  f  collected  nine  examples  of  this  kind ;  Mayo  Robson, J  Chfford  AU- 
butt,§  and  Osier  ||  refer  to  other  cases. 

Death  may  be  due  to  another  cause,  viz.,  rupture  of  the  gall-bladder 
or  bile-ducts  during  severe  spasm,  and  perforative  peritonitis  due  to  the 
leakage  of  infected  bile.  Courvoisier**  has  collected  41  examples  of  this 
result. 

In  nearly  all  cases  recovery  takes  place  from  the  actual  attack,  but 
it  is  seldom  that  the  first  attack  is  the  last.  Usually  there  are  a  number 
of  further  attacks  which  are  less  severe  than  the  first.  As  a  rule,  after 
a  series  of  these  attacks  the  patients  become  free  from  any  further  trouble. 
But  a  calculus  is  sometimes  left  in  the  common  bile-duct  and  the  symp- 
toms of  intermittent  hepatic  fever  develop,  or  there  is  constantly  re- 
curring pain  from  the  presence  of  adhesions  around  the  gall-bladder 
(vide  p.  749).  The  prognosis  in  some  degree  depends  on  the  presence  or 
absence  of  facets  on  a  calculus  found  in  the  stools.  If,  after  a  first  attack, 
a  smooth  gall-stone  without  any  facets  is  found  in  the  fseces,  it  may  rea- 
sonably be  hoped  that  no  further  attacks  will  follow.  If,  on  the  other 
hand,  the  calculus  is  facetted,  there  are  other  calculi  in  the  gall-bladder 
and  the  probability  of  another  attack  must  be  faced.  The  patient's 
habit  of  life,  his  wdllingness  or  refusal  to  adopt  means  to  avoid  conditions 
which  favour  catarrhal  cholecystitis  and  the  production  of  fresh  gall- 
stones, all  bear  on  the  prognosis. 

Treatment. — The  treatment  of  biliary  colic  consists  in  that  of  the 

*  de  Havilland  Hall:  Lancet,  1902,  vol.  i,  p.  593.  Trans.  Med.  Soc,  vol.  xxv, 
p.  19L  t  Naunyn:  Cholelithiasis,  p.  89.     Transl.  New  Sydenham  Soc. 

t  Mayo  Robson :  Gall-stones,  1S92,  p.  77. 
§  Chfford  Allbutt:  System  of  Medicine,  vol.  iii,  p.  471. 
II  Osier,  W. :  Practice  of  Medicine,  p.  56.5,  4th  ed. 
**  Courvoisier:  Beitrage  z.  Path.  u.  Chirurg.  d.  Gallenwege,  1890. 


734  DISEASES    OF   THE    BILE-DUCTS. 

painful  paroxysm  and  of  the  patient  during  the  intervals  between  the 
attacks. 

In  acute  biliary  colic  the  pain  is  often  so  agonising  that  it  will  yield 
to  nothing  except  hypodermic  injections  of  morphia  or  inhalations  of 
chloroform.  After  a  hypodermic  injection  has  been  given,  a  few  whiffs 
of  chloroform  will  relieve  the  pain  until  the  effect  of  the  morphia  makes 
.  the  patient  comfortable.  One-fourth  of  a  grain  of  morphia  combined 
with  y-g-Q  grain  of  atropine  may  be  injected  in  these  cases,  and  if  an 
inhalation  of  chloroform  is  not  advisable,  20  ininims  of  chloroform  in 
water  may  be  given  by  the  mouth,  as  directed  by  Oilman  Thompson.* 

In  a  severe  attack  a  hypodermic  injection  of  morphia  is  very  much 
better  than  opium  by  the  mouth,  both  because  it  acts  more  rapidly  and 
because  the  repeated  vomiting  which  frequently  accompanies  severe 
biliary  colic  may  lead  to  rejection  of  everything  taken  by  the  mouth. 
The  hypodermic  syringe  should,  of  course,  never  be  entrusted  to  the 
patient,  as  there  is  very  considerable  risk  in  cases  where  the  attacks  are 
frequently  repeated  of  the  morphia  hal^it  being  acquired. 

A  short  but  graphic  account  of  the  intense  suffering  involved  in  breaking  off 
the  morphia  habit  acquired  from  repeated  bihary  colic  is  given  by  Keay  in  his  book 
on  the  Medical  Treatment  of  Gall-stones,  p.  105. 

Antipyrin,  if  given  at  the  beginning  of  an  attack,  has  been  thought 
to  give  considerable  relief.  Kraus  f  considers  that  it  does  good  chiefl}'' 
by  inducing  profuse  perspiration,  and  insists  on  its  futility  in  cases  where 
the  attack  has  already  lasted  two  to  three  hours  and  on  the  danger  of 
collapse  from  its  use. 

Naunyn  %  has  had  favourable  results  with  a  single  dose  of  salicylate 
of  soda  (30-45  grains)  given  at  the  beginning  of  an  attack.  Some  ob- 
servers have  found  that  copious  draughts  of  warm  water  or  several  ounces 
of  olive  oil  give  relief,  even  though  promptly  vomited.  In  fact,  pro- 
viding fluid  for  the  stomach  to  reject  gives  relief.  Washing  out  the 
stomach  has  also  been  thought  to  alleviate  the  pain.     (Baruch.§) 

The  vomiting  accompanying  the  biliary  colic  hardly  recpires  any 
special  treatment  apart  from  that  of  the  pain,  as  it  will  cease  with  it. 
Bismuth,  soda,  dilute  hydrocyanic  acid,  and  iced  apollinaris  or  soda- 
water  may  be  given.  Large  draughts  of  water  containing  bicarbonate 
of  soda  (3j  to  Oj),  recommended  by  Prout,  reheve  purposeless  retching 
by  giving  the  stomach  something  to  bring  up.  If  retching  persists  and 
the  patient  be  collapsed,  iced  champagne  may  be  given;  otherwise  it  is 
better  to  give  nothing  by  the  mouth,  to  apply  poultices  to  the  epigas- 
trium, and  keep  the  patient  under  the  influence  of  moiphia  administered 
hypodermically. 

In  less  severe  cases  the  patient  may  be  put  in  a  hot  bath  (104°  F.) 
and  given  tincture  of  belladonna  (^^xx)  in  spirits  of  chloroform  to  relieve 

*  Oilman  Thompson:  Medical  News  (N.  Y.),  April  29,  1897. 

t  Kraus:  On  CJall-stones,  p.  83.     English  translation,  1896. 

i  Naunyn :  Cholelitliiasis,  p.  178.     Transl.  New  Sydenham  Soc. 

§  Baruch:  The  Principles  and  Practice  of  Hjalrotherapj',  p.  235,  1900. 


CHOLELITHIASIS.  735 

spasm.     Hot  fomentations  or  poultices  may  be  tried  over  the  liver  and 
antipyrin  given  by  the  mouth. 

The  external  application  of  salicylate  of  metliyl  over  the  hver  has  been  recom- 
mended in  hepatic  colic  :  a  drachm  to  2  drachms  may  be  painted  on  daily  and  covered 
with  gutta-percha  to  favour  absorption.  Cliambart-Henon  *  says  it  gives  relief 
in  half  an  hour. 

Surgical  Treatment. — During  an  attack  of  biliary  cohc  operation 
is  justified  only  in  the  presence  of  some  severe  complication  which  would 
otherwise  prove  fatal.  These  complications  are  (i)  rupture  of  the  gall- 
bladder or  bile-ducts,  with  severe  collapse  and  signs  of  perforative 
peritonitis ;  (ii)  widespread  peritonitis  due  to  acute  infective  inflamma- 
tion of  the  gall-bladder,  and  (iii)  signs  of  acute  intestinal  obstruction 
due  to  volvulus  of  the  intestine  from  exaggerated  peristalsis. 

When,  in  spite  of  medical  treatment,  attacks  of  cohc  continually 
recur  and  the  patient  becomes  incapacitated  and  is  in  danger  of  con- 
tracting the  morjDhia  habit,  surgical  measures  must  be  considered.  The 
gall-bladder  should  be  opened,  calculi  removed,  and,  if  necessary,  the 
gall-bladder  itself  removed,  or  Mayo's  modified  operation,  removal  of 
the  mucous  membrane,  performed.  Some  difference  of  opinion  has, 
perhaps  naturally,  existed  between  physicians  and  surgeons  as  to  the 
recurrence  of  cholelithiasis  after  the  operative  removal  of  calculi  from 
the  gall-bladder.  Keay,t  in  a  vigourous  plea  in  favour  of  the  medical 
treatment  of  gall-stones,  unhesitatingly  states  that  recurrence  occurs, 
and  Homans  t  and  Kehr  §  have  reported  cases  where  fresh  calculi 
formed  around  sutures  introduced  into  the  wall  of  the  gall-bladder  during 
an  operation  for  the  removal  of  calcuH.  Mayo,  ||  from  the  surgeon's 
point  of  view,  insists  that  recurrence  does  not  occur. 

It  would  appear,  therefore,  that  when  operation  is  rec[uired  in  re- 
current biliary  colic,  the  gall-bladder  should  either  be  removed  or  so 
treated  that  no  fresh  formation  of  gall-stones  in  it  is  possible.  The  treat- 
ment during  the  intervals  is  the  general  treatment  of  cholelithiasis  de- 
scribed on  page  763. 

THE  MECHANICAL  EFFECTS  OF  GALL-STONES. 

The  purely  mechanical  effects  of  gall-stones  will  be  considered  seriatim 
under  the  following  heads : 

(1)  In  the  gall-bladder. 

(2)  In  the  cystic  duct. 

(3)  In  the  common  bile-duct. 

(4)  In  the  ampulla  of  Vater. 

(5)  Intestinal  obstruction. 

(1)  Mechanical  Effects  of  Gall-stones  in  the  Gall-bladder. — The 
mechanical  effects  pure  and  simple  of  calculi  in  thc^  gall-l)lad(ler  are  not 

*  Ga^.  Med.  de  Paris,  1,S9S,  p.  40.S. 

t  Keay:  The  Medical  'I'rcutinent  of  (lall-stoncs,  p.  96. 

X  Homans:  .Annals  of  Surgery,  vol.  xxvi,  p.  114,  1897. 

§  Kehr:  Diagnosis  of  (iall-stono  Di.sea.se,  p.  105.     American  translation,  1901. 

II  Mayo:  Bo.ston  Medical  and  Surgical  .lourii.,  vol.  cxlviii,  p.  545. 


736  DISEASES    OF   THE    BILE-DUCTS. 

very  frequent,  or,  as  a  rule,  very  important.  A  large  calculous  gall- 
bladder may  give  rise  to  a  dragging  sensation  or  feeling  of  heaviness  and 
discomfort  in  the  region  of  the  liver. 

The  gall-bladder,  when  full  of  tightly  packed  calculi  or  containing 
a  single  large  gall-stone,  may  exert  pressure  on  the  adjacent  structures. 
By  pressing  on  the  pylorus  or  duodenum  it  may  produce  pyloric  ob- 
struction, dilatation  of  the  stomach,  and  thus  imitate  carcinoma  of  the 
pylorus.  (Naunyn,*  Potherat.t)  In  these  cases  examination  of  the 
gastric  contents  may  be  of  use  in  settling  the  diagnosis.  Some  free  hy- 
drochloric acid  should  be  present  in  cholelithiasis,  while  in  gastric  car- 
cinoma it  should  be  absent.  Gall-stones  in  the  gall-bladder  do  not,  as 
a  rule,  obstruct  the  outflow  of  food  from  the  stomach  simply  and  solely 
in  a  mechanical  way,  but  set  up  adhesions  between  the  pylorus  and  the 
gall-bladder  (vide  p.  749)  which  contract  and  slowly  lead  to  pyloric  ob- 
struction. 

In  cases  where  a  large  single  calculus  is  in  process  of  ulcerating  out 
of  the  gall-bladder  into  the  duodenvim,  the  calculus  may  mechanically 
obstruct  the  pylorus  (vide  Intestinal  Obstruction  Due  to  Gall-stones, 
p.  742).  There  may  be  a  combination  of  cholecystogastric  fistula,  adhe- 
sions around  the  pylorus,  and  mechanical  obstruction  of  the  lumen  of 
the  pylorus  by  a  calculus. 

From  the  pressure  of  a  large  calculous  gall-bladder  the  common  bile- 
duct  might  be  compressed  and  jaundice  set  up.  Thrombosis  of  the  portal 
vein  from  this  cause  has  been  reported. J  From  traction  exerted  by  a 
heavy  gall-bladder  containing  calculi  the  right  lobe  of  the  liver  may  be 
elongated  into  the  formation  known  as  a  Hied  el's  lobe. 

When  the  gall-bladder  is  filled  with  calculi,  it  may  be  felt  as  a  hard 
tumor  through  the  abdominal  wall,  sometimes  just  below  the  costal 
arch;  in  other  cases,  owing  to  the  right  lobe  of  the  liver  being  elongated 
into  the  formation  known  as  Riedel's  lobe,  the  gall-bladder  is  considerably 
depressed  and  may  be  found  in  the  neighbourhood  of  the  right  iliac  fossa. 
Unless  fixed  by  adhesions,  the  calculous  gall-bladder  moves  with  respira- 
tion and  can  be  displaced  in  a  lateral  direction.  When  there  are  numerous 
calculi,  a  grating  feeling  of  crepitus  may  be  detected  on  palpation  over 
the  tumor,  but  this  is  often  absent  even  when  there  are  several  calculi 
in  the  gall-bladder.  A  number  of  calculi  may  become  loosely  cemented 
together  so  as  to  form  a  large  composite  calculus  which  does  not  give 
rise  to  any  crepitus  and  so  resembles  a  large  single  calculus  as  big  as  a 
hen's  egg.  From  absorption  of  bile  the  walls  of  the  gall-bladder  may 
become  adherent  to  the  surface  of  a  contained  calculus  and  be  separated 
from  it  with  difficulty. 

When  the  gall-bladder  is  filled  with  a  number  of  gall-stones  and  its 
walls  are  much  atrophied,  it  is  possible  that  spontaneous  rupture  may 
occur;   but  in  most  cases  ulceration  and  softening  due  to  inflammation 

*  Naunyn:  On  Cholelithiasis,  p.  151. 

t  Potherat :  Soc.  de   Chirurg.  Paris,  June  10,  1903. 

t  Donkin :  Medical  Times  and  Gazette,  1868,  vol.  ii,  p.  396. 


CHOLELITHIASIS.  737 

must  be  regarded  as  the  important  antecedents  of  rupture  of  a   gall- 
bladder containing  calculi. 

The  presence  of  calculi  in  the  gall-bladder  disposes  to  the  development 
of  primary  carcinoma ;  this  is  perhaps  the  result  of  irritation  rather  than 
a  purely  mechanical  effect,  but  until  the  causation  of  carcinoma  is  estab- 
hshed,  the  role  of  gall-stones  in  the  production  of  carcinoma  of  the  gall- 
bladder must  remain  undecided.  The  association  of  cholelithiasis  and 
primary  carcinoma  is  discussed  under  Carcinoma,  of  the  Gall-bladder, 
{Vide  p.  627.) 

According  to  Schroeder,  14  per  cent,  of  patients  with  cholelithiasis  eventually 
develop  carcinoma  of  the  gall-bladder.  In  149  cases  of  gall-stones  examined  at 
Guy's  Hospital  there  were  17,  or  11  per  cent.,  of  cases  of  primary  carcinoma  of  the 
gall-bladder  (Keay*).  Among  242  cases  of  gall-stones  at  St.  George's  Hospital 
there  were  10  cases  of  primary  carcinoma  of  the  gall-bladder,  or  4.1  per  cent. 

(2)  Mechanical  Effects  of  Calculi  in  the  Cystic  Duct. — When  a 
calculus  passes  into  the  cystic  duct,  it  stretches  the  walls  and  sets  up 
spasm  and  bihary  cohc.  {Vide  p.  723.)  A  calculus  may  remain  impacted 
in  the  cystic  duct  for  long  periods;  sometimes  no  definite  liistory  of  past 
colic  is  forthcoming  in  such  cases  to  mark  the  time  of  impaction.  The 
calculus  is  nearly  always  fixed  close  to  the  neck  of  the  gall-bladder.  It 
may  completely  obstruct  the  flow  of  bile  into  the  gall-bladder,  which  then 
becomes  distended  with  mucus,  at  first  mixed  with  bile,  but  later  quite 
clear.  This  is  hydrops  vesicae  fellese,  or  dropsy  of  the  gall-bladder. 
Infection  and  cholecystitis  are  very  prone  to  occur  under  these  conditions. 
The  distended  gall-bladder  may  be  the  site  of  painful  spasmodic  contrac- 
tions resembhng bihary  cohc  in  their  chnical  aspect,  except  that  jaundice 
is  usually  absent;  in  some  of  these  cases  the  condition  is  very  likely  to  be 
regarded  as  indigestion.  Jaundice  may,  however,  be  brought  about  by 
extension  of  spasm  to,  or  by  concomitant  catarrhal  inflammation  of, 
the  common  bile-duct.  According  to  Riedel,t  jaundice  is  present  in 
from  10  to  15  per  cent,  of  the  cases  where  a  calculus  is  impacted  at  the 
neck  of  the  gall-bladder.  Attacks  of  painful  spasm  in  a  distended  gall- 
bladder have  been  explained  as  depending  on  a  calculus  in  the  neck 
of  the  gall-bladder  acting  as  a  valve  and  allowing  bile  to  enter  the  gall- 
bladder but  not  to  leave  it.  It  is,  however,  more  probable  that  the  dis- 
tension of  the  gall-bladder  is  not  purely  mechanical  and  due  to  a  valvular 
action  of  a  calculus,  but  that  there  is  inflammation  of  the  mucous  mem- 
brane of  the  gall-bladder,  which  accounts  for  both  the  cHstension  and 
the  pain. 

A  distended  gall-bladder  appears  as  an  abdominal  tumor  in  the  right 
half  of  the  abdomen;  in  very  rare  instances  it  is  so  large  as  to  occupy 
the  greater  part  of  the  abdomen,  and  has  been  mistaken  for  ascites 
and  tapped.  Usually  it  is  not  larger  than  one's  closed  fist.  The  dilated 
gall-bladder  may  be  associated  witli  an  elongated  condition  of  the  right 
lobe  of  the  liver,  Riedel's  linguiform  lobe,  and  as  a  result  the  gall-bladder 
may  form  a  tumor  in  the  right  iliac  fossa  and  might  imitate  appendicitis. 

*  Keay:  The  Medical  Treatment  of  Gall-stones,  p.  67. 
t  Riedel:  Berlin.  kUn.  Wochen.,  .Jan.  21,  1901,  S.  78. 

47 


738  DISEASES    OF    THE    BILE-DUCTS. 

H.  J.  Waring  *  figures  a  gall-bladder  which  entered  into  a  right  femoral 
hernia.  It  forms  a  smooth,  tense,  pear-shaped  tumor  mth  the  apex 
upwards  and  the  base  do'\\T.iwards.  It  usually  moves  with  respiration 
and  can  be  displaced  laterally,  but  not  downwards.  It  is  separated  from 
the  liver  by  a  groove  or  depression,  is  immediately  under  the  abdominal 
walls,  and  in  thin  patients  may  be  visible  as  a  raised  surface.  It  is  not 
tender  unless  there  is  concomitant  inflammation.  It  may  be  resonant 
on  percussion.  A  gall-bladder  which  has  been  distended  ^xith  mucus 
from  obstruction  of  the  cystic  duct  may  subsequently  shrivel  up  and 
become  very  contracted. 

A  distended  gall-bladder  must  be  distinguished  from  a  floating  kidney, 
a  renal  tumor  or  hydronephrosis,  a  tumor  of  the  pylorus,  a  growth  in 
the  transverse  colon,  etc.  Confusion  is  most  likely  to  arise  between  a  dis- 
tended gall-bladder  and  a  floating  kidney  on  the  right  side,  since  they 
are  both  commoner  in  women  and  may  both  be  accompanied  by  attacks 
of  severe  pain  followed  by  Jaundice.  An  enlarged  gall-bladder  forms 
a  tumor  which  is  much  more  constant  and  does  not  disappear  or  vary 
in  position  in  the  same  way  as  a  floating  kidney.  A  gall-bladder  is 
usually  movable,  but  is  limited  by  its  attachment  to  the  liver  and  cannot 
be  displaced  into  the  false  pelvis  hke  a  floating  kidney.  If  displaced 
backwards  towards  the  loin,  it  returns  to  its  former  position  directly  the 
pressure  is  removed,  while  a  floating  kidney  tends  to  remain  there  as 
long  as  the  patient  is  in  the  reciunbent  position. 

A  distended  gall-bladder  does  not  escape  from  one's  grasp  in  the 
same  way  that  a  floating  kidney  does.  A  careful  bimanual  examination 
should  always  be  made.  Morris  f  points  out  that  too  much  stress  is 
apt  to  be  laid  on  hollowness  and  diminished  resistance  in  the  loin  as 
signs  of  floating  kidney. 

Distension  of  the  colon  with  air  (Ziemssen's  test)  may  be  useful,  as- 
it  should  press  the  gall-bladder  forwards  and  displace  a  floating  kidney 
backwards;  but  it  is  not  infallible.  INIayo  Robson  met  ^^^Lth  a  case  in 
which  it  pushed  a  growth  of  the  right  suprarenal  body  forw^ards.  Kehr 
also  distrusts  this  test,  as  the  colon  may  pass  in  front  of  the  gall-bladder. 
In  a  fat  person  it  may  be  very  difficult  to  be  certain  whether  one  is  deahng 
with  a  floating  kidney  or  a  distended  gall-bladder,  and  in  such  cases  an 
exploratory  operation  may  be  the  only  means  of  settling  the  diagnosis. 
In  some  cases  a  floating  kidney  and  a  distended  gall-bladder  ma}"  both 
be  present. 

Chance  J  described  a  case  of  a  dilated  gall-bladder  containing  200  calculi  -^vhich 
exactly  imitated  a  tuberculous  kidne3^ 

A  tumor  of  the  pylorus  lies  in  a  plane,  roughly  speaking,  at  right 
angles  to  that  of  the  gall-bladder  and  is  harder  and  painful.  In  gall- 
bladder cases  there  may  be  gastric  symptoms  and  some  dilatation  of  the 
stomach  from  pyloric  obstruction,  but  the  gastric  symptoms  are  not  sO' 

*  Waring,  H.  J. :  Diseases  of  the  Liver,  p.  235. 

t  Morris,  H. :  Brit.  Med.  Journ.,  1895,  vol.  i,  p.  238. 

J  Chance:  Medical  Chronicle,  vol.  xxxvii,  p.  120,  Nov.,  1902. 


CHOLELITHIASIS.  739 

prominent  as  in  pyloric  new-growth.  A  tumor  of  tlie  transverse  colon 
is  less  sharply  defined  than  a  dilated  gall-bladder,  and,  like  the  pyloric 
tumor,  tends  to  have  its  long  axis  at  right  angles  to  that  of  a  distended 
gall-bladder.  Faecal  impaction  in  the  transverse  colon  vn\l  usually  be 
accompanied  by  faecal  masses  elsewhere  in  the  abdomen,  and  the  con- 
dition will  be  cleared  up  or  altered  by  the  use  of  enemata.  It  may  be 
impossible  to  distinguish  between  a  small  dependent  hydatid  cyst  and 
a  dilated  gall-bladder  until  the  abdomen  is  opened.  Aspiration  would 
probably  settle  the  matter,  but  this  is  too  dangerous  a  method  to  be 
recommended. 

In  a  woman  aged  forty  a  dilated  gall-bladder  containing  eleven  pints  of  liquid, 
due  to  a  calculus  impacted  in  the  cystic  duct,  imitated  a  parovarian  cvst.  (L. 
Tait.*) 

Naunyn  t  quotes  two  cases  in  w^hich  a  calculus  in  the  cystic  duct 
exerted  direct  pressure — on  the  portal  vein  in  one  instance,  and  on  one 
of  its  branches  in  the  other — and  set  up  pylethrombosis.  Haematemesis 
may  thus  be  an  indirect  result  of  cholelithiasis.  A  calculus  in  the  cystic 
duct  may  possibly  exert  pressure  on  the  common  hepatic  duct  and  so 
give  rise  to  jaundice. 

The  passage  of  calculi  along  the  cystic  duct  .leads  to  dilatation  and 
to  straightening  out  of  the  tortuous  lumen  of  the  duct,  and  so  facilitates 
the  subsequent  passage  of  calculi  from  the  gall-bladder.  The  valves  of 
Heister,  which  under  ordinary  conditions  obstruct  the  return  of  a  calculus 
from  the  duct  into  the  gall-bladder,  become  almost  obhterated  and  only 
appear  as  slight  elevations  of  the  mucous  membrane;  when  thus  altered, 
they  may  allow  a  calculus  to  travel  towards  the  gall-bladder. 

In  a  case  under  my  care  a  large  gall-stone  in  the  common  duct  was  displaced 
at  a  laparotomy,  undertaken  for  its  removal,  by  manipulation,  and  was  thought 
to  have  passed  into  the  duodenum.  At  the  autopsy,  however,  it  was  found  in  the 
gall-bladder. 

(3)  Mechanical  Effects  of  Gall-stones  in  the  Common  Bile-duct. 

— The  passage  of  a  calculus  through  the  common  bile-duct  sets  up  biliary 
colic.  {Vide  p.  723.)  A  calculus  may,  however,  pass  into  the  common 
duct  and  become  permanently  lodged  there  ^\ithout  giving  rise  to  the 
symptoms  of  colic. 

Situation  of  the  Calculi  in  the  Common  Duct. — Statistics  A'ary  as  to 
the  commonest  site  for  a  calculus.  The  general  im]3ression  is  that  the 
termination  of  the  duct  in  the  biliary  papilla  and  the  ampulla  ^^ateri 
are  the  commonest  situations  for  calculi. 

Courvoisier's  statistics  bear  this  out:  in  123  ol)servations  the  calculi  were  found 
to  occupy  the  whole  of  the  common  bile-duct  in  26;  the  upper  segment  in  17;  the 
middle  segment  in  19 ;  to  be  close  to  the  duodenum  in  20 ;  in  the  orifice  of  the  biliary 
papilla  in  41 ;  so  that  in  almost  exactly  half  the  cases  the  calculus  was  close  to  the 
lower  end  of  the  duct.  In  380  operation  cases  Mayo  Robson  %  found  the  calculus 
in  the  duodenal  end  in  67  per  cent.,  in  the  middle  portion  in  18  per  cent.,  and  at 
the  upper  end  in  1.5  per  cent. 

*  Lancet,  1S89,  vol.  i,  p.  1294. 

t  Xaunyn:  Cholelithia.sis,  p.  133.     Transl.  New  Sydenliam  Soc. 

X  Mayo" Robson:  Diseases  of  the  Gall-bladder  and  Bile-ducts,  p.  278,  1904. 


740  DISEASES    OF   THE    BILE-DUCTS. 

Ill  a  smaller  number  of  cases  Vautriii  *  comes  to  the  opposite  conclusion : 
number  of  cases,  47 ;  calculi  in  part  of  the  duct  above  the  duodenimi,  27 ;  in  part 
of  duct  in  contact  with  the  duodenum,  18 ;  in  the  ampulla  Vateri,  2.  This  distri- 
bution he  explained  by  the  fact  that  the  duct  is  readily  dilatable  above  the  duo- 
denum, but  resists  dilatation  where  it  is  supported  by  the  pancreas. 

Number  of  Calculi  in  the  Common  Duct. — In  the  great  majority  of 
cases  there  is  a  single  calciihis;  thus  in  149  observations  Coiirvoisier  f 
found  that  in  95  there  was  a  single  calculus,  in  36  instances  there  were 
from  two  to  six  calcuH,  and  in  the  remaining  18  there  were  a  dozen  or 
more  calculi  in  the  duct.  A  single  calculus  is  usually  firm,  but  there 
may  be  a  soft,  cnmibhng  mass  wliich  fills  up  the  whole  of  the  dilated 
duct  and  may  extend  into  the  common  hepatic  duct.  Several  soft 
crumbhng  calcuH  may  be  found.  Mayo  Robson  has  removed  88  calculi 
from  the  common  duct. 

In  very  rare  instances  a  calculus  in  the  common  bile-duct  may  me- 
chanically compress  the  portal  vein  and  give  rise  to  thrombosis.  Cases 
of  this  nature  have  been  reported  by  Naunyn,{  WesterLhoffer,§  Korte.  |1 

It  is  possible  that  the  reflex  irritation  of  calcuh  in  the  common  duct, 
quite  apart  from  catarrh,  may  give  rise  to  vomiting.  Leclerc  **  reports 
a  case  in  which  vomiting  persisted  for  forty  days  until  two  calculi  were 
removed  from  the  common  duct ;  there  was  no  cause,  such  as  adhesions 
or  pyloric  obstruction,  for  the  vomiting. 

A  calculus  may  completely  obstruct  the  common  duct,  partially 
occlude  the  lumen  so  that  some  bile  can  run  past  it  into  the  duodenum, 
or  be  floating  in  the  common  duct  and  exert  a  ball-valve  action.  A 
calculus  which  at  first  is  firmly  impacted  and  completely  occludes  the 
common  duct  may  subsequently  become  loose.  This  is  due  to  several 
factors :  the  obstruction  dilates  the  ducts  above  and  thus  leads  to  widen- 
ing of  the  duct  at  the  point  of  impaction;  the  constant  pressure  of  the 
calculus  produces  atrophy  of  the  waUs  of  the  common  duct,  while  in- 
flammator}^  softening  and  ulceration  are  extremely  likely  to  occur.  It 
is,  therefore,  rare  for  absolute  biliary  obstruction  to  persist  for  a  long 
time,  but  jaundice  may  be  kept  up  both  from  intermittent  obstruction 
depending  on  the  ball-valve  action  of  a  calculus  described  by  Osier  ft 
and  by  Fenger,JJ  and  also  from  concomitant  inflammation  of  the  bile- 
ducts — either  the  larger  extra-hepatic  or  the  small  intra-hepatic. 

Jaundice  which  has  been  marked  early  in  the  course  of  the  impaction 
may  wane  and  finally  disappear,  and  after  death  a  loose  calculus  ma}^ 
be  found  in  the  duct. 

Griffon  §§  records  4  cases  of  this  kind  where  the  calculus  was  found  just  above 
the  biliary  papilla. 

*  Vautrin:  Rev.  de  Chirurg.,  1S96,  p.  454. 

t  Courvoisier :  Path.  u.  Chir.  d.  Gallenwege,  1890. 

X  Namiyn :  Cholelithiasis,  p.  133.     Transi.  New  Sydenham  Soc. 

§  Westenhoffer :  La  Semame  Medicale,  1903,  p.  33. 
II  Korte :  Ibid. 
**  Leclerc:  Lvon  Medical,  tome  c,  p.  737. 
tt  Osier,  W.  TMed.  Times  and  Gaz.,  July  31,  1881. 
%%  Fenger,  C.:  American  Jouni.  of  Med.  Sciences,  vol.  cxi,  p.  125,  1896. 
§§  Griffon:  Bull.  Soc.  Anat.,  July,  1896,  p.  513. 


CHOLELITHIASIS.  741 

Chronic  obstruction  of  the  bile-duct  with  calcuh  may,  however,  induce 
long-standing  jaundice.  In  these  cases  there  may  be  a  large  crumbling 
calculous  mass  occupying  a  considerable  extent  of  the  common  bile-duct. 
A  calculous  accumulation  of  this  kind  grows  from  deposit  of  bilirubin- 
calcium  and  is  accompanied  by  infective  cholangitis.  When  the  duct 
contains  a  single  calcidus,  jaundice,  though  present  for  a  time,  usually 
passes  away. 

As  the  result  of  obstruction  of  the  common  duct  by  calculi  there  may 
be — (i)  Cyhndrical  or  (ii)  saccular  dilatation  of  the  duct. 

(i)  Cylindrical  dilatation  of  the  common  bile-duct  is  the  commoner. 
The  duct  is  not  infrequently  the  size  of  a  test-tube,  and  may  be  larger 
and  become  comparable  to  a  piece  of  intestine.  The  cylindrical  dilata- 
tion may  spread  through  the  common  and  hepatic  ducts  into  the  liver 
and  give  rise  to  dilatation  of  the  intra-hepatic  bile-ducts.  The  dilatation 
is  more  marked  on  the  surface  of  the  organ,  and  is  often  more  prominent 
in  the  left  lobe,  probably  because  there  is  less  resistance  on  the  surface 
of  the  liver  and  especially  in  the  smaller  left  lobe.  Local  saccular  dila- 
tations of  the  varicose  bile-ducts  on  the  surface  of  the  liver  may  occur. 

(ii)  Saccidar  Dilatation. — In  rare  instances  the  common  bile-duct  may 
form  a  large  cyst  which  may  be  diagnosed  as  a  dilated  gall-bladder,  a 
pancreatic  cyst,  a  hydatid  cyst,  etc.  The  condition  is  like  that  described 
on  page  651.  Occasionally  there  are  local  cystic  dilatations  in  the  intra- 
hepatic branches  of  the  bile-ducts  on  the  surface  of  the  liver;  this  local 
dilatation  may  be  superimposed  on  a  widespread  cylindrical  dilatation. 

Simply  from  distension  with  bile  the  liver  becomes  at  first  enlarged. 
Subsequently  atrophy  of  the  liver  cells  occurs,  with  proininence  of  the 
existing  fibrous  tissue.  The  question  whether  mere  stasis  of  the  bile 
can  lead  to  genuine  hepatic  cirrhosis  has  given  rise  to  considerable  dis- 
cussion {vide  p.  329)  and  experimental  investigation.  The  conclusions 
from  human  morbid  anatomy  are  that  biliary  obstruction  alone  does  not 
induce  real  cirrhosis,  but  if  infection  of  the  bile-ducts  occurs,  pericholan- 
gitic  fibrosis  will  result.  In  obstruction  of  the  ducts  with  calculi  infective 
cholangitis  is  readily  produced,  and  thus  fibrosis  of  the  liver  may  result. 

(4)  The  Mechanical  Effects  of  a  Calculus  in  the  Ampulla  of 
Vater, — An  important  difference  between  the  mechanical  effects  of  a 
calculus  in  this  situation  and  of  one  in  the  lower  end  of  the  bile-duct  is 
that  when  the  calculus  occupies  the  ampulla  of  Vater,  it  may  in  addition 
obstruct  the  outflow  of  pancreatic  juice  from  Wirsung's  duct.  The 
accessory  duct  of  Santorini  may,  however,  carry  off  the  secretion  into 
the  duodenum,  and  so  preA-ent  any  accumulation  of  the  pancreatic  juice 
in  the  ducts.  In  about  one-third  of  the  cases,  however  (Schirmer  *), 
there  is  no  conmiunication  between  the  two  ducts,  and  in  these  cases 
obstruction  of  the  orifice  of  Wirsung's  duct  would  lead  to  its  distension 
with  pancreatic  secretion. 

As  a  matter  of  fact,  however,  there  is  nearly  always  some  additional 
inflammatory  change  Avhen  a  calculus  is  in  the  anijMilla  of  Vater.     This 

*  Schirmer:  Inaug.  Dissert.,  Basel.  Quoted  by  C»pie:  Anier.  Jour.  Med.  Sci., 
vol.  cxxi,  p.  30. 


742  DISEASES    OF   THE    BILE-DUCTS. 

sets  up  pancreatitis  and  leads  to  enlargement  and  fibrosis  of  the  pan- 
creas, dilatation  of  Wirsung's  duct,  and  in  some  instances  to  the  forma- 
tion of  pancreatic  calculi.  The  chronic  interstitial  pancreatitis  which 
results  from  obstruction  of  the  ducts  hardly  ever  destroys  the  islands 
of  Langerhans,  and  hence  glycosuria  and  diabetes  do  not  result.     (Opie.*) 

Wlien  a  small  calculus  is  impacted  in  the  ampulla  of  Vater  close  to 
the  biliary  papilla  and  is  not  sufficiently  large  to  obstruct  the  opening 
of  the  main  duct  of  the  pancreas  into  the  ampulla  Vateri,  the  direct 
mechanical  obstruction  to  the  flow  of  bile  into  the  duodenum  results  in 
the  passage  of  bile  into  the  pancreatic  duct.  This  has  been  shown  by 
Halsted  and  Opie  f  to  have  occurred  in  a  fatal  case  of  hsemorrhagic 
pancreatitis.  Opie  has,  moreover,  proved  by  experiments  on  dogs  that 
the  passage  of  bile  into  the  pancreatic  duct  induces  hsemorrhagic  pan- 
creatitis. The  reason  why  impacted  calculi  in  the  diverticulum  of  Vater 
only  rarely  induce  hsemorrhagic  pancreatitis  is  that  usually  the  calculi 
are  sufficiently  large  to  obstruct  the  orifice  of  Wirsung's  duct  and  so 
interfere  with  the  entrance  of  bile  into  the  pancreatic  duct. 

(5)  Mechanical  Obstruction  of  the  Intestines  by  Gall-stones. — 
Incidence. — When  a  large  gall-stone  ulcerates  out  of  the  gall-bladder  into 
the  duodenum,  or  in  rare  instances  into  the  colon,  it  may  produce  me- 
chanical obstruction  of  the. bowel.  This  is  a  decidedly  rare  event  in 
ordinary  practice,  as  is  shown  by  the  fact  that  at  the  Leeds  Infinxiary, 
where  a  large  number  of  gall-stone  operations  are  done,  only  one  case 
has  occurred  in  ten  years. J  Only  one  case  occurred  at  St.  George's 
Hospital  in  fifteen  years.  But  from  the  interest  attaching  to  such 
rare  and  striking  cases  a  large  number  have  been  reported,  and  Mores- 
tin,  §  in  1900,  was  able  to  refer  to  as  many  as  242  cases.  The  relative 
frequency  of  this  cause  to  other  causes  of  intestinal  obstruction  has  been 
variously  estimated  at  from  1  to  13  to  1  to  45. 

In  295  cases  of  intestinal  obstruction  Fitz  found  23  clue  to  gall-stones,  or  1  in 
13;  Gibson,  |  40  in  696,  or  1  in  17;  Leichtenstein,  41  in  11.52,  or  1  in  28;  while  in 
360  consecutive  cases  of  intestinal  obstruction  in  eight  years  at  the  London  Hospital 
Barnard  **  found  8,  or  1  in  45,  due  to  gall-stones. 

Entrance  of  the  Calculus  into  the  Intestine. — It  is  probably  ver}^  seldom 
that  a  calculus  which  passes  down  the  bile-duct  into  the  duodenum  is 
of  sufficient  size  to  occlude  mechanically  the  ileocsecal  valve.  In  some 
instances  a  large  calculus  is  found  projecting  from  the  lower  end  of  the 
bile-duct,  and  it  is  conceivable  that  such  a  calculus,  after  squeezing 
through  the  biliary  papilla  into  the  duodenum,  would  be  large  enough 
to  obstruct  the  ileocsecal  valve.  Most  writers,  however,  are  agreed  that 
a  calculus  which  passes  down  the  common  bile-duct  into  the  duodenum 
is  hardly  ever  large  enough  to  obstruct  the  intestine  mechanically.     It  is 

*  Opie,  E.  L.:  Jour.  Exper.  Med.,  vol.  v,  p.  397,  1901. 

t  Halsted  and  (Jpie:  Johns  Hopkins  Hospital  Bull.,  vol.  xii,  Nos.  121,  122,  123, 
April,  May,  June,  1901. 

X  Vide  Moynihan:  Medical  Chronicle,  vol.  xxxviii,  p.  277,  1903. 
§  Morestin:  Bull.  Soc.  Anat.  Paris,  1900,  p.  196. 
II  Gibson,  C.  L. :  Annals  of  Surgery,  October,  1900,  p.  506. 
**  Barnard,  H.  L. :  Annals  of  Surgery,  Aug.,  1902,  p.  161. 


CHOLELITHIASIS.  743 

probable  that  a  comparatively  small  calcuhis,  after  passing  into  the 
intestine,  may  increase  in  size  from  addition  of  phosphates  to  its  surface, 
as  in  Eve's  case,*  and  so  become  large  enough  to  cause  obstruction  in 
the  ileum  or  ileocsecal  valve.  Treves  t  removed  a  calculus,  with  a  diam- 
eter in  its  long  axis  of  1^  inches,  from  the  ileum  of  an  old  lady  who  for 
years  had  taken  carbonate  of  magnesia  daily.  Its  nucleus  was  a  small 
gall-stone,  and  its  large  size  was  due  to  layers  of  magnesia  and  ftecal 
material. 

In  other  and  verv  rare  instances  intestinal  obstruction  may  be  due 
to  impaction  of  a  congeries  of  small  calcidi  in  the  intestine  (Cantlie  J). 
A  calculus  which  is  not  sufficiently  large  to  obstruct  the  normal  small 
intestine  ma}^,  if  the  intestine  is  narrowed  from  some  other  cause,  com- 
pletely obstruct  the  stricture. 

Thus  Mayo  Robson  §  found  a  calculus  entangled  in  a  pouch  laetween  two  tuber- 
culous strictures  of  the  ileum.  Garrett  ||  found  a  gall-stone  arrested  just  above  a 
point  where  the  small  intestine  passed  under  an  omental  cord ;  the  bowel  was  thus 
completely  occluded. 

A  comparativeh'  small  calculus  may,  especially  if  it  is  angular,  set 
up  spasm  of  the  intestinal  wall  around  the  calculus,  and  so  lead  to  closure 
of  the  lumen  of  the  bowel;  this  theory  explains  the  fact  that  in  some 
fatal  cases  of  gall-stone  obstruction  the  calculus  has  been  found  loose 
in  the  bowel.  Another  method  by  which  a  comparatively  small  calculus 
may  cause  intestinal  obstruction  is  b}'-  setting  up  localised  inflammation 
of  the  mucous  membrane  of  the  bowel  in  its  immediate  neighbourhood. 
The  resulting  swelling  and  spasm  of  the  wall  of  the  bowel  may  then  lead 
to  impaction  of  the  calculus. 

In  the  vast  majority  of  cases  mechanical  ol^st ruction  of  the  intestine 
by  gall-stones  is  clue  to  a  large  calculus  which  has  ulcerated  out  of  the 
gall-bladder  into  the  duodenum,  or  less  commonly  into  the  transverse 
colon.  Intestinal  obstruction  is  much  more  likely  to  follow  the  passage 
of  a  calculus  into  the  duodenum,  as  it  has  then  to  pass  through  the  duo- 
denum, jejunum,  and  the  narrowed  lower  part  of  the  ileum,  than  in  cases 
where  a  calculus  ulcerates  directly  from  the  gall-bladder  into  the  colon. 

It  is  a  curious  fact  that  a  calculus  may  enter  the  intestine  and  remain 
there  comparatively  c^uietly  for  days,  months,  or  even  years,  and  yet 
eventually  give  rise  to  intestinal  obstruction.  When  a  calculus  is  in  the 
intestine,  it  may  give  rise  to  repeated  attacks  of  colic,  vomiting,  and 
pain,  suggesting  mild  olistructioii.  and  finally  bring  al^out  acute  ob- 
struction. 

In  Sir  T.  Smith's  **  case  the  calculus  was  thought  to  have  enteretl  the  intestine 
fifteen  years  before  acute  obstruction  was  produced. 

As  there  ma}'  be  two  calculi  in  the  intestine,  attacks  of  transient  ob- 
struction may  recur  even  after  a  calculus  has  been  passed  by  the  l)owel. 

*  Eve,  F. :  Trans.  Clmic.  Soc,  vol.  xxviii,  p.  91. 

t  Treves,  F. :  Intestinal  Obstruction,  p.  19.3,  2(1  ed.,  1S99. 

tCantlie,  J.:  Brit.  Med.  Jour.,  1904,  vol.  i,  p.  LSI. 

§  Mavo  Robson:  Trans.  Chn.  Soc,  vol.  xxxv,  p.  .58. 

Ij  Garrett:  Brit.  Med.  Journ.,  1902,  vol.  ii,  p.  789.  **  Lancet,  Dec.  3,  1887. 


744  DISEASES    OF   THE    BILE-DUCTS. 

As  already  pointed  out,  there  may  be  a  want  of  proportion  between 
the  size  of  the  gall-stone  and  the  intestinal  manifestations  produced  by 
it.  Thus  a  comparatively  small  but  angular  calculus  may  set  up  so 
much  spasm  that  the  symptoms  of  obstruction  are  produced,  while  a 
smooth  calculus  of  much  larger  dimensions  may  be  passed  by  the  rectum 
with  little  pain. 

It  is  probable  that  all  large  calculi  spontaneously  passed  by  the 
bowel  have  entered  the  transverse  colon  from  the  gall-bladder  by  a 
cholecysto-colic  fistula,  for  a  calculus  with  a  diameter  of  an  inch  or  more 
would  almost  certainly  become  impacted  at  the  ileocsecal  valve.  Among 
Gibson's  *  40  cases  the  largest  gall-stone  weighed  three  and  one-half 
ounces. 

Site  of  the  Obstruction.— The  obstruction  is  most  frequent  in  the  lower 
end  of  the  ileum  near  the  ileocsecal  valve.  When  a  large  calculus  ulcer- 
ates from  the  gall-bladder  into  the  duodenum,  the  site  of  the  obstruction  ■ 
may  be  in  the  duodenum  itself,  at  its  junction  with  the  jejunum,  or  in 
the  ileum.  Wlien  a  calculus  ulcerates  into  the  colon,  the  obstruction 
may  occur  in  the  sigmoid  flexure  or  close  to  the  anus. 

In  53  cases  Courvoisier  f  found  the  site  of  obstruction  to  be  in  the  ileum  in 
65.4  per  cent.;  in  the  duodenum,  21.4  per  cent.;  at  the  ileocsecal  valve,  10  per 
cent.,  and  in  the  sigmoid  flexure,  2.4  per  cent.  In  40  cases  collected  by  Gibson  J 
the  calculus  was  impacted  in  the  large  intestine  in  one  case  only;  in  the  ileocEecal 
valve  in  one  instance,  and  in  all  the  other  cases  in  the  small  intestine. 

Sex. — Intestinal  obstruction  due  to  gall-stones  is  very  much  com- 
moner in  women  than  in  men.  This  is  a  natural  result  of  the  great  fre- 
quency of  cholelithiasis  in  women. 

In  Natmyn's  127  cases  34  were  men  and  93  women.  In  50  recent  cases  which 
I  have  collected  there  were  42  females  and  8  males. 

The  average  age  is  over  fifty  years  of  age.  In  50  recent  cases  the 
average  age  was  62.7  years,  and  many  cases  between  70  and  80  years 
of  age  have  been  reported. 

Clinical  Picture. — The  onset  is  sudden.  In  some  cases  it  has  been 
preceded  by  attacks  of  vomiting  and  pain,  but  usually  signs  suggesting 
that  the  calculus  has  been  for  some  time  in  the  bowel  are  absent,  and 
there  may  be  no  evidence  of  former  gall-bladder  trouble  or  of  chole- 
lithiasis. In  41  out  of  120  cases  the  onset  was  preceded  by  symptoms 
which  could  be  referred  to  ulceration  of  the  calculus  into  the  intestine. 
(Naunyn.)  Although  the  bowel  is  obstructed,  it  is  not  strangidated, 
and  as  the  circulation  through  its  walls  is  not  interfered  with,  they  do 
not  become  paralysed  and  hence  tympanites  is  usuall}''  absent,  while 
flatus  and  faeces  are  often  passed  by  the  bowel.  A  calculus  has  been 
known  to  ulcerate  out  of  the  bowel  and  set  up  peritonitis.  §  At  first 
pain  and  collapse  are  not  marked.  Vomiting  is  usually  an  early  symp- 
tom, and  when  the  calculus  is  impacted  in  the  duodenum  or  in  the 

*  Gibson:  Annals  of  Surgery,  Oct.,  1900,  p.  506. 
t  Courvoisier :  Patholog.  u.  Chirurg.  der  Gallenwege,  1900. 
t  Gibson,  C.  L. :  Annals  of  Surgery,  Oct.,  1900,  p.  506. 
§  .Jeatfreson:  Brit.  Med.  Jour.,  1868,  vol.  i,  p.  531. 


CHOLELITHIASIS.  745 

Upper  part  of  the  small  intestine,  the  vomited  matter  is  bihous  and 
does  not  become  stercoraceous.  It  may  contain  blood  from  haemorrhage 
produced  in  the  process  of  ulceration  of  the  calculus  into  the  duodenum. 

The  impaction  may  persist,  so  that  unless  reheved  by  operation  death 
occurs  from  acute  obstruction;  in  about  50  per  cent,  the  symptoms  are 
spontaneously  reheved,  sometimes  quite  suddenly,  so  that  the  patient 
at  once  knows  that  his  condition  has  improved.  In  some  instances,  even 
though  the  patient  has  been  relieved  from  the  acute  symptoms  of  ob- 
struction, the  wall  of  the  bowel  is  so  damaged  that  perforation  or  leakage 
from  an  ulcer  occurs  and  sets  up  peritonitis. 

Duration  and  Prognosis. — In  fatal  cases  death  usually  occurs  within 
five  to  ten  days  after  the  onset  from  collapse.  In  Sands'  case  *  recovery 
took  place  after  the  condition  had  lasted  for  twenty-eight  days ;  this  is 
the  longest  case  on  record.  About  50  per  cent,  of  the  cases  die  if  not 
operated  upon.  The  statistics  of  cases  operated  upon  show  a  high  mor- 
tahty;  thus  in  Schuller's  82  cases  there  was  56  per  cent.;  in  J.  Hutchin- 
son's (Sr.),  50  per  cent.;  and  in  Courvoisier's  125  cases  of  operation,  44 
per  cent.,  of  deaths. 

Diagnosis. — ^Wlien  there  is  a  definite  history  of  gall-stones  in  the 
past  and  acute  obstruction  comes  on  suddenly  with  the  presence  of  a 
hard,  rounded  tumor  in  the  abdomen,  the  diagnosis  would  appear  to  be 
fairly  clear.  But,  unfortunately,  in  a  number  of  the  cases  there  is  no 
definite  history  of  cholelithiasis,  and  the  gall-stone  is  hardly  ever  felt 
in  the  abdomen  before  the  operation. 

In  two  cases  reported  by  Barnard  t  the  calculus  was  felt  before  operation. 

It  is  possible  that  examination  under  an  anaesthetic  might  enable  a 
calculus  to  be  felt  in  a  certain  number  of  cases.  But  as  a  matter  of  fact, 
the  condition  is  very  seldom  correctly  diagnosed  before  the  abdomen  is 
opened  or  the  calculus  is  spontaneously  passed  by  the  rectum. 

Treatment. — ^As  the  symptoms  are  those  of  intestinal  obstruction  and 
it  is  seldom  possible  to  make  a  certain  chagnosis  of  mechanical  obstruction 
of  the  intestine  by  a  gall-stone,  the  safest  course  is  to  open  the  abdomen 
and  remove  the  stone  by  incising  the  bowel.  In  cases  where  the  stone 
is  comparatively  small  and  is  impacted  at  the  lower  end  of  the  ileum, 
it  iTiight  be  pressed  on  into  the  colon.  It  is  important  that  if  an  operation 
is  necessary,  it  should  be  undertaken  as  soon  as  possible,  for  the  patients 
are  usually  elderly  and  are  often  wanting  in  vitality. 

Medical  treatment  has  been  successful  in  a  certain  number  of  cases. 
The  most  reasonable  method  seems  to  be  to  give  belladonna  or  atropine 
in  order  to  relieve  spasm,  and  so  to  allow  of  the  onward  passage  of  the 
calculus;  this  method  should  be  adopted  in  less  severe  cases  in  which 
there  is  any  reason  to  suspect  or  believe  that  the  cause  of  obstruction  is 
an  impacted  calculus  in  the  intestine,  and  at  an  early  stage.  In  such 
cases  Mayo  Robson  X  advises  moiphia  to  relieve  the  pain,  and  extract 

*  Quoted  by  Treves:  Intestinal  Obstruction,  2d  ed.,  p.  3S8. 

t  Barnard,  H.  L. :  Annals  of  Surgery,  Aug.,  1902,  p.  161. 

i  Mayo  Robson:  Diseases  of  the  Gall-bladder  and  Bile-ducts,  p.  157,  1904. 


746  DISEASES    OF   THE    BILE-DUCTS. 

of  belladonna  (|  gr.)  every  four  hours,  while  chloroform  anaesthesia  may 
be  of  use  in  two  ways — by  allowing  a  thorough  examination  of  the  abdo- 
men, by  which  the  diagnosis  may  be  cleared  up  if  it  is  doubtful,  and 
possibly  by  allowing  manipulation  to  reduce  or  remove  the  obstruction. 
If  these  measures  fail,  operation  should  be  undertaken  without  further 
delay. 

J.  Hutchinson  *  has  advocated  a  poUcy  of  surgical  non-interference 
in  cases  of  gall-stone  obstruction,  and  has  urged  the  use  of  anaesthetics, 
opium,  and  rectal  injections  with  air  or  fluid  to  diminish  spasm  and 
assist  in  the  passage  of  the  calculus.  Massage  has  been  known  to  lead 
to  a  cure. 

Treves  f  quotes  a  case  of  Martin's  J  in  Avhicli  massage  was  employed  on  the 
sixth  day  of  obstruction  and  on  the  next  day  a  large  gall-stone  and  ten  smaller 
stones  were  evacuated. 

INFLAMMATORY  AND  INFECTIVE  CHANGES  SET  UP  BY  GALL-STONES, 

The  inflammatory  and  infective  changes  due  to  gall-stones  include 
a  large  number  of  the  irregular  symptoms  of  cholelithiasis,  and  will  be 
conveniently  described  under  the  various  headings  of  changes  in  con- 
nexion with  — (A)  The  gall-bladder;  (B)  the  cystic,  and  (C)  the  common 
bile-duct  and  ampulla  of  Vater;  while  an  account  of  the  various  fistulse 
due  to  cholelithiasis  will  be  given. 


SYNOPSIS. 

(A)  Gall-bladder: 

Cholecystitis. 

Ulceration. 

Haemorrhage. 

Scars;  hour-glass  contraction. 

Perforation;  fistulse. 

Pericholecystic  adhesions  to  pylorus,  duodenum,  colon,  etc. 

(B)  Cystic  duct: 

Swelling. 

Obliteration. 

Diverticulum. 

(C)  Common  bile-duct  and  ampulla  of  ^^ater: 

Intermittent  hepatic  fever. 

Extension  to  pancreatic  duct — pancreatitis ;  cysts.     • 
Extension  to  portal  vein — ^pylephlebitis. 
Fistulse. 

(A)  Inflammatory  and  Infective  Changes  in  the  Gall-bladder.— 

Although  gall-stones  are  due  to  inflammation,  of  a  comparatively  mild 
character,  of  the  gall-bladder,  their  presence  disposes  to  fresh  infection 
of  the  gall-bladder  and  thus  to  cholecystitis  and  to  a  vicious  circle. 

*  Hutchinson,  J. :  Archives  of  Surgery,  April,  1896. 
t  Treves:  Intestinal  Obstruction,  p.  467,  2d  ed.,  1899. 
X  Martin:  Bull.  Soc.  Anat.  Paris,  1875,  p.  195. 


CHOLELITHIASIS.  747 

Mieczkowski,*  from  examination  of  the  bile  of  15  patients  whose  gall-bladders 
were  health}^  and  were  extirpated  during  laparotomj''  for  other  conditions,  concludes 
that  human  bile  is  sterile.  In  23  cases  of  cholelithiasis  investigated  by  him  the 
bile  was  infected  in  IS.  Gall-bladders  containing  gall-stones,  therefore,  are  usuallj' 
infected  and  are  thus  prone  to  fresh  attacks  of  cholecystitis. 

Cholecystitis. — Inflammation  of  various  degrees  of  severity  may  super- 
vene in  a  gall-bladder  containing  gall-stones.  There  may  be  acute  in- 
fective cholecystitis,  serous,  serofibrinous,  or  purulent,  which  may  go 
on  to  ulceration  and  perforation  or  gangrene;  or  there  may  be  chronic 
serous  or  purulent  cholecystitis;  the  latter  condition  is  often  spoken 
of  as  empyema  of  the  gall-bladder.  Descriptions  of  these  various  forms 
of  cholecystitis  are  given  elsewhere.     {Vide  p.  596.) 

Acute  cholecystitis  may  set  up  local  peritonitis,  and  by  paralysing 
the  peristaltic  movements  of  the  intestines,  may  imitate  acute  intestinal 
obstruction. 

Ulceration  of  the  mucous  membrane  of  the  gall-l^ladder  may  give 
rise  to:  (1)  Changes  in  the  gall-bladder — (a)  Haemorrhage.  (5)  Scars, 
(c)  Hour-glass  contraction  and  diverticula.  (2)  Perforation  of  the 
gall-bladder:  (a)  Into  the  general  cavity  of  the  peritoneum.  (6)  Into 
part  of  the  peritoneum  shut  off  by  adhesions,  (c)  Into  the  duodenum, 
colon,  etc.  (vide  FistulEe,  p.  756).  (d)  Into  other  adjacent  structures, 
such  as  bile-ducts,  portal  vein,  hepatic  artery,     (e)  Into  the  liver. 

(a)  Hcemorrhage. — ^As  the  result  of  an  ulcer  due  to  cholecystitis 
haemorrhage  may  take  jilace  into  the  gall-bladder.  This  may  depend  on 
erosion  of  a  small  vessel  in  the  wall  of  the  gall-l^ladder,  but  in  rare  in- 
stances ulceration  of  the  gall-bladder  may  involve  the  trunk  of  the  hepatic 
artery  and  give  rise  to  the  formation  of  an  aneurysm  {vide  p.  43)  which 
may  subsequently  rupture. 

(b)  Scars. — As  a  result  of  the  healing  of  an  ulcer  in  the  mucous  mem- 
brane of  the  gall-bladder  a  scar  results.  In  343  cases  of  cholelithiasis 
tabulated  by  Schloth  j  there  were  14  with  cicatrices.  These  are  more 
commonly  seen  at  the  fundus  or  close  to  the  origin  of  the  cystic  duct. 
Their  site  depends  to  some  extent  on  the  mechanical  irritation  of  the 
calculus.  It  may  be  pointed  out,  however,  that  what  looks  like  a  scar 
on  the  surface  of  the  gall-bladder  may  in  realit}'  be  a  ^^ery  early  stage 
of  primary  carcinoma  of  the  gall-bladder. 

(c)  Hour-glass  Contraction. — Cicatrisation  following  inflammation 
and  ulceration  may  lead  to  the  production  of  hour-glass  contraction  of 
the  gall-bladder.  The  gall-bladder  may  thus  become  divided  into  two 
compartments  which  conmumicate  by  a  narrow  channel.  One  or  both 
of  these  two  divisions  may  contain  calculi.  The  communication  between 
the  two  may  become  impervious,  so  that  the  fimdus  no  longer  com- 
municates with  the  cystic  duct. 

Kehr  J  records  such  a  case  in  which  one  comj^artment  contained  pus,  the  other 
clear  bile.     In  Donald's  §  case  the  peripheral  part  onh^  contained  mucus. 

*  Mieczkowski:  Mitt.  a.  d.  Grenzgeb.  d.  Med.  u.  Chir.,  1900,  Bd.  vi.     Abstract 
in  American  .Journ.  Med.  Sciences,  1902,  vol.  cxxiii,  p.  372. 
t  Schlotli :  Diss.,  '\^'urzburg,  1887.     Quoted  by  Xaiuiyn. 
t  Kehr:  Diagnosis  of  Gall-stone  Disease.     American  translation,  p.  48. 
§  Donald:  Glasgow  Medical  .louni.,  1898,  p.  .348. 


748 


DISEASES    OF   THE    BILE-DUCTS. 


Courvoisier  collected  15  examples  of  hour-glass  gall-bladder,  and 
others  have  been  recorded  since  his  monograph  was  pubUshed  in  1890. 
Much  the  same  kind  of  change  is  in  progress  in  cases  where  a  number  of 
septa  spring  from  the  walls  of  the  gall-bladder  and  form  ridges  between 
a  succession  of  calculi.  In  this  way  the  gall-bladder  may  become  divided 
into  a  number  of  loculi  or  compartments  communicating  by  narrow 
orifices. 

H.  L.  Barnard  *  described  a  ease  where  the  gall-bladder  contained  four  such 
compartments,  one  of  which  opened  into  the  duodenum. 

(2)  Perforation  of  the  Gall-bladder. — (a)  Into  the  General  Cavity  of 
the  Peritoneum. — When  perforation  or  rup- 
ture of  an  inflamed  gall-bladder  takes  place 
and  the  general  cavity  of  the  peritoneum  is 
not  shut  off  by  old  or  recent  adhesions,  the 
bile  and  even  gall-stones  pass  into  the  peri- 
toneum and  set  up  severe  and  usually  fatal 
peritonitis.  This  is  seen  in  cases  of  phleg- 
monous and  gangrenous  cholecystitis  {vide 
pp.  610  and  612). 

(6)  Into  a  Localised  Pocket  of  the  Perito- 
neum Cut  off  hy  A  dhesions. — A  local  abscess 
formed  in  connexion  with  perforation  of  a 
calculous  gall-bladder  into  part  of  the  peri- 
toneum previously  cut  off  by  adhesions  may 
contain  gall-stones,  and  may  open  in  one  or 
more  of  a  number  of  different  situations, 
such  as  the  duodenum,  stomach,  on  the 
surface  of  the  abdomen,  etc.  {vide  Bihary 
Fistulse),  or  present  as  a  subphrenic  abscess, 
or  give  rise  to  an  empyema  on  the  right 
side. 

(c)  Ulceration  of  the  Gall-bladder  into  the 
Substance  of  the  Liver. — Ulceration  of  the 
gall-bladder  may  extend  directly  into  the 
substance  of  the  liver;  it  may  then  give 
rise  to  an  abscess  cavity  in  the  hver  com- 
municating with  the  gall-bladder,  or  to 
haemorrhage  into  the  gall-bladder. 

Arbuthnot  Lane  t  described  a  case  where  an  encj'sted  cavity  in  the  liver,  which 
contained  calculi,  opened  into  the  gall-bladder;  and  a  second  casej  in  which  rupture 
of  the  gall-bladder,  which  probably  contained  a  calculus,  on  its  anterior  surface, 
extended  into  the  substance  of  the  liver  and  gave  rise  to  profuse  haemorrhage  into 
the  gall-bladder. 

This,  however,  is  a  very  rare  event. 

{d)  Ulceration  of  the  gall-bladder  may  extend  into  the  common  bile- 

*  Barnard,  H.  L. :  Annals  of  Surgery,  Aug.,  1902,  p.  161. 

t  Lancet,  189.3,  vol.  ii,  p.  874.  X  Trans.  Clinic.  Soc,  vol.  xxviii,  p.  160. 


Fig.  96. — Hour-glass  Contrac- 
tion OP  Gall-bladder. 
The  fundus,  which  commu- 
nicates with  the  remainder  of  the 
gall-bladder  through  a  minute 
orifice  admitting  a  bristle,  con- 
tains two  calculi,  one  above 
the  other,  partially  separated 
from  each  other  by  a  septum  from 
the  wall  of  the  gall-bladder, 
(Drawn  by  Dr.  G.  H.  Goldsmith.) 


CHOLELITHIASIS.  749 

ducts,  portal  vein,  and  hepatic  artery  in  the  lesser  omentum.  These 
events  are  also  referred  to  under  the  head  of  bihary  fistulse  (vide  p.  756) : 
they  are  very  rare.  Ulceration  of  the  hepatic  artery  may  give  rise  to 
the  production  of  an  aneurysm  (vide  p.  43). 

Ulceration  of  the  gall-bladder  with  the  formation  of  fistulse  in  con- 
nexion with  various  internal  organs  and  with  the  outside  of  the  body 
is  dealt  with  below  (vide  p.  756). 

Pericholecystic  Adhesions. — As  the  result  of  inflammation  around  the 
gall-bladder  adhesions  readily  form  and  unite  it  to  adjacent  organs, 
especially  the  pyloric  end  of  the  stomach  or  the  duodenum.  According 
to  the  thickness  and  density  of  the  adhesions  symptoms  of  a  varying 
degree  of  intensity  are  induced.  In  the  slighter  cases  there  is  pain  after 
food,  or  ''adhesion  dyspepsia"  due  to  interference  with  the  gastric  move- 
ments and  to  dragging  on  adhesions.  These  cases  come  under  observa- 
tion as  indigestion  or  gastralgia,  and  imitate  "adhesion  dyspepsia"  due 
to  the  effects  of  a  past  gastric  ulcer.  When  the  adhesions  are  firmer 
and  dense,  the  pylorus  or  the  duodenum  may  be  so  constricted  or  kinked 
that  pyloric  obstruction  is  induced,  and  the  case  may  closely  resemble 
carcinoma  of  the  pylorus  with  secondary  dilatation  of  the  stomach. 

Mayo  Robson,*  Tufiier  and  Marchais,t  Thomas,t  Page,§  Villard,l| 
and  others  have  drawn  attention  to  pyloric  obstruction  due  to  adhesions 
of  pericholecystitic  origin. 

These  cases  are  frequently  recognised  during  the  course  of  operations 
on  the  gajl-bladder  for  cholelithiasis.  In  many  of  the  cases  the  symptoms 
come  on  very  gradually  and  a  considerable  time  after  definite  symptoms 
of  gall-stones,  so  that  their  clinical  relationship  is  very  much  obscured. 

In  a  few  of  the  cases  hsematemesis  has  been  recorded,  thus  making 
the  resemblance  to  primary  gastric  disorder  even  more  definite. 

When  dieting  and  thorough  medical  treatment  fail  to  relieve  these 
cases  of  pyloric  stenosis  due  to  adhesions  set  up  by  calculous  cholecystitis 
and  the  patient's  life  is  made  a  burden  by  the  continual  pain  and  inva- 
lidism, exploratory  laparotomy  is  justified. 

Dr.  Fiitterer,  of  Chicago,  has  kindly  sent  me  photographs  of  the  gall-bladder  in  a 
case  where  old  adhesions  between  a  gall-bladder  containing  calculi  and  the  pylorus 
were  the  means  of  conveying  carcinoma  from  the  pylorus  to  the  gall-bladder. 

In  cases  where  a  gall-stone  has  ulcerated  into  the  duodenum  the 
cicatricial  contraction  which  follows  may  give  rise  to  stricture  of  the 
duodenum  and  so  to  obstruction.**  In  some  instances  adhesions  due 
to  past  cholecystitis  may  form  bands  which  lead  to  constriction  of  the 
colon  or  of  the  small  intestine  and  so  produce  acute  intestinal  obstnic- 
tion. 

*  Mayo  Robson:  Trans.  Clinic.  Soc,  vol.  xxvii,  p.  1,  L893-4.  Diseases  of  Gall- 
bladder and  Bile-ducts,  1st  ed.,  p.  73,  1897. 

t  Tuther  and  Marchais:  Rev.  de  (hirurg.,  Feb.,  L897. 
X  Thomas:  Rev.  Med.  de  la  Suisse  Romande,  Jan.,  L897 
§  Page,  F. :  Brit.  Med.  Journ.,  L897,  vol.  i,  p.  205. 
II  Villard :  Lyon  Medical,  1902,  p.  737. 
**  Labadie-Lagrave  and  Magdelaine :  Journ.  des  Praticiens,  June  25,  1S98. 


750  DISEASES    OF   THE    BILE-DUCTS. 

Xiles  *  reported  a  case  of  stenosis  of  the  liepatic  flexure  by  pericholecystitic 
adhesions  Avhich  was  cured  by  dividing  the  adhesions  and  removing  60  small  calculi 
from  the  gall-bladder. 

Adhesions  ma}'  be  formed  between  the  gall-bladder  and  the  vermiform 
appendix  as  the  result  of  inflammation  of  the  gall-bladder.  This  may 
explain  the  fact  that  cholelithiasis  often  gives  rise  to  pain  suggesting 
appendicitis. 

(B)  Results  of  Inflammation  in  the  Cystic  Duct.^The  impaction 
or  passage  of  a  calculus,  especially  an  angular  one,  along  the  cystic  duct 
may  set  up  severe  inflammatory  changes,  ulceration,  and  subsecpently 
cicatricial  contraction  of  the  duct.  In  some  cases  inflammatory  adhesions 
around  the  cystic  duct  may  involve  and  lead  to  constriction  of  the  neigh- 
bouring common  hepatic  and  common  bile-clucts.  A  calculus  when 
impacted  may  lead  to  ulceration  and  bulging  of  the  walls  of  the  duct, 
so  that  the  calculus  becomes  encysted  in  a  diverticulum  of  the  cystic 
duct.  When  so  placed,  the  calculus  may  exert 
pressure  on  the  cystic  duct,  as  in  a  case  reported 
b}^  W.  W.  Cheyne,t  or  possibly  on  the  common 
hepatic  duct. 

In  a  woman  Avho  died  of  bronchitis  in  St.  George's  Hos- 
pital the  liver  was  very  freely  movable  and  showed  evidence 
of  tight  lacing.  The  neck  of  the  gall-bladder  was  long,  and 
just  at  the  commencement  of  the  cystic  duct  there  was  a 
recess  containing  a  gall-stone  (vide  Fig.  97).  The  gall-blad- 
der was  not  dilated,  and  bile  could  easily  be  driven  from  the 
gall-bladder  into  the  duodenum. 

„      „_     ^  The  process  of  ulceration  mav  lead  to  the  calculus 

Fig.  97. — Ctall-blad-  J^  "... 

DEK  WITH  Elon-     worklug  Its  way  out  of  the  duct  and  giving  rise  to  a 

Diverticulum  AT     localised  abscess  in  the  immediate  neighbourhood. 

of'c^Itic^duct  (C)  Inflammation    and   Infective    Changes    in 

Calculus'"'       ^      the  Common  Bile-duct.— The  inflammation  of  the 

common  bile-duct  associated  with  the  presence  of  a 

gall-stone    may   possibly   be    an    extension  of   the   cholecystitis  which 

originally  drove  the  calculus  out  of  the  gall-bladder,  but  probably  in 

most  cases  the  presence  of  the  calculus  favours  an  ascending  infection 

of  the  common  bile-duct  from  the  duodenum. 

Calculi  in  the  common  duct  may  set  up  chronic  or  intermittent  in- 
flammation, which  is  described  below  in  detail  as  intermittent  hepatic 
fever.  It  may  give  rise  to  ulceration  of  the  duct  and  to  perforation 
and  the  formation  of  a  local  abscess,  or  to  suppurative  cholangitis  (vide 
p.  663)  and  multiple  aljscesses  in  the  liver. 

INTERMITTENT  HEPATIC  FEVER: 
S)/now/m:  Recurrent  Hepatic  Fever. 

A  characteristic  result  of  calculi  in  the  conmion  bile-duct  is  a  group 
of  symptoms  collectively  descril^ed  as  intermittent  hepatic  fever.     Its 

*  Niles,  H.  D. :  Annals  of  Surgery,  part  cxi,  p.  .344,  March,  1902. 
t  Cheyne,  W.  W. :  King's  College  Hospital  Reports,  vol.  iii,  p.  94. 


CHOLELITHIASIS.  751 

clinical  features  Avere  first  noted  by  Charcot,*  but  have  been  especially 
insisted  upon  by  Osier, f  and  are  now  thoroughly  well  recognised. 

Anatomically  the  calculus  "floats"  near  the  lower  end  of  the  common 
bile-duct,  which  is  often  greatly  dilated.  The  calculus  is  movable,  and 
is  spoken  of  as  exerting  a  ball-valve  action  (Osler,t  C.  Fenger  §).  In 
many  cases  the  dilatation  of  the  duct  around  and  above  the  gall-stone, 
which  often  lies  in  a  pathologically  dilated  ampulla  of  ^"ater,  allows  bile 
to  trickle  past  into  the  duodenum,  so  that  jaundice  may  be  transient, 
intermittent,  or  if  at  one  time  marked,  may  gradually  pass  away.  There 
may,  in  fact,  be  no  jaundice  at  all. 

Griffon  ||  records  4  cases  and  Bernard  **  one  where  a  calculus  just  above  the 
biliary  papilla  existed  without  any  jaundice. 

The  gall-stone  often  bulges  the  biliary  papilla  out  as  a  projection  in 
the  duodenum.  The  common  and  other  bile-ducts  are  dilated,  often 
very  greatly,  and  their  walls  thickened,  but  the  mucous  membrane, 
though  inflamed,  is  usually  free  from  ulceration.  The  liver  often  shows 
adhesions  over  its  convexity,  due  to  past  attacks  of  perihepatitis.  The 
intra-hepatic  bile-ducts  may  be  dilated,  and  from  pericholangitis  there 
is  an  increased  amount  of  fibrous  tissue  around  them  with  some  atrophy 
of  the  Hver  substance;  this  constitutes  the  condition  often  described  as 
obstructive  biliary  cirrhosis. 

The  gall-bladder  is  usually  small,  thickened,  and  contracted  from 
past  cholecystitis  in  accordance  with  Courvoisier's  ft  well-known  law  that 
in  jaundice  due  to  gall-stones  the  gall-bladder  is  small,  Avhereas  in  icterus 
due  to  the  pressure  of  a  growth  on  the  ducts  the  gall-bladder  is  distended. 
There  are  frequently  adhesions  between  the  gall-bladder  and  the  adjacent 
viscera,  especially  the  omentum,  stomach,  and  the  transverse  colon. 
There  may  be  no  gall-stones  in  the  gall-bladder,  but  in  some  instances 
it  contains  a  number  of  calculi.  The  head  of  the  pancreas  tends  to  be 
enlarged  from  chronic  interstitial  pancreatitis. 

There  is  infective  catarrhal  inflammation  of  the  common  bile-duct. 

Charcot  originally  regarded  the  fever  as  due  to  absorption  of  poisons  from  the 
bile-ducts.  Netter  and  Martha, |  J  Abbott,  and  Pick  §§  have  found  micro-organisms, 
especially  tlie  colon  bacillus,  in  the  ducts.  Budd  ||  j|  drew  an  analog}'  between 
urethral  fever  following  catheterization  and  intermittent  hepatic  fever,  while  Mur- 
chison  and  Ord  ***  regarded  the  fever  as  merely  the  reflex  result  of  irritation  ex- 
erted by  the  calculus. 

The  striking  intermissions  in  the  symptoms  may  possibly  depend  on 
the  micro-organisms  which  have  set  up  acute  catarrhal  swelling  of  the 

*  Charcot :  Le(,'ons  sur  les  Maladies  du  foie  et  des  Voies  biliaires,  p.  178,  1877. 

t  Osier:  Johns  Hopkins  Hospital  Reports,  vol.  ii.  1890.     Lancet,  1897,  vol.  i. 

i  Osier,  W.:  Medical  Times  and  Gazette,  July  31,  1881,  p.  111. 

§  Fenger,  C. :  .\merican  Journal  Med.  Sciences,  vol.  cxi,  p.  125,  Feb.,  1896. 

II  Griffon:  Bull.  Soc.  Anat.  Paris,  July,  189G,  p.  513. 
**  Bernard:  Ibid.,  p.  510. 

tt  Courvoisier:  Beitrilge  zur  Pathologie  u.  ("Iiirurg.  d.  Gallenwegen,  1890. 
Xt  Netter  and  Martha:  .\rchiv  de  Physiolog.  norm,  et  path.,  1880,  p.  7. 
§§  Pick:  Brit.  Med.  Journ.,  1898,  vol.  i,  Fpitome,  No.  229. 
nil  Budd:  Diseases  of  the  r>ivcr,  2d  ed..  p.  37r.,  1857. 
***Ord,  W.  M.:  Brit.  .Med.  .Idurn..  1S,S7,  vol.  i,  p.  496. 


752  DISEASES    OF    THE    BILE-DUCTS. 

mucous  membrane  of  the  duct  and  biliary  obstiiiction,  j^assing  away 
into  the  duodenum.  Or,  on  the  other  hand,  periodic  inten^als  of  im- 
munity may  be  developed  with  the  result  that  the  symptoms  disappear, 
only  to  reappear  when,  inmiimity  being  exliausted,  the  micro-organisms, 
which  in  the  interval,  though  present,  have  remained  latent,  set  up  a 
fresh  and  acute  cholangitis. 

Clinical  Picture. — The  symptoms  may  come  on  many  years  after 
the  original  attack  of  cholecystitis  which  gave  rise  to  the  gall-stone,  and 
there  may  be  an  inter\'al  lasting  for  years,  -uith  freedom  from  symiDtoms, 
or  there  may  be  recurrent  attacks  of  biliary  colic  eventually  terminating 
in  intermittent  hepatic  fever. 

W.  Moore  *  reported  a  case  in  a  woman  aged  fifty-four  who  first  had  jaundice 
when  nineteen  years  old.  For  twenty-five  years  she  had  had  yearly  attacks  of 
biliary  colic,  which  recently  had  been  accompanied  by  jaundice  and  shivering. 
Recover jr  followed  removal  of  a  calculus  from  the  common  bile-duct  and  21  calculi 
from  the  gall-bladder. 

The  clinical  aspect  of  these  cases  may  be  summed  up  in  the  occur- 
rence of  ague-like  attacks  of  pain,  fever,  rigors,  and  increase  in  the 
jaundice,  wliile  in  the  inter^-als  the  patients  are  fairty  well  and  even 
able  to  live  their  ordinary  lives.  The  disease  may  continue  for  years, 
but  eventually  may  terminate  in  suppurative  inflammation  of  the  ducts, 
the  liver,  or  in  the  neighbourhood  of  the  calculus. 

The  attacks,  which  sometimes  closely  resemble  ague  in  their  periodic- 
it}^,  are  accompanied  by  fever,  the  temperature  going  up  as  high  as 
103°,  rigors,  and  sweating.  The  pain  is  felt  in  the  region  of  the  liver 
and  epigastrium,  and  may  be  as  severe  as  that  of  ordinary  bihary  colic 
and  necessitate  relief  by  hy]Dodermic  injection  of  morpliine.  There  may 
be  tenderness  in  the  back,  close  to  the  tenth  dorsal  spine  on  the  right 
side.  Jaundice,  wliich  is  usually  present  in  a  slight  degree  in  the  intervals, 
becomes  more  intense  and  may  be  accompanied  by  itching  of  the  skin. 
Vomiting  is  often  present  during  the  attack,  and  dyspepsia  and  gastric 
pain  from  adhesions  between  the  gall-bladder  and  stomach  are  frequently 
troublesome.  The  liver  may  be  somewhat  enlarged  and  tender  during 
an  attack,  but  the  gall-bladder  cannot  be  felt.  The  spleen  is  usually 
palpable  during  the  attacks.  Examination  of  the  blood  shows  that 
there  is  a  leucoc}^osis  during  the  attack,  but  not  in  the  intervals.  (Pick.t) 

Complications. — Inflammation  and  ulceration  of  the  common  bile- 
duct  in  rare  instances  lead  to  cicatricial  contraction  of  the  duct.  Ex- 
amples of  this  curioush'  infrequent  sequela  are  given  on  page  653  (Simple 
Stricture  of  the  Ducts). 

Kehr  J  records  a  case  where  complete  obliteration  of  the  common  bile-duct  at 
its  junction  with  the  cystic  duct  was  due  to  this  cause. 

The  inflammation  may  be  acute  and  lead  to  widespread  suppurative 

cholangitis  throughout  the  liver.     This  unfortunate  result  is  described 

on  page  663. 

*  Moore,  W. :  Intercolonial  Med.  Journ.  of  Australasia,  Aug.  20,  1899. 

t  Pick,  E. :  Brit.  Med.  Journ.,  1898,  vol.  i.  Epitome,  No.  229. 

%  Kehr :  Diagnosis  of  Gall-stone  Disease,  American  translation,  p.  48. 


CHOLELITHIASIS.  753 

Diag)wsis. — The  periodicity  of  the  febrile  attacks  may  closely  imitate 
malaria,  but  there  is  no  reaction  to  quinine  and  the  malarial  parasite 
is  not  found  in  the  blood.  The  presence  of  jaundice  in  the  intervals 
and  its  intensification  during  the  attacks  should  always  suggest  chole- 
lithiasis. The  diagnosis  of  gall-stones  by  x-rays  cannot  be  relied  upon, 
as  no  shadow  may  be  obtained  from  them.  Probably  a  good  deal 
depends  on  the  experience  of  the  radiographer.  A  negative  result  is  of 
no  value. 

It  is  important  to  distinguish  the  condition  from  suppurative  inflam- 
mation of  the  bile-ducts,  which,  as  has  been  pointed  out,  may  supervene 
in  intermittent  hepatic  fever.  In  suppurative  cholangitis  the  fever  is 
much  more  continuous,  the  paroxysms  are  more  frequent,  and  intervals 
of  comparatively  good  health  do  not  occur;  the  patient  is  much  worse, 
the  liver  is  more  enlarged,  the  gall-bladder  may  be  palpable,  while  the 
jaundice  is  not  so  marked. 

In  hepatic  abscess  the  fever  is  continuous,  the  liver  is  more  enlarged, 
and  leucocytosis,  if  present,  is  constant  and  does  not  pass  away  as  it 
does  in  intermittent  hepatic  fever. 

In  malignant  disease  the  liver  is  more  enlarged  and  the  course  of  the 
disease  is  more  rapid  and  not  accompanied  by  periodic  attacks  of  fever 
and  pain.  In  malignant  disease  pressing  on  the  ducts,  as  in  carcinoma 
of  the  head  of  the  pancreas,  the  jaundice  is  deep  and  the  motions  are 
devoid  of  bile.  The  gall-bladder  is  generally  distended  and  the  tem- 
perature is  not  raised. 

From  chronic  cholangitis  due  to  infection  of  the  ducts  with  micro- 
organisms of  no  great  virulence  the  diagnosis  is  difficult,  but  the  pain 
and  intermittent  fever  are  more  severe  and  prominent  in  the  cases  com- 
plicated by  cholelithiasis. 

Hypertrophic  biliary  cirrhosis  in  rare  instances  comes  on  acutely  and 
might  imitate  a  calculus  passing  into  the  duct;  the  periodic  attacks  of 
fever,  pain,  and  increased  jaundice  are  much  less  severe  in  bihary  cirrho- 
sis; further,  splenic  enlargement  is  a  prominent  feature  in  biliary  cirrhosis, 
and  is  practically  absent  in  the  intervals  between  the  attacks  in  inter- 
mittent hepatic  fever. 

The  prognosis  is  rather  bad,  as  suppuration  may  supervene,  as  already 
pointed  out,  in  the  bile-ducts,  the  liver  itself,  or  in  the  neighbourhood. 
The  outlook  is  much  better  if  the  cases  are  submitted  to  iaperation  and 
the  stone  or  stones  removed  from  the  common  bile-duct.  In  10  cases 
tabulated  by  Osier,*  spontaneous  recovery  occurred  in  five. 

Treatment. — In  cases  where  the  attacks  occur  at  considerable  intervals 
medical  treatment  should  be  tried.  The  patient  should  take  a  light, 
digestible  diet,  avoid  stimulants,  and  keep  the  bowels  open.  The  dieting 
of  cases  with  gastric  pain  is  often  very  disajjj^ointing,  a  result  which  can 
hardly  be  wondered  at  since  the  pain  and  gastralgia  depend  in  some 
degree  on  the  adhesions  around  the  pylorus.  Carlsbad  water  at  home, 
or  better  a  cure  there  or  at  Neuenahr,  Kissingen,  Salzschlirf,  Homburg, 
is  advisable,  and  it  is  well  to  increase  the  flow  of  bile  over  the  calculus 

*  Osier:  Lancet,  1897,  vol.  i,  p.  1319. 

48 


754  DISEASES    OF   THE    BILE-DUCTS. 

in  the  hope  of  dissolving  its  surface  sufficiently  to  allow  it  to  sHp  into 
the  duodenum. 

For  the  pain  hot  applications,  fomentations,  or  poultices  may  be 
tried;  but  in  many  cases  morphia  is  required  and  there  is  the  danger 
that  the  habit  may  be  acquired.  Antipyrin  and  phenacetin  may  be 
tried,  or  a  mixture  containing  belladonna  and  spiritus  chloroformi  may 
be  given  to  allay  spasm.  TurjDentine  and  ether  have  been  given  vrith 
the  same  object.  With  the  exception  of  morpliia,  these  measures  often 
fail.  Massage  is  unsafe,  and  olive  oil  by  the  mouth  of  no  real  good  so 
far  as  removal  or  solution  of  the  calculus  is  concerned.  If  no  improve- 
ment follows  medical  treatment,  operative  measures  should  be  advised 
before  the  patient  loses  too  much  flesh  or  gets  deeply  jaundiced;  as  these 
conditions  render  the  operative  interference  dangerous. 

Operative  interference  should  not  be  delayed  when  it  becomes  clear 
that  medical  treatment  is  imsuccessful,  as  there  is  always  the  possible 
danger  that  suppurative  cholangitis  may  supervene.  In  addition  long- 
continued  inflammation  of  the  ducts  may  eventually  lead  to  fibrotic  and 
atrophic  changes  in  the  hver,  while  the  irritation  of  other  calcuh  in  the 
gall-bladder  may  lead  to  primary  carcinoma  there.  In  cases  of  long 
standing  dense  adhesions  form  aroimd  the  gall-bladder  and  ducts  and 
make  operative  interference  both  more  difficult  and  more  dangerous. 

The  most  radical  and  effective  treatment  is  laparotomy  and  removal 
of  the  stone  from  the  common  duct.  It  is  probable  that  in  most  cases 
removal  of  the  gall-bladder,  unless  it  is  entirely  shrivelled  up,  should  also 
be  carried  out,  so  as  to  avoid  any  possibility  of  recurrence.  The  foIlo"uing 
case  illustrates  the  features  of  the  disease  and  its  successful  surgical 
treatment : 

A  lady  aged  fifty-seven  had  an  attack  of  biliary  colic  with  fever  in  Maj%  1902, 
from  which  she  recovered  and  went  in  the  following  month  to  Buxton,  where  the 
pain  suddenly  returned  while  vmdergoing  abdominal  massage.  In  the  middle  of 
September  she  had  another  attack  of  jaundice,  pain,  and  fever  lasting  three  weeks; 
after  a  short  interv-al  of  fair  health  pain  recurred  and  was  more  or  less  constant 
from  the  end  of  November  until  January,  1903,  when  she  was  seen  in  consultation 
with  Dr.  Swan  and  operation  advised  for  a  gall-stone  in  the  common  duct.  The  liver 
was  not  enlarged;  the  gall-bladder  could  not  be  felt.  There  was  tenderness  over 
the  common  bile-duct,  and  pain  in  the  epigastriimi.  There  was  a  slight  degree 
of  jaundice  and  the  temperature  oscillated.  The  pain  necessitated  morphia  injections. 
The  history  showed  that  twenty-five  years  ago,  after  the  birth  of  a  child,  she  had 
had  an  attack  of  severe  pain  like  gaU-stone  colic.  On  January  17th  Mr.  Mayo 
Robson  operated  and  removed  a  gaU-stone  from  the  lower  end  of  the  common 
bile-duct  by  pressing  it  into  the  duodenum  and  incising  the  intestine.  The  gall- 
bladder was  shrivelled  up  and  united  by  very  old  and  firm  adhesions  to  the  duo- 
denum and  colon.  Its  mucous  membrane  was  removed  according  to  Mayo's 
method.  The  common  bile-duct  was  much  dilated.  The  operation  was  rendered 
very  difficult  bj^  the  extensive  adhesions.  There  was  a  rudimentary  Riedel's  lobe. 
The  patient  recovered  without  a  bad  sjmiptom. 

Probably  in  some  cases  operation  short  of  this  may  do  good ;  mere 
manipulation  of  the  ducts  may  drive  a  softened  stone  into  the  duodenum 
and  effectually  remove  it. 

A  woman  aged  fifty-four  Avho  had  had  about  20  attacks  within  the  year  came 
under  my  care  in  1896  in  St.  George's  Hospital.  During  an  attack  the  temperature 
went  up  to  104°,  jaundice  became  more  marked,  bile  appeared  in  the  urine,  and 


CHOLELITHIASIS.  755 

there  was  marked  tenderness  over  the  common  bile-duct.  Mr.  Sheild  explored 
the  abdomen,  broke  down  adhesions  aromid  the  common  bile-duct,  which  felt 
thickened,  but  did  not  open  the  duct,  as  no  calculi  were  palpable.  After  this  the 
patient  remained  free  from  any  further  attacks. 

Extension  of  Inflammation  and  Infection  to  the  Pancreas. — Gall-stones 
in  the  common  duct,  especially  when  in  their  usual  situation,  viz.,  the 
lower  end,  readily  give  rise  to  catarrhal  inflammation  of  Wirsung's  duct 
of  the  pancreas.  In  this  manner  acute  or  chronic  pancreatitis  maj^  be 
set  up. 

Thirty-two  cases  of  acute  pancreatic  lesions,  such  as  haemorrhage,  suppiiration, 
acute  pancreatitis,  have  been  collected  by  Opie  *  in  which  gall-stones  were  present. 
He  concludes  that  with  few  exceptions  the  gall-stones  caused  the  pancreatic  dis- 
ease. I  had  previously  called  attention,  though  on  a  much  smaller  number  of  cases, 
to  the  production  of  pancreatitis  by  cholelithiasis. f 

The  production  of  suppuration  in  the  pancreas  by  calculi  in  the 
common  bile-duct  was  described  in  1883  by  Norman  Moore. J  The  fol- 
lowing case  illustrates  this  point: 

A  man  aged  sixty-three,  who  had  had  an  attack  of  jaundice  and  abdominal 
pain  five  years  before,  was  seized  with  abdominal  pain  a  week  before  his  death. 
He  was  admitted  to  St.  George's  Hospital  in  a  jaundiced,  drowsy,  and  exhausted 
condition.  His  temperature  was  101°,  there  was  tenderness  in  the  upper  part  of 
the  abdomen,  and  he  sweated  profusely,  without  any  shivering.  He  died  from 
exhaustion  within  twenty-four  hours  of  admission.  At  the  autopsy  there  were 
three  large  crumbling  calculi  in  the  common  bile-duct,  which  was  dilated  to  the 
size  of  one's  thumb  and  had  a  granular,  thickened  condition  of  its  mucous  mem- 
brane. The  cystic  duct  was  dilated,  there  was  an  ulcer  in  the  fimdus  of  the  gall- 
bladder, which  contained  bile-stained  mucopus  but  no  calculi.  The  intra-hepatic 
ducts  were  slightly  dilated  and  showed  pericholangitic  fibrosis,  but  there  was  no 
suppuration.  The  pancreatic  duct  contained  dirty  jdus  and  there  were  spots  of 
suppuration  in  the  pancreas. 

As  a  result  of  pancreatitis,  infection  of  the  peritoneum  of  the  lesser 
sac  of  the  peritoneum — ^the  omental  bursa  of  American  writers — ^may 
occur.  The  inflammation  of  the  peritoneum  in  the  lesser  sac  leads  to 
closure  of  the  foramen  of  Winslow  and  to  an  inflammatory  exudate. 
Cholelithiasis  may  thus  set  up  a  peripancreatic  effusion  in  the  lesser  sac, 
the  contents  being  either  serous  or  purulent.  Many  so-called  pancreatic 
cysts  are  probably  of  tliis  nature. 

The  following  case  is  of  interest  in  this  connexion: 

A  man  aged  twenty-five  years  was  seized  two  weeks  before  his  death  with  vomit- 
ing, which  persisted  until  his  death,  and  pain,  never  very  acute,  in  the  lower  part 
of  the  abdomen.  He  had  never  had  jaundice,  a  blow  on  the  abdomen,  or  any  serious 
illness.  An  indistinct  tumor  was  felt  in  the  left  hypochondrium,  with  the  stomacli 
resonance  above  it.  At  the  autopsy  there  were  59  small  calculi  in  the  gall-bladder 
and  one  in  the  cystic  duct,  which  was  very  long  and  joined  the  common  hepatic 
duct,  I  inch  above  the  biliary  papilla.  The  cystic  duct  was  inflamed,  and  it  seemed 
possible  that  inflammation  had  spread  froin  it  to  the  pancreas.  There  was  a  localised 
effusion  distending  the  lesser  sac  of  tlie  peritoneum  into  a  cyst  as  large  as  one's 
head,  the  foramen  of  Winslow  being  closed.  The  fluid  contained  a  fat-splitting 
ferment.  The  pancreas  showed  acute  pancreatitis  under  the  microscope.  There 
were  scattered  islands  of  fat  necrosis  all  around  the  cyst.     This  peripancreatic 

*  Opie:  American  Joum.  of  the  Medical  Sciences,  vol.  cxxi,  p.  27,  Jan.,  1901. 
t  Rolleston:  Trans.  Path.  Soc,  vol.  xlix,  p.  149,  1898. 
X  Moore,  N. :  Trans.  Path.  Soc,  vol.  xxxiii,  p.  186. 


756  DISEASES    OF   THE    BILE-DUCTS. 

cyst  was  evidently  secondary,  just  as  pleurisy  is  to  pneumonia,  to  acute  inflamma- 
tion of  the  pancreas,  which  in  its  turn  was  associated  with  cholelithiasis.* 

More  or  less  chronic  pancreatitis  from  extension  of  inflammation  from 
the  common  bile-duct  via  Wirsimg's  duct  is  probably  a  frequent  accom- 
paniment of  calculi  in  the  lower  part  of  the  common  bile-duct.  The  head 
of  the  pancreas  may  thus  become  so  hard  that  when  felt  during  the  course 
of  an  operation  for  gall-stones  the  surgeon  may  assume  that  there  is 
malignant  disease  of  the  head  of  the  pancreas  and  abandon  the  operation. 
The  inflammatory  changes  thus  started  may  progress,  even  though  the 
calculi  which  caused  it  have  passed  into  the  duodenum.  (Mayo  Robson^f 
Barhng.J)  Subsequently  the  enlarged  head  of  the  gland  undergoes 
atrophy  from  cicatricial  contraction  of  the  newly  formed  fibrous  tissue, 
and  imitates  a  hard,  slowly  growing  carcinoma  of  the  head  of  the  pan- 
creas by  compressing  the  common  bile-duct  and  producing  chronic 
jaundice. 

The  treatment  of  such  cases  is  to  establish  free  drainage  for  the  gall- 
bladder; if  this  is  kept  up  for  some  time,  the  condition  of  the  pancreas 
will  improve.  It  seems  safer  and  better  to  drain  the  gall-bladder  ex- 
ternally and  not  to  do  cholecystenterostomy. 

Inflammatory  Effects  of  a  Calculus  in  the  Ampulla  of  Voter. — A  calculus 
in  the  diverticulum  Vateri  often  obstructs  the  main  pancreatic  duct,  but 
as  there  is  usually  a  communication  in  the  pancreas  between  the  main 
duct  and  the  accessory  or  Santorini's  duct,  the  pancreatic  secretion  is 
not  prevented  from  entering  the  duodenum.  But  as  the  result  of  con- 
tinued chronic  pancreatitis,  cicatricial  contraction  may  result  and  com- 
press both  the  ducts,  giving  rise  to  retention  of  the  secretion,  dilatation 
of  the  ducts,  and  sometimes  to  the  formation  of  cysts  in  the  gland.  The 
chronic  interstitial  pancreatitis  which  results  from  obstruction  of  the 
ducts  very  seldom  destroys  the  islands  of  Langerhans,  and  glycosuria 
and  diabetes  therefore  hardly  ever  result.     (Opie.  §) 

Pi/ZepAZe&iYts.— Inflammation  of  the  bile-ducts  may  give  rise  to  sup- 
purative pylephlebitis.  The  inflammation  may  spread  to  the  main  trunk 
of  the  portal  vein  or  to  its  intra-hepatic  branches.  In  some  instances  the 
infection  may  spread  to  the  portal  vein  by  the  lymphatics  or  by  the  small 
veins  of  the  bile-ducts  which  open  into  the  branches  of  the  portal  vein. 
This  subject  is  fully  discussed  u'nder  the  causation  of  pylephlebitis. 
(Ftrfep.  71.) 

BILIARY  FISTULA. 

Abnormal  passages  between  the  gaU-bladder  and  bile-ducts  and  other 
viscera  or  the  outside  of  the  body  are  in  the  great  majority  of  instances 
due  to  gall-stones  and  inflammatory  processes  accompanying  them. 

External  fistulas  may  result  from  other  causes,  such  as  operations  on 
the  gall-bladder  and  ducts,  or  on  hepatic  abscesses  and  hydatid  cysts, 
while  an  internal   fistula  between  the  gall-bladder  and  the  colon  may 

*  RoUeston:  Trans.  Path.  Soc,  vol.  xlix,  p.  145. 
t  Mavo  Robson :  Lancet,  1900,  vol.  ii,  p.  236. 
%  Barling:,  G. :  Brit.  Med.  Jour.,  1900,  vol.  ii,  p.  1766. 
§  Opie,  E.  L.:  Jour.  Exper.  Med.,  vol.  v,  p.  397,  1901. 


CHOLELITHIASIS.  757 

depend  on  malignant  disease.  It  is  worthy  of  note  that  while  gall-stones 
most  commonly  give  rise  to  a  fistula  between  the  gall-bladder  and  duo- 
denum, malignant  disease  of  the  gall-bladder  is  much  more  prone  to  set 
up  a  fistula  between  the  colon  and  the  gall-bladder  than  between  the 
duodenum  and  the  gall-bladder.  The  following  remarks  on  biliary  fistulas 
refer  to  those  associated  with  calculi. 

External  or  Cutaneous  Biliary  Fistulas. — Suppuration  in  the  gall- 
bladder may  eventually  discharge  through  the  abdominal  walls.  This 
is  the  commonest  recognised  form  of  biliary  fistula,  probably  because  its 
presence  is  so  manifest  that  it  cannot  be  overlooked. 

Naunyn  *  collected  184  examples  out  of  a  total  of  384  biliary  fistulse  due  to 
cholelithiasis,  the  next  most  frequent  form  of  fistula  being  that  between  the  gall- 
bladder and  duodenum  (108). 

The  communication  between  the  gall-bladder  and  the  opening  in  the 
abdominal  wall  is  often  by  a  long  fistulous  tract  which  may  be  tortuous 
and  difficult  to  follow.  The  fistula  may  be  the  opening  of  an  abscess 
formed  in  the  neighbourhood  of  the  gall-bladder  or  may  lead  directly 
into  the  cavity  of  the  suppurating  gall-bladder. 

External  biliary  fistulse  usually  open  near  the  umbihcus;  this  depends 
partly  on  the  vicinity  of  the  gall-bladder  and  partly  on  the  fact  that 
the  falciform  ligament  seems  to  direct  the  suppurative  process  in  this 
direction.  Not  uncommonly  the  opening  is  in  the  right  hypochon- 
drium.  In  rare  instances  there  may  be  a  discharging  abscess  in  the  right 
iliac  fossa  which  imitates  an  appendicular  abscess.  The  following  case 
illustrates  this  point  : 

Gibson  j  explored  a  spontaneous  sinus  in  the  right  iliac  fossa,  |  inch  below 
and  2^  inches  internal  to  the  anterior-superior  spine  of  the  ilium,  and  removed  52 
calculi,  after  which  the  fistula  healed. 

In  very  rare  instances  a  biliary  fistula  may  be  established  in  the  thigh. 
Forges  {  has  recorded  the  discharge  of  gall-stones  from  a  fistula  in  this 
situation. 

Fistulas  Between  the  Biliary  and  Gastro-intestinal  Tracts. — In 
many  instances  where  this  condition  is  found  after  death  there  have  been 
no  clinical  manifestations  of  the  process,  such  as  intestinal  obstruction 
from  a  large  gall-stone,  or  the  passage  of  a  calculus  in  the  faeces,  and 
its  existence  has  not  been  suspected  during  life.  A  fistula  may  be  sus- 
pected when  a  large  calculus  is  passed  by  the  bowel,  but  this  often  occurs 
when  no  absolute  proof  of  a  fistula  is  forthcoming. 

In  111  cases  where  a  large  calculus,  viz.,  one  the  size  of  a  nut,  was  passed  by 
the  bowel,  the  method  by  which  it  gained  entrance  into  the  bowels  was  quite  un- 
known in  69.     (Le  Ro5\§) 

Duodenal  fistidce  are  the  most  frequent.  In  a  list  of  384  biliary  fistulas 
due  to  cholelithiasis  the  duodenum  was  involved  in  108.     (Naunyn.  ||) 

*  Naunvn :  Cholelithiasis,  p.  143. 

t  Gibson,  ,J.  H. :  Philadelphia  Med.  News,  .Tan.  19,  1901. 

i  Forges:  Wiener  khn.  Wochen.,  1900,  S.  597. 

§  Le  Roy,  C. :  These  Paris,  No.  474,  1902. 

II  Naunyn:  On  Cholelithiasis,  p.  143.     Translation  New  Sydenham  Soc. 


758  DISEASES    OF    THE    BILE-DUCTS. 

As  a  rule,  there  is  a  communication  between  the  fundus  of  the  gaU- 
bladder  and  the  duodenum,  but  in  a  certain  number  of  cases  a  calculus 
ulcerates  through  the  walls  of  the  conmion  bile-duct  into  the  first  part 
of  the  duodenum,  above  the  biliarj^  papilla. 

Cholecystoduodenal  Fistulce. — This  was  the  form  present  in  9-3  out  of 
the  108  cases  mentioned  above.  The  fundus  of  the  gall-bladder  com- 
municates with  the  first  part  of  the  duodenum.  The  process  of  ulceration 
may  give  rise  to.  severe  gastro-intestinal  haemorrhage.  Such  cases  may 
very  easily  be  misinterpreted  and  regarded  as  examples. of  simple  gastric 
or  duodenal  ulceration.  In  some  instances  cicatrisation  of  the  fistulous 
communication  may  lead  to  stricture  of  the  duodenum  and  to  symptoms 
of  pyloric  obstruction.  Dense  adhesions  between  the  gall-bladder  and 
the  duodenum  may  imitate  malignant  disease  even  when  the  parts  are 
exposed  in  the  course  of  an  exploratory  laparotomy.  The  mucous 
membrane  around  the  fistulous  opening  mto  the  duodenum  may  become 
extensively  ulcerated  and  set  up  persistent  vomiting;  this  may  occur 
without  any  cicatricial  stenosis  of  the  duodenum  or  pylorus. 

A  calculus  may  ulcerate  out  of  the  gall-bladder,  but  fail  to  pass  into 
the  duodenum,  and  may  set  up  so  much  cicatricial  contraction  around  the 
duodenum  that  obstrviction  results.  A  case  of  this  kind  is  reported  by 
Labadie-Lagrave  and  Magdelaine.*  Occasionally  an  abscess  formed 
around  a  gall-stone  which  is  ulcerating  out  of  the  gall-bladder  or  com- 
mon bile-duct  discharges  in  several  directions  and  a  complicated  fistula 
results,  vnth  openings  into  the  duodenum,  stomach,  and  gall-bladder. 

A  woman  aged. fifty-four  years  died  in  St.  George's  Hospital  after  removal  of 
the  right  big  toe.  She  had  diabetes  of  pancreatic  origin  and  was  jaundiced.  The 
gall-bladder  was  shrivelled  up  on  a  gall-stone,  and  commimicated  by  a  fistula  with 
the  first  part  of  the  duodenum.  There  was  a  soft,  crumbling  calculus  the  size  of 
a  pigeon's  egg  in  the  lower  part  of  the  common  bile-duct.  Near  this  calciilus,  but 
not  in  actual  continuity,  there  was  an  abscess,  partly  in  the  head  of  the  pancreas 
and  partly  in  the  lesser  omentum  and  left  lobe  of  the  liver.  This  abscess  communi- 
cated by  two  small  openings  with  the  duodenum,  and  by  two  more  fistulse  with  the 
stomach  on  its  posterior  wall.     The  pancreas  was  markedly  fibrotic. 

Choledochoduodenal  Fistula. — A  communication  between  the  common 
bile-duct  and  the  first  part  of  the  duodenum  is  probably  commoner  than 
is  beheved.  Naunyn  points  out  that  in  some  cases  where  the  calculus  is 
seen  projecting  into  the  duodenum  the  orifice  is  not  the  biliary  papilla, 
as  is  too  often  assumed,  merely  because  there  is  an  opening  there,  but 
a  fistulous  passage.  Naunyn  thinks  it  not  improbable  that  in  reahty 
fistulge  between  the  duodenum  and  the  common  bile-duct  are  as  common 
as  those  between  the  duodenum  and  gall-bladder.  But  of  his  108  col- 
lected cases  of  duodenal  fistulas  15  were  between  the  common  duct  and 
the  duodenum,  and  the  remaining  93  between  the  gall-bladder  and  the 
duodenum. 

Biliary  Gastric  Fistulos. — ^Although  duodenal  fistulae  are  common, 
communications  between  the  stomach  and  biliary  tract  are  ver}'  rare, 
and  when  they  do  occur,  are  in  some  instances  due  to  an  abscess,  arising 
in  connexion  with  the  gall-bladder  or  ducts,  opening  into  the  stomach 

*  Labadie-Lagrave  and  Magdelaine :  Joum.  des  Praticiens,  June  25,  1890. 


CHOLELITHIASIS.  759 

and  also  into  the  duodenum  or  colon,  or  both,  as  in  a  case  reported  by 
Voelcker.* 

XaunjTi  t  quotes  12  gastrobiliar}^  fistulae,  8  of  which  were  between  the  gall- 
bladder and  4  between  the  ducts  and  the  stomach.  In  a  recent  case  of  NichoUs'  J 
the  patient  was  a  woman  aged  eiglity-five.  In  a  comphcated  case  reported  by 
Lejonne  and  Milanoff  §  there  was  a  commimication  between  the  stomach  and  the 
gaU-bladder,  and  a  second  fistula  between  the  common  bile-duct,  which  contained  a 
calculus,  and  the  first  part  of  the  duodenum.  The  gaU-bladder  showed  primary 
carcinoma,  but  the  fistulte  probably  depended  on  cholelithiasis.  The  patient  was 
a  woman  aged  eighty-seven  years.  Cholecystogastric  fistulae  due  to  gaU-stones 
have  also  been  recorded  by  Ochsner  1|  and  Snively.** 

A  cholecysto-gastric  fistula  may  be  brought  to  light  in  separating  dense 
adhesions  during  an  operation  in  cases  where  no  symptoms  of  the  fistula 
existed. 

In  a  woman  aged  sixty  who  had  had  attacks  of  gall-stone  pain  for  fifteen  months, 
lately  very  frequently,  followed  by  slight  jaundice  and  constant  dyspepsia  with 
frequent  vomiting  and  loss  of  flesh.  Mayo  Robson  ft  found  the  stomach  and  gall- 
bladder firmly  adherent.  On  separating  the  adhesions  a  fistula  between  the  gall- 
bladder and  stomach  was  found.  The  gaU-bladder  contained  calculi;  the  patient 
made  a  good  recovery. 

Vomiting  of  gall-stones  has  been  thought  to  be  good  evidence  of  a 
gastro-biliary  fistula,  but  there  seems  to  be  no  convincing  reason  for  this 
belief,  for  if  bile  can  be  regurgitated  into  the  stomach,  as  it  commonly 
is  in  vomiting,  small  calculi  should  be  so  too.  But  when,  as  extremely 
rarely  happens,  a  large  calculus  is  vomited,  the  probabilities  are  that  a 
gastro-biliary  fistula  exists. 

Thompson  tj  recorded  the  case  of  a  woman  aged  ninety-four  who  vomited  a 
calculus  the  size  of  a  nutmeg.  Jeaffreson  §§  quoted  a  case  where  a  large  calculus 
was  vomited  and  after  death  the  stomach  was  found  adherent  to  the  gaU-bladder. 
In  12  cases  in  which  gall-stones  were  vomited  there  was  only  one  in  which  a  gastro- 
cholecystic  fistula  was  shown  to  exist  (Murchison  ||  ||).  Mayo  Robson,***  Nicholls,ttt 
Kellett  Smith  and  Bailey,tJJ  Crooke,§§§  and  others  have  reported  more  recent 
cases  in  which  gaU-stones  were  vomited. 

Cholecystocolic  Fistulce. — A  fistulous  communication  between  the  bili- 
ary tract  and  the  colon  is  less  frequent  than  one  involving  the  duodenum 
as  the  result  of  cholelithiasis. 

Naunyn  1|  ||  ||  gives  49  examples  of  fistulsc  between  the  gaU-bladder  and  the  colon 
and  one  between  the  common  bile-duct  and  the  colon. 

*  Voelcker:  Trans.  Path.  Sec,  vol.  xlvi,  p.  78,  1895. 

t  Naunyn:  On  Cholelithiasis,  p.  143.     Transl.  New  Sydenham  Soc,  1892. 
%  NichoUs:  Montreal  Med.  .Joum.,  Nov.,  1898. 
§  Lejonne  et  Milanoff:  Bull.  Soc.  Anat.,  1900,  p.  33. 
II  Ochsner:  Annals  of  Surgery,  vol.  xxxv,  p.  712,  1902. 
**  Snively:  Joum.  American  Medical  Association,  April  11,  1903,  p.  963. 
tt  Mayo  Robson:  Brit.  Med.  Joum.,  1903,  vol.  i,  p.  185. 
X%  Thompson:  Trans.  Path.  Soc,  vol.  xii,  p.  129. 
§§  Jeaffreson:  Brit.  Med.  Joum.,  May  30,  1868,  vol.  i,  p.  531. 
II II  Murchison :  Diseases  of  Liver,  1885,  p.  548. 
***  Mayo  Robson:  Lancet,  1897,  vol.  i,  p.  1526. 
ttt  Nicholls,  A.  G.:  Montreal  Med.  Joum.,  Nov.,  1898,  p.  829. 
XXt  Kellett  Smith  and  Bailey:  Liverpool  Medico-Chirurg.  Joum.,  p.  74,  1902. 
§§§  Crooke:  Ibid.  ||||||  Naunyn:  On  Cholelithiasis,  p.  143. 


760  DISEASES    OF    THE    BILE-DUCTS. 

As  an  indirect  result  of  gall-stones,  viz.,  from  carcinoma  of  the  gall- 
bladder, a  fistulous  opening  into  the  colon  may  result.  In  nine  cases  of 
cholecystocolic  fistulse  mentioned  by  ^Murcliison  6  were  associated  with 
carcinoma  of  the  gall-bladder. 

As  a  rare  sequela  of  a  cholecj^stocolic  fistula  fseces  may  pass  into 
the  gall-bladder  and  set  up  suppuration  in  the  liver. 

This  is  exemplified  in  the  following  case,  under  the  care  of  my  colleague,  Dr- 
Ewart,  ra  St.  George's  Hospital.  A  woman  aged  thirty-one  years  had  had  jaimdice, 
without  anj'  definite  biliary  colic,  for  one  and  one-half  years  before  her  death; 
the  jaundice  varied  from  time  to  time,  but  became  very  dark  before  death.  She 
was  thought  to  have  malignant  disease,  and  an  exploratory  operation  was  performed, 
but  it  was  impossible  to  do  anj-thing.  At  the  autopsy  the  gaU-bladder  had  ulcerated 
into  the  colon,  and  the  parts  around  were  firmly  matted  together  by  dense  adhe- 
sions. There  were  gaU-stones  and  fseces  in  the  gaU-biadder,  the  right  hepatic 
duct  contained  fsecal  material,  and  there  were  multiple  abscesses  in  the  liver.  (Vide 
coloured  plate  7.) 

Fistulce  Between  the  Biliary  Tract  and  the  Small  Intestine. — ^A  direct 
communication  between  the  gall-bladder  or  ducts  and  any  part  of  the 
small  intestine  except  the  duodenum  is  most  exceptional,  and  hardly  any 
cases  are  on  record.  The  small  intestine  is,  from  its  position,  less  Hkely 
to  become  adherent  to  the  gall-bladder,  and  its  free  mobility  further 
protects  it. 

Naunjm  *  refers  to  two  cases,  one  in  which  the  jejunum.  (Gaston),  and  the 
other  in  which  the  Uemn,  commimiicated  with  the  gaU-bladder. 

Results  of  the  Passage  of  Calculi  into  the  Intestines. — ^A  calculus  may 
obstruct  the  lumen  of  the  bowel  and  mechanically  give  rise  to  intestinal 
obstruction.  This  condition  is  described  on  page  742.  It  may  set  up 
inflammation  of  the  wall  of  the  bowel,  and  may  thus  give  rise  to  the 
formation  of  a  diverticulum  in  which  the  calculus  is  contained.  The 
waU  of  the  bowel  may  be  so  damaged  that  it  undergoes  gangrene.  In 
most  exceptional  instances  a  smaU  gall-stone  has  been  described  as  passing 
into  the  vermiform  appendix.  -As  the  result  of  ulceration  between  the 
gall-bladder  and  duodenum  or  colon  cicatricial  contraction  and  stricture 
of  the  bowel  may  occur.  Cicatrisation  of  a  fistula  is,  however,  a  rare 
event  (Naunyn  f)  or  is  rarety  recognised  at  the  autops5^ 

Bronchobiliary  Fistulas. — In  35  cases  collected  by  Graham  %  of 
this  condition,  including  24  of  Coun^oisier's,  19  were  due  to  cholehthiasis, 
11  to  hj^datids,  2  to  ascarides;  in  2  the  cause  was  not  forthcoming,  and 
in  one  it  was  referred  to  traumatism.  As  cholelithiasis  is  far  the  most 
frequent  cause  of  bronchobiliary  fistulae,  a  general  account  of  the  condi- 
tion wdll  be  given  here.  GaU-stones  maj^  give  rise  to  a  bronchobilian,' 
fistula  in  several  waj^s : 

(a)  Gall-stones  in  the  common  duct  set  up  infecti^■e  cholangitis  and 
an  abscess  in  the  liver  which  perforates  the  diaphragm,  and  after  setting 
up  adhesions  between  the  diaphragm  and  the  base  of  the  lung,  ruptures 
into  the  latter;  or  the  liver  abscess  ma}^  perforate  first  into  the  pleura 
and  subsequently  into  the  lung. 

*  Naunyn :  On  Cholelithiasis,  p.  14S.  t  Naunjm :  On  Cholelithiasis,  p.  150. 

%  Graham.  J.  E. :  Trans.  Assoc.  American  Physicians,  vol.  xii,  p.  247. 


Plate  7. 


Section  op  Liver  Showing  Abscess  duk  to  Infection  of  thk  Bile-ducts   in  a  Case  of 
Oholecystocolic  Fistula  from  CiiOLicLiTiriAsis. 


CHOLELITHIASIS.  761 

(&)  Intra-hepatic  calculi  may  give  rise  to  a  similar  sequence  of  events. 

(c)  A  calculus  msiy  ulcerate  out  of  the  gall-bladder  or  ducts,  and  set 
up  an  intra-peritoneal  abscess  which  perforates  the  diaphragm  and 
either  opens  into  the  lung  direct  or  first  into  the  pleura  and  subsequently 
into  the  lung. 

(d)  A  suppurating  gall-bladder  associated  with  cholelithiasis  msiy  set 
up  a  subphrenic  abscess  which  perforates  the  diaphragm  and  eventually 
opens  into  the  lung. 

(e)  In  very  rare  cases,  as  in  Mandard's,*  the  gall-bladder  may  per- 
forate directlj'  through  the  diaphragm  into  the  lung. 

Sym'ptoms. — Irritating  cough  may  be  accompanied  by  orthopnoea 
and  the  expectoration  of  large  quantities  of  bile,  sometimes  almost  pure. 
Graham  speaks  of  expectoration  of  as  much  as  700  c.c.  of  bile  in  the 
twenty-four  hours.  In  a  few  cases  the  patients  have  coughed  up  biliary 
calculi. 

Signs. — There  may  be  duhiess  in  the  right  inframammary  and  axillary 
regions,  extending  back  for  a  variable  extent,  the  breath-sounds  over 
this  area  being  coarse  and  accompanied  by  rales.  On  the  other  hand, 
there  may  be  no  dulness  on  percussion,  and  merely  the  signs  of  broncliitis. 
When  the  discharge  of  bile  is  free,  there  may  be  no  obstructive  jaundice 
and  no  bile  in  the  urine,  as  in  Smith  and  Rigby's  f  case. 

The  diagnosis  depends  on  the  expectoration  of  bile  in  considerable 
quantities.  In  jaundiced  patients  with  bronchitis  or  pneumonia  the 
sputum,  like  other  excretions,  is  bile-stained,  but  the  amount  of  bile  is 
much  less.  Fragments  of  liver  tissue  may  also  be  found  in  the  sputum. 
When  the  existence  of  a  bronchobiliary  fistula  is  determined,  its  cause 
is  sometimes  difficult  to  make  out;  other  signs  of  cholelithiasis,  or  in 
rare  cases  the  expectoration  of  biliary  calculi,  would  settle  the  diagnosis, 
but  in  many  cases  that  recover  or  are  not  examined  postmortem  the  cause 
remains  doubtful. 

Prognosis. — Recovery  may  occur  spontaneously  or  after  operative 
interference  on  the  biliary  apparatus.  Wlien  spontaneous  recover}- 
occurs,  there  is,  generally  speaking,  no  liability  to  return  of  the  fistula; 
a  relapse  has,  however,  been  known  to  occur. 

In  a  case  reported  by  J.  E.  Graham  a  patient,  after  expectorating  bile,  "was 
free  for  ten  years  from  any  symptoms;  at  the  end  of  this  time  tliey  recurred  and 
proved  fatal. 

Treatment. — If  the  condition  does  not  tend  to  pass  away  and  undergo 
spontaneous  cure,  laparotomy,  with  the  view  of  relieving  the  obstniction 
to  the  passage  of  bile  into  the  intestine,  should  be  undertaken;  when 
gall-stones  are  removed  from  the  common  duct,  the  fistulous  channel 
into  the  lung  should  heal  up. 

Other  and  Rare  Forms  of  Fistulas. — Fistula;  Between  the  Bile-ducts 
Themselves. — Naunyn,J  who  quotes  8  cases,  adds  that  they  are  merely  of 
anatomical  interest. 

*  Mandard:  Th^se  Paris,  1854.     Quoted  by  Naunyn. 

t  Smith  and  Riffby:  Brit.  Med.  Journ.,  1903,  vol.  ii,  p.  313. 

i  Naunyn:  On  Cholelithiasis,  p.  149.     Translation  New  Sydenhani  Soc. 


762  DISEASES    OF   THE    BILE-DUCTS. 

Fistula  Between  Gall-bladder  and  the  Portal  Vein. — This  is  a  very  rare 
condition.  Naimyn  quotes  3  cases,  but  does  not  admit  Bristowe's  * 
case.  According  to  tradition,  there  were  three  calcuH  in  the  portal  vein 
of  Ignatius  Loyola,  but  Galliard  f  considers  this  doubtful,  and  it  is 
probable  that  the  calculi  were  really  in  the  common  bile-duct,  which  was 
mistaken  for  the  portal  vein.  Ulceration  of  a  calculus  into  the  portal 
vein  would,  of  course,  tend  to  set  up  suppurative  pylephlebitis. 

Ulceration  of  the  Hepatic  Artery. — A  communication  between  the  gall- 
bladder or  the  bile-ducts,  on  the  one  hand,  and  the  hepatic  artery  or  its 
branches,  on  the  other  hand,  leads  to  profuse  or  even  fatal  haemorrhage 
which  runs  down  the  ducts  into  the  alimentary  canal.  Most  of  these 
cases  have  been  regarded  as  examples  of  aneurysms  of  the  hepatic  artery 
or  its  branches,  rupturing  into  the  bihary  tract.  But  it  must  be  remem- 
bered that  ulceration  of  the  gall-bladder  or  bile-ducts  in  cholelithiasis 
may  erode  the  walls  of  the  hepatic  artery  or  its  branches  and  first  give 
rise  to  an  aneurysmal  bulging  and  subsequently  to  rupture  of  the  vessel 
into  the  biliary  tract. 

According  to  Naunyn,±  Lebert's  case  of  an  hepatic  aneurysm  rupturing  into 
the  gall-bladder  was  probably  of  this  nature,  while  M.  B.  Schmidt  recorded  a  clear 
case  of  ulceration  of  a  bile-duct,  due  to  a  calculus,  producing  an  hepatic  aneurysm. 

Fistulce  Between  the  Gall-bladder  and  the  Kidneys. — ^This  form  of 
fistula  is  very  rare.  Courvoisier§  quotes  five  cases.  The  fistulous 
passage  is  usually  between  the  gall-bladder  and  the  pelvis  of  the  right 
kidney.  Eisner  |1  has  reported  another  case  which  showed  a  gall-stone 
in  the  pelvis  of  the  right  kidney. 

Fistulce  Between  the  Gall-bladder  and  Urinary  Bladder,  etc. — ^This  is  a 
very  infrequent  event.  Barnard,**  however,  refers  to  a  number  of  cases. 
H.  Faber,  in  1839,  wrote  an  octavo  volume  on  the  subject.  Kosthn 
and  Wucherer  have  described  fistulge,  and  Abt,  Giiterbock,tt  and  Hahn, 
biliary  calculi  in  the  urinary  bladder. 

A  case  of  cholecystovaginal  fistula  has  been  reported.  It  is  quite 
conceivable  that  an  elongated  gall-bladder  with  an  abscess  in  connexion 
with  it  may  track  into  the  pelvis. 

A  communication  between  the  pericardium  and  the  biliary  tract  is 
one  of  the  rarest  fistulse.     In  1892  Naunyn  only  knew  of  one  case. 

Rupture  and  Perforation  of  the  Gall-bladder  into  the  Peritoneum. — It 
is  most  unlikely  that  a  healthy  gall-bladder  would  rupture  merely  from 
the  weight  of  contained  gall-stones,  but,  as  a  matter  of  fact,  the  gall- 
bladder is  very  seldom  healthy  in  cholelithiasis.  It  may  be  thinned  from 
distension,  and  rupture  may  then  take  place  from  traumatism,  or  as 
the  result  of  sudden  pressure  brought  to  bear  on  the  gall-bladder  by  con- 
traction of  the  abdominal  walls  in  violent  straining,  coughing,  etc.,  or 

*  Bristowe:  Trans.  Path.  Soc,  vol.  ix,  p.  285. 

t  Galliard:  Medecine  Modeme,  Nov.  20,  1895. 

X  Naunyn:  On  Cholelithiasis,  p.  141. 

§  Courvoisier:  Pathologie  u.  Chirurgie  der  Gallenwege,  1890. 

!|  Eisner:  Medical  News  (N.  Y.),  Feb.  5,  1898. 
**  Barnard,  H.  L. :  Annals  of  Surgery,  Aug.,  1902,  vol.  xxxvi,  p.  161. 
tt  Giiterbock :  Virchow's  Archiv,  Bd.  Lxvi,  S.  273. 


CHOLELITHIASIS.  763 

in  the  vigourous  abdominal  contractions  of  delivery.  In  such  cases  there 
may  be  no  active  inflammation  or  previous  ulceration  of  the  gall-bladder. 
If  the  bile  is  free  from  microbic  infection,  the  peritoneum  may  be  Httle 
the  worse.  Cases  have  occurred  in  which  large  quantities  of  bile  have 
been  removed  from  the  abdominal  cavity,  but  this  chiefly  occurs  in  cases 
when  a  hydatid  cyst  in  connexion  with  a  bile-duct  ruptures  into  the 
cavity  of  the  peritoneum.     (Vide  p.  412.) 

Usually  rupture  of  the  gall-bladder  is  disposed  to  by  recent  inflamma- 
tion of  its  walls  or  by  definite  ulceration.  Under  these  conditions  the 
contents  of  the  gall-bladder  are  infected,  and  if  they  pass  into  the  general 
cavity  of  the  peritoneum,  generalised  peritonitis  will  be  set  up. 

In  some  instances,  as  the  result  of  adhesions  around  the  gall-bladder, 
the  rupture  or  perforation  sets  up  a  localised  peritoneal  abscess,  which 
may  contain  calculi,  in  communication  with  the  gall-bladder.  An  abscess 
of  this  kind  may  open  either  externally  on  the  surface  of  the  body  or  into 
one,  or  even  into  several,  of  the  abdominal  or  thoracic  viscera,  and  thus 
give  rise  to  fistulse,  which  may  be  multiple  and  extremely  complicated. 

In  rare  instances  a  localised  abscess  is  formed  behind  the  peritoneum, 
the  gall-bladder  having  become  adherent  to  the  posterior  abdominal 
wall. 

In  other  cases  calculi  may  ulcerate  out  of  the  gall-bladder  and  be 
found  surrounded  by  adhesions. 

Mo3Tiihan  *  describes  a  case  in  which  three  gall-stones,  each  the  size  of  a 
Barcelona  nut,  had  ulcerated  almost  through  the  walls  of  a  gall-bladder  showing 
chronic  sclerosing  cholecystitis.  Two  of  these  calculi  lay  in  pockets  in  the  omen- 
tum and  the  third  was  almost  hidden  in  a  cavity  in  the  liver. 


TREATMENT  OF  CHOLELITHIASIS. 

Prophylaxis. — In  fat  people,  especially  women,  and  after  typhoid 
fever,  influenza,  malaria,  and  pregnancy,  it  may  sometimes  be  within 
the  medical  man's  power  to  advise  a  change  in  the  patient's  mode  of  life 
which  will  tend  to  prevent,  or  diminish  the  liability  to,  catarrhal  inflam- 
mation of  the  gall-bladder  and  bile-ducts.  These  measures  are,  in  the 
main,  on  the  same  lines  as  those  for  the  general  hygienic  treatment  of 
cholelithiasis  in  the  intervals  between  the  attacks.  The  points  to  be 
borne  in  mind  are  to  prevent  stagnation  of  bile  in  the  biliary  tract,  and 
to  obviate  or  remove  any  inflammatory  condition  of  the  mucous  mem- 
brane of  the  duodenum,  biliary  papilla,  bile-ducts,  etc.  Thus  gentle 
exercise,  in  the  fresh  air  if  possible,  short'  of  fatigue,  so  as  to  favour  the 
passage  of  bile  into  the  intestines,  is  advisable.  When  this  is  not  prac- 
ticable, breathing  exercises  to  increase  the  movements  of  the  diaphragm 
and  liver  should  be  instituted.  Stooping  over  desks  and  working  in  a 
cramped  position  must  be  corrected,  while  the  use  of  tight  corsets,  belts, 
etc.,  should  be  discontinued.  The  patient  should  be  warmly  clad,  so 
as  to  avoid  chills.  A  visit  to  one  of  the  spas  mentioned  on  page  769 
is  a  valuable  precautionary  measure. 

*  Moynihan:  But.  Mod.  Journ.,  1903,  vol.  i,  p.  186. 


764  DISEASES    OF   THE    BILE-DUCTS. 

GENERAL  TREATMENT. 

The  general  medical  treatment  of  cholelithiasis  and  its  various  mani- 
festations may  be  considered  under  the  following  heads: 

To  prevent  stagnation  of  bile. 

To  prevent  the  occurrence  of  catarrhal  inflammation  of  the  gall- 
bladder and  bile-ducts. 

To  remove  catarrhal  inflamixiation  when  it  has  appeared. 

To  attempt  to  dissolve  and  remove  calculi  from  the  gall-bladder 
and  ducts. 

Spa  treatment. 

To  Prevent  Stagnation  of  Bile. — Stagnation  of  bile  in  the  gall- 
bladder favours  infection  and  cholecystitis,  and  therefore  the  production 
of  gall-stones,  or  if  these  are  already  present,  an  immediate  attack  of 
colic.  It  is,  therefore,  important  that  stagnation  should,  as  far  as 
possible,  be  prevented,  and  for  this  object  the  following  methods  may  be 
adopted : 

Exercise,  which  leads  to  increased  movements  of  the  diaphragm  and 
liver  and  so  to  an  increased  flow  of  bile  into  the  duodenum.  In  com- 
paratively young  and  vigourous  persons  active  exercise,  rather  than  a 
''constitutional"  w^alk,  is  needed.  Horse  exercise  is  perhaps  the  best, 
but  bicycling,  climbing,  tennis,  and  rowing  are  excellent.  In  cases  where 
active  open-air  exercise  is  not  possible,  deep  respirations  should  be  prac- 
tised so  as  to  induce  vigourous  movements  of  the  diaphragm  and  Uver, 
while  in  some  cases  abdominal  massage  is  useful  in  increasing  the  tone 
of  the  abdominal  muscles  and  the  flow  of  bile.  After  pregnancy  the  lax 
condition  of  the  abdominal  wall,  which  favours  enteroptosis,  hepato- 
ptosis,  and  stagnation  of  bile,  may  be  met  by  massage  to  the  abdominal 
muscles,  care  being  taken  not  to  bring  direct  pressure  to  bear  on  the 
gaU-bladder,  since  cholecystitis  may  thus  be  set  up. 

The  factor  of  dress,  especially  the  corset,  tight  waist-bands,  and 
heavy  skirts,  in  constricting  the  lower  part  of  the  chest  and  preventing 
free  diaphragmatic  respiration,  has  been  referred  to  in  the  consideration 
of  the  greater  incidence  of  gaU-stones  in  women  {vide  p.  717).  These 
causes  should  be  obviated,  and  the  wearing  of  tight  belts  in  men  dis- 
continued. 

By  the  Administration  of  Food  and  Drink. — When  food  passes  into 
the  duodenum,  bile  is  driven  out  of  the  gall-bladder  into  the  duodenum. 
Meals  at  short  intervals,  therefore,  are  more  effective  in  preventing  biliary 
stagnation  than  larger  meals  at  longer  intervals.  Kehr,*  in  fact,  suggests 
that  one  factor  which  accounts  for  the  much  greater  frequency  of  gall- 
stones in  German  women  is  that  the  wives  do  not  share  in  the  late  suppers 
taken  by  their  husbands.  In  addition  to  meals  at  comparatively  short 
intervals  some  supper  should  be  eaten  before  going  to  bed,  and  it  is  a 
good  plan  to  have  some  food  available,  so  that  in  case  the  individual 
wakes,  a  small  meal  may  be  taken  during  the  night.  The  details  of  the 
diet  will  be  considered  later.     {Vide  p.  769.) 

*  Kehr:  Diagnosis  of  Gall-stone  Disease,  p.  70,  American  translation. 


CHOLELITHIASIS.  765 

Though  experimental  results  show  that  water  cannot  be  considered 
a  cholagogue,  good  results  undoubtedly  follow  the  taking  of  large  draughts 
of  hot  water.  Vichy,  Carlsbad,  or  Contrexeville  waters  have  a  good 
effect,  or  hot  water  containing  some  sulphate  or  phosphate  of  soda.  The 
action  of  an  increased  amount  of  water  is  probably  complex  :  the  bile 
is  diluted  and  rendered  more  copious,  while  catarrh  of  the  ducts  and 
intestine  is  relieved.  In  order  to  get  the  maximum  effect  from  water  it 
should  be  taken  before  meals,  when  the  stomach  is  empty.  Thus  it  may 
be  taken  the  last  thing  at  night  or,  as  is  more  frequently  done,  early  in 
the  morning.  It  should  then  be  sipped  in  the  intervals  of  dressing,  or 
later  in  the  day  while  walking  about  in  a  garden. 

The  water  should,  of  course,  not  be  taken  in  excessive  quantities  or 
too  hot,  otherwise  dilatation  of  the  stomach  may  occur.  Dr.  Wightwick 
has  told  me  of  a  patient  who,  having  some  knowledge  of  medicine,  treated 
himself  for  gall-stones  by  copious  draughts  of  water  as  hot  as  he  could 
bear,  and  as  a  result  developed  very  acute  dilatation  of  the  stomach 
which  nearly  proved  fatal. 

Copious  enemata  of  hot  water  have  been  recommended  and  have 
been  thought  to  induce  muscular  contraction  of  the  gall-bladder  and 
expulsion  of  the  contained  bile. 

Cholagogues. — Although  a  number  of  drugs  have  been  credited 
with  the  power  of  increasing  the  secretion  and  flow  of  bile,  it  is  now 
generally  agreed  that  salicylate  of  soda  and  bile  itself  are  the  only  drugs 
which  really  increase  the  secretion  of  bile.  Mercury,  podophyllin,  iridin, 
rhubarb,  senna,  aloes,  turpentine,  and  other  drugs  may  increase  the 
peristaltic  contraction  of  the  ducts  and  so  lead  to  a  temporary  increase 
in  the  amount  of  bile  discharged  into  the  duodenum,  but  do  not  really 
augment  the  secretion  of  bile.     (Rutherford  and  Vignal,*  Mayo  Robson.f) 

Toluylendiamin  at  first  increases  the  flow  of  bile,  but  later  the  bile 
becomes  more  viscid  from  an  increased  quantity  of  mucus  in  it.  (Stadel- 
mann,t  Hunter.  §)  This  body  has  only  very  occasionally  been  employed 
in  medicine,  and  is  dangerous  from  its  hsemolyiic  or  destructive  action 
on  the  red  blood-corpuscles  and  its  tendency  to  produce  inflammation 
of  the  small  bile-ducts  and  jaundice. 

Secretin,  which,  as  Starling  and  Baylis  !|  have  shown,  is  manufactured  in  the 
duodenal  mucous  membrane  and  stimulates  the  secretion  of  the  pancreas,  also 
increases  the  secretion  of  bile. 

Ox  bile  is  sometimes  given  in  capsules,  but  it  is  better  to  give  the 
salts  of  the  bile  acids  alone,  since  the  bile-pigments  are  themselves  some- 
what poisonous. 

Gautier**  met  with  complete  relief  from  attacks  of  biliary  colic,  which  had  ex- 
tended over  five  years,  after  a  prolonged  course  of  ox  bile. 

*  Rutherford  and  Vignal:  Jour.  Anat.  and  Phys.,  vol.  x. 
t  Mayo  Kobson:  Proc.  Royal  Soc,  vol.  xlvii,  p.  21,  1890. 
%  Stadehnann:  Archiv  f.  exper.  Path.  u.  Pharmak.,  1887. 
§  Hunter,  W. :  Journ.  Path,  and  Bacter.,  vol.  iii,  p.  259. 
II  Starling  and  Baylis:  Proc.  Roy.  Soc,  1902,  vol.  Ixix,  p.  352. 
**  Gautier:  Rev.  M6d.  dc  la  Suisse  Roniande,  June  20,  1898. 


766  DISEASES    OF   THE    BILE-DUCTS. 

Salicylate  of  soda  has  the  advantage  that  it  not  only  increases  the 
secretion  of  bile,  but  that  it  acts  as  an  intestinal  antiseptic  and  so  tends 
to  diminish  intestinal  catarrh.  It  may  be  given  in  10-grain  doses  twice 
or  three  times  daily  with  an  equal  quantity  of  bicarbonate  of  soda.  The 
most  satisfactory  treatment  from  the  point  of  view  of  inducing  an  in- 
creased flow  of  bile  is  to  give  salicylate  of  soda  combined  with  plenty  of 
alkaline  waters.  Aspirin  (acetylo-salicylic  acid)  may  also  be  given,  but 
is  incompatible  with  bicarbonate  of  soda. 

Chauffard  *  combines  salicylate  of  soda  with  benzoate  of  soda  for 
periods  of  twenty,  fifteen,  ten  days  in  every  month  for  a  year  or  two, 
the  duration  of  the  course  diminishing  as  time  goes  on.  Iodide  of  potas- 
sium has  been  found  of  use  in  checking  frequent  attacks  of  colic.  Its 
method  of  action  is  doubtful ;  possibly  it  may  increase  the  mucous  secre- 
tion from  the  walls  of  the  biliary  tract  and  so  increase  the  flow  of  fluid 
through  the  ducts  and  thus  relieve  catarrh.  It  is  also  conceivable  that, 
like  chloroform  and  ether,  it  may  diminish  spasm. 

The  Prevention  of  Catarrhal  Inflammation. — Indigestion  and 
gastritis,  which,  by  leading  to  gastro-duodenal  catarrh,  might  set  up 
catarrhal  inflanunation  of  the  bile-ducts,  must  be  treated  by  careful 
dieting,  drugs,  and  the  prevention  of  constipation.  The  food  should  be 
bland,  nutritious,  and  eaten  slowly.  The  condition  of  the  teeth  should  be 
seen  to,  so  that  the  food  can  be  properly  masticated,  and  further  that 
there  is  no  oral  sepsis  to  set  up  gastritis.  Worry  and  anxiety  are  frequent 
causes  of  dyspepsia,  and  in  this  way  may  be  instrumental  in  favouring 
infection  of  the  ducts  and  gall-bladder.  Constipation  and  the  attendant 
tendency  to  indigestion  and  gastro-intestinal  fermentation  and  putre- 
faction should  be  prevented  by  gentle  purgatives ;  the  use  of  vigourous 
purges  must  be  avoided,  as  enteritis  may.  thus  be  induced.  Salines,  such 
as  half  a  tumbler  of  natural  Carlsbad  water  with  a  little  hot  water  before 
breakfast,  or  one  or  two  drachms  of  Carlsbad  salts  dissolved  in  hot  water 
are  useful.  Phosphate  of  soda  in  drachm  doses  may  also  be  given  in 
water  early  in  the  morning.  The  Carlsbad  salts  are  better  borne  by  the 
stomach  if  a  little  of  the  infusion  of  quassia  or  cinchona  is  added  to  the 
draught  (Stewart  f)-  After  taking  the  salts  the  patient  should  walk 
about,  or  better,  practise  systematic  exercises  \^dth  deep  inspiratorv^ 
movements  so  as  to  favour  the  descent  of  the  diaphragm,  and  should 
not  have  any  food  until  an  hour  after  the  draught  has  been  taken. 

To  Remove  Catarrhal  Inflammation  of  the  Biliary  and  Intestinal 
Tracts, — It  is  most  important  to  remove  inflammation  of  the  gall- 
bladder, because  calculi  are  formed  as  a  result  of  catarrhal  cholecystitis 
and  are  not  likely  to  be  dissolved  so  long  as  the  gall-bladder  is  inflamed. 
Harley  and  Barrett  J  have  shown  that  calculi  introduced  into  dogs' 
gall-bladders  are  dissolved  by  the  bile  when  the  gall-bladders  are  healthy, 
but  not  when  cholecystitis  is  kept  up. 

The  methods  already  referred  to,  by  which  the  flow  of  bile  is  increased 

*  Traite  de  M6d.  (Bouchard,  Brissaud),  t.  v,  p.  85. 

t  Stewart,  D.  D. :  American  Journ.  of  the  Medical  Sciences,  vol.  cxxv,  p.  851. 

X  V.  Harley  and  Barrett:  Journ.  of  Physiology,  vol.  x.xix,  p.  341,  1903. 


CHOLELITHIASIS.  767 

and  the  bile-passages  washed  down,  are  of  use  in  removing  catarrhal  in- 
flammation of  the  gall-bladder  and  bile-ducts.  Carlsbad  salts,  phos-. 
phate  of  soda,  Epsom  salts  in  hot  water,  or  table  waters,  such  as  Con- 
trexeville,  Homburg,  etc.,  should  be  taken  so  as  to  remove  catarrhal 
inflammation  of  the  intestines  and  keep  the  bowels  loose.  Vigourous 
purgatives  should  be  avoided,  as  the}'  tend  to  set  up  inflammation  of 
the  mucous  membrane. 

The  abdomen  should  be  kept  warm,  so  as  to  avoid  chills,  and  in  cases 
where  there  is  tenderness  over  the  gall-bladder  poultices,  hot  packs,  or 
fomentations,  or  heat  by  means  of  the  thermophore,  may  be  applied 
over  the  right  hj-pochondrium. 

A.  E.  Wright  *  has  tentatively  suggested  that  patients  should  be  immunised 
against  the  colon  bacillus,  so  that  the  cholecystitis  due  to  colon  infection  should  be 
arrested  and  that  when  this  has  been  brought  about,  the  calculi  might  gradually 
dissolve  in  the  bile. 

Attempts  to  Dissolve  Calculi. — Numerous  drugs  have  been  tried 
and  recommended  with  a  \-iew  to  dissolving  calculi,  but  with  very  little, 
if  any,  success.  A  very  famous,  ancient  remedy  was  Durande's,  which 
consisted  of  a  mixture  of  ether  (vri  xv)  and  turpentine  (n^  x)  in  a  capsule. 
Although  this  remedy  may  do  good  by  virtue  of  the  antispasmodic  action 
of  ether  or  of  the  expulsive  action  of  turpentine, — radically  opposed  as 
these  actions  are, — there  is  no  reason  to  believe  that  the  calcuh  in  the 
gall-bladder  are  acted  upon  directly  by  the  drugs.  Chloroform,  which 
has  been  employed  as  a  solvent,  probably  acts  chiefly  as  an  antispas- 
modic. 

Olive  oil  has  been  wddety  used  to  relieve  the  symptoms  of  cholelithiasis. 
It  has  been  shown  to  dissolve  calculi  out  of  the  body  (Brockbank,t  L. 
Scott  t),  but  there  is  no  evidence  that  olive  oil  given  by  the  mouth, 
much  less  when  injected  per  rectum,  can  act  on  calculi  in  the  gall-bladder. 
In  fact,  there  is  a  well-known  fallacy  about  some  of  the  good  effects 
ascribed  to  the  use  of  olive  oil,  namely,  that  the  oil  itself  may  be  so 
digested  and  altered  as  to  imitate  softened  calculi  when  passed  by  the 
bowel. 

Delepine  §  described  a  case  where  a  patient  taking  olive  oil  for  cholelithiasis  . 
passed  40  round  or  oval  bodies  which  were  at  first  regarded  as  biliary  calculi  and 
as  evidence  of  the  success  of  the  treatment.     They  turned  out  to  be  masses  of 
crystals  of  fatty  acids  derived  from  tlie  oil. 

It  is  quite  conceivable,  however,  that  olive  oil  might  exert  a  solvent 
action  on  a  calculus  impacted  in  the  actual  orifice  of  the  biliary  papilla. 
It  has  also  been  thought  that  fatty  acids  and  glycerine  absorbed  from 
the  bowel  may  reach  the  liver  and  lead  to  an  increased  flow  of  bile  into 
the  gall-bladder.  Bile  acids  dissolve  cholesterin,  hence  the  more  bile 
passes  over  a  calculus,  the  better  the  chance  of  some  absoiption  taking 
place.     Some  of  the  good  effects  of  r)il  may  be  due  to  its  soothing  and 

*  Wright,  A.  E. :  Brit.  Med.  .Journ.,  1903,  vol.  i,  p.  1073. 
t  Broclvbank,  E.  M. :  Med.  Clironicle,  vol.  xix,  p.  155. 
i  Lindley  Scott:  Brit.  Med.  Journ.,  1897,  vol.  ii,  p.  798. 
§  Dclcpinc,  S. :  Trans.  Path.  Soc,  vol.  xli,  p.  111. 


768  DISEASES    OF    THE    BILE-DUCTS. 

antispasmodic  action  on  the  intestine.  Olive  oil  is  given  in  quantities 
of  from  6  to  12  ounces  a  day  by  the  mouth,  but  is  far  from  a  pleasant 
thing  to  take.  Some  writers  (Chauffard,  Dupre  *),  however,  speak  highly 
of  the  good  effects  of  olive  oil  in  cholelithiasis.  Pure  olive  acid  (Merck) 
and  eunatrol,  or  pure  oleate  of  soda,  have  been  recommended  instead  of 
the  oil.  Fat  and  cream  may  also  be  taken  in  place  of  the  oil,  unless 
they  disturb  digestion. 

Since  the  bile  acids  dissolve  cholesterin,  any  increase  in  the  secretion 
of  bile,  such  as  is  induced  by  salicylates  or  by  the  administration  of  bile 
by  the  mouth,  may  be  regarded  as  a  means  of  dissolving  calculi.  Since 
proteid  food  increases  the  percentage  of  bile  acids  in  the  bile,  meat  has 
been  regarded  as  an  important  element  in  the  diet  of  patients  suffering 
from  gall-stones.  As  already  pointed  out,  Harley  and  Barrett's  experi- 
ments show  that  calculi  are  dissolved  by  the  bile  provided  cholecystitis 
is  absent.  It  is,  therefore,  important  to  prevent  or  remove  inflammation 
of  the  gall-bladder. 

Attempts  to  Remove  Gall-stones. — Measures  such  as  massage  and 
drugs  such  as  turpentine  and  purgatives  which  lead  to  muscular  contrac- 
tion of  the  gall-bladder  and  bile-ducts  have  bfeen  employed  to  favour 
the  expulsion  of  calculi.  At  the  commencement  of  a  course  at  Carlsbad 
it  not  uncommonly  happens  that  a  patient  experiences  an  attack  of 
biliary  colic  and  passes  calculi.  Turpentine  has  been  recommended  by 
Ralfe  t  in  cases  of  irregular  biliary  colic  to  favour  the  passage  of  calculi. 
Increasing  the  flow  of  bile  by  salicylates  and  ox  bile  cannot  be  regarded 
as  likely  to  drive  calculi  out  of  the  gall-bladder,  though  their  good  effects 
in  reducing  catarrh  of  the  ducts  and  the  possibility  that  calculi  may, 
as  already  pointed  out,  be  dissolved,  must  not  be  forgotten.  Measures 
intended  to  lead  to  the  expulsion  of  gall-stones  are  somewhat  uncertain 
in  their  action.  Massage  of  the  gall-bladder  and  bile-ducts  in  order  to 
effect  ''the  extrusion  of  gaU-stones  by  digital  manipulation"  was  advo- 
cated by  the  late  Dr.  George  Harley  J  in  1888,  and  has  been  widely  con- 
demned as  a  dangerous  method  of  working  in  the  dark.  No  doubt  it 
might  lead  to  the  expulsion  of  soft  calculous  masses  lying  in  the  common 
bile-duct,  but  in  many  cases  it  would  be  quite  powerless  to  do  any  good 
and  might  easily  do  harm  by  leading  to  rupture  of  an  ulcerated  gall- 
bladder or  duct.  If  it  were  possible  to  recognise  with  certainty  cases 
with  soft  calculous  material  in  the  conn^non  duct,  gentle  massage  might 
be  recommended,  but,  unfortunately,  our  methods  of  diagnosis  are  not 
sufficiently  sure  to  enable  us  to  do  so,  and,  according^,  massage  in  chole- 
lithiasis is  a  haphazard  and,  it  must  be  admitted,  a  dangerous  method 
of  treatment. 

Spa  Treatment. — Mineral  waters  dilute  and  increase  the  flow  of  bile 
and  may  thus  lead  to  some  degree  of  solution  of  calculi  in  the  ducts  and 
gall-bladder  and  to  their  ultimate  discharge  into  the  duodenum.  The 
increased  flow  of  bile  flushes  the  bile-ducts  and  thus  tends  to  remove 

*  Chauffard,  Dupre :  Soc.  Med.  des  Hop.  Paris,  Oct.  12,  1888. 

t  RaKe:  Lancet,  1891,  vol.  ii. 

t  Harley,  G. :  Illustrated  Med.  News,  Oct.  20,  1888. 


CHOLELITHIASIS.  769 

infective  catarrh  and  so  to  prevent  the  further  formation  of  calcuH  and 
possibly  to  favour  absor|3tion  of  calculi.  It  is  not  absolutely  necessary 
to  go  to  a  spa  in  order  to  undergo  the  treatment,  for  it  can  be  carried 
out  under  medical  advice  at  home,  but  the  patient  probably  gains  by 
going  to  the  original  source  from  the  change  of  scene  and  from  the  influ- 
ence exerted  by  the  regular  life,  the  regime,  and  the  freedom  from  business 
cares  and  worries. 

Carlsbad,  Vichy,  Marienbad,  Kissingen,  Homburg,  Neuenahr,  Ems, 
Bertrich,  Brides,  are  appropriate  spas  on  the  Continent.  In  England 
Harrogate,  Llandrindod  Wells,  enjoy  some  reputation,  while  in  America 
Bedford,  Pa.,  Las  Vegas  Hot  Springs,  Sharon,  White  Sulphur,  are  recom- 
mended for  the  treatment  of  gall-stones. 

At  Carlsbad  and  Vichy  it  not  infrequently  happens  that  calculi  are 
passed  after  the  course  of  treatment  has  begun;  patients  should,  there- 
fore, be  warned  that  they  may  have  a  return  of  colic  with  jaundice. 
Neuenahr  and  Bertrich  are  less  depressing  than  Carlsbad,  wliile  the 
waters  at  Salzschlirf,  Wiesbaden,  Nauheim,  and  Soden  are  sometimes 
reconmiended. 

Diet. — Food  should  be  taken  at  comparatively  short  intervals  and 
the  amount  at  each  meal  should  not  be  large,  while  overeating  must,  of 
course,  be  prevented.  As  to  the  kind  of  food  most  suitable  for  patients 
with  gall-stones,  considerable  divergence  of  opinion  has  been  expressed. 
It  is  unnecessary  to  insist  on  the  fact  that  the  food  should  be  digestible 
and  not  too  bulky.  The  amount  of  starchy  food  should  be  much  re- 
stricted, and  bread  should  be  taken  sparingly  and  preferably  as  toast, 
while  sugar  must  only  be  allowed  in  small  quantities.  Porridge  and  rice 
may  be  taken  in  moderation.  It  is  particularly  with  regard  to  fatty 
food  that  contradictory  statements  have  been  made.  Some  writers  be- 
lieve that  fats  favour  the  production  of  calculi;  others  that  fats  are 
indicated  as  solvents  of  gall-stones.  It  is  probable  that  fatty  food  has 
no  particular  action  in  dissolving  calculi  in  the  bile-ducts  or  gall-bladder, 
and  that  it  only  does  harm  indirectly,  viz.,  when  it  gives  rise  to  acid 
dyspepsia.  As  a  general  rule,  fatty  food  should  be  taken  in  small  quanti- 
ties and  carefully  watched ;  when  any  signs  of  dyspepsia  or  fermentation 
appear,  it  should  be  diminished  in  amount,  or,  if  need  be,  discontinued. 

Proteid  food  may  be  taken  with  greater  freedom  and  may  consist  of 
mutton,  beef,  game  in  small  quantities,  and  vegetables  containing  a  good 
deal  of  albumin.  It  has  been  thought  that  proteid  food,  by  increasing 
the  amount  of  the  bile  acids,  may  assist  in  dissolving  cholesterin;  tliis, 
however,  is  problematical.  Alcohol  is  best  avoided,  and  if  required  for 
other  reasons,  should  be  well  diluted.  Light  claret,  still  Moselle,  or  a 
little  whisky  may  be  taken  in  this  way.  Beer,  stout,  champagne,  and 
especially  liqueurs  should  be  forbidden.  The  importance  of  taking  plenty 
of  water  before  meals  has  already  been  insisted  on. 


49 


770  DISEASES    OF   THE    BILE-DUCTS. 


SURGICAL  INTERFERENCE  IN  CHOLELITHIASIS. 

It  has  already  been  pointed  out  that  in  acute  bihary  cohc  operative 
interference  is  justifiable  only  when  hfe  is  threatened  by  some  extremely 
grave  complication,  such  as  rupture  of  the  gall-bladder  or  bile-ducts 
with  resulting  peritonitis,  or  when,  as  rarely  happens,  concoixdtant  acute 
infective  cholecystitis  sets  up  widespread  peritonitis,  or  when  signs  of 
acute  intestinal  obstruction  appear. 

The  effects  of  chronic  or  irregular  cholelithiasis  which  require  surgical 
interference  may  be  arranged  as  follows : 

(i)  When  there  is  acute  inflammation  in  the  region  of  the  gall-bladder 
with  the  signs  of  severe  localised  peritonitis. 

(ii)  When,  in  a  case  with  a  history  of  gall-stones,  there  are  symptoms 
pointing  to  acute  perforative  peritonitis,  such  as  might  be  set  up  by  per- 
foration of  the  gall-bladder. 

(iii)  When,  from  the  presence  of  fever,  pain,  jaundice,  etc.,  there  is 
evidence  that  severe  infective  inflannnation  of  the  bile-ducts  has  devel- 
oped. Under  these  conditions  the  gall-bladder  and  ducts  should  be 
freely  drained. 

(iv)  When  acute  intestinal  obstruction  occurs  in  patients  with  a  his- 
tory of  gall-stones. 

(v)  When  there  is  a  large  tumor  constantly  present  in  the  position 
of  the  gall-bladder,  such  as  might  be  due  to  distension  of  the  gaU-bladder 
by  serous  or  mucous  fluid  (dropsy  of  the  gall-bladder),  by  pus  (empyema), 
or  by  a  collection  of  calculi. 

(vi)  Wlien  jaundice  in  a  patient  with  a  history  of  gall-stones  becomes 
chronic.  The  period  which  should  be  aUowed  to  elapse  after  the  onset 
of  permanent  jaundice  varies  very  considerably.  Hanot  fixed  the  period 
at  three  months.  Boix  *  shortened  it  to  six  weeks,  while  C.  Beck  f 
argued  in  favour  of  four  weeks.  If  medical  measures  are  quite  ineffectual 
and  the  patient  loses  ground,  the  chance  of  relief  from  operation  is  cer- 
tainly diminished  by  delay,  as  the  liver  cells  are  further  damaged  by 
the  prolonged  stagnation  of  the  bile  in  the  intra-hepatic  bile-ducts.  There 
is  also  the  danger  that  infective  catarrh  may  supervene  in  the  dilated 
bile-ducts  or  in  the  liver.  Further,  the  marked  tendency  to  hsemorrhage 
which  exists  in  so  many  deeply  jaundiced  patients  makes  operative  inter- 
ference difficult  and  dangerous.  No  hard-and-fast  rule  can  be  laid  down 
as  to  the  time  which  should  be  allowed  to  elapse  before  a  patient  with 
chronic  jaundice  is  operated  upon.  The  patient's  condition,  general 
nutrition,  presence  or  absence  of  symptoms,  and  response  to  treatment 
must  all  be  considered.  If  improvement  occurs  under  medical  treatment, 
it  would  obviously  be  unwise  to  adopt  operative  measures.  As  a  general 
rule,  operation  should  be  advised  earher  in  poor  patients  whose  liA'e- 
lihood  depends  on  their  ability  to  work  than  in  well-to-do  patients 
who  can  afford  a  cure  at  Carlsbad,  Neuenahr,  etc. 

(vii)  In  intermittent  hepatic  fever,  where  there  is  a  calculus  in  the 

*  Boix:  Archiv.  general,  de  Med.,  Oct.,  1901,  p.  470. 
t  Carl  Beck:  The  Medical  Week,  1897,  p.  137. 


CHOLELITHIASIS.  771 

common  bile-duct  which  sets  up  recurrent  attacks  of  fever,  pain,  and 
jaundice,  medical  treatment  should  always  be  given  a  good  trial,  and  if 
the  attacks  become  less  frequent  and  severe  and  gradually  disappear, 
there  is,  of  course,  no  need  for  operation.  On  the  other  hand,  if  the 
attacks  become  more  frequent  or  no  improvement  occurs,  operation 
should  be  considered  and  should  be  carried  out  before  the  patient  be- 
comes too  run  down  in  strength  and  resistance. 

(viii)  In  recurrent  biliary  cohc,  without  the  passage  of  calcuU  in  the 
stools,  which  leads  to  serious  impairment  of  the  patient's  health  and 
threatens  to  induce  a  condition  of  chronic  invahdism,  the  question  of 
operative  interference  must  be  considered.  A  poor  man  who  cannot 
afford  the  loss  of  time  and  expense  involved  by  a  cure  at  Carlsbad, 
Neuenahr,  Harrogate,  etc.,  should  be  advised  to  submit  to  operation.  A 
rich  patient  should  be  given  the. chance  of  a  course  of  spa  treatment 
under  careful  mecUcal  supervision  before  an  operation  is  undertaken.  An 
additional  reason  for  operating  in  some  cases  is  that  carcinoma  of  the 
gall-bladder  occurs  in  from  14  to  4  per  cent,  of  all  the  persons  wdth  gall- 
stones, and  that  removal  of  the  gall-stones  or,  if  necessary,  of  the  gall- 
bladder may  prevent  this  sec[uela.  In  a  case  of  recurrent  attacks  of 
biliary  colic  it  would  probabty  be  safer  to  advise  operative  interference 
at  any  earUer  date  in  patients  who  have  a  family  histor}^  of  carcinoma 
than  other  patients. 

(ix)  When,  from  adhesions  between  the  gall-bladder  and  pyloric  end 
of  the  stomach,  continued  and  severe  gastric  sjaiiptoms  are  produced. 
{Vide  p.  749.) 

(x)  In  patients  who  are  acquiring  the  mor^jhia  habit  as  the  result 
of  prolonged  suffering  operative  interference  is  necessary  to  prevent  the 
estabhshment  of  this  pernicious  habit. 

(xi)  In  some  cases  of  fistulse,  both  external  and  internal. 

For  the  details  of  the  surgical  operation  the  reader  must  consult  the 
text-books  on  operative  surger}^ 


NDEX 


Abdomen,  tympanitic  distension  of,  in  portal 

pyaemia,  76 
Abdominal   aorta,   aneurysm   of,    as   cause   of 
jaundice,  550 
conditions  displacing  liver,  19 
backwards,  21 
downwards,  19 
forwards,  20 
upwards,  20 
cysts,  differentiation  from  ascites  in  cirrhosis, 

250 
sympathetic,    neuralgia    of,     differentiation 

from  biliary  colic,  732 
tumors,  differentiation  from  ascites  in  cirrho- 
sis, 249  __  _ 
veins,    superficial,    dilatation    of,    in  portal 

thrombosis,  63 
wall,   anterior,  conditions  in,  differentiation 
from  hydatid  cysts  of  liver,  403 
Abnormal  lobulation  of  liver,  1 
Abnormalities,  anatomical,  of  liver,  1 
in  size  and  shape  of  gall-bladder,  590 
of  bile-ducts,  639 
of  gaU-bladder,  589 
Abscess,  120 

amcEbic,  histological  appearances  in,  132 
cerebral,  complicating  tropical  abscess,  146 
multiple,  156 

in  connexion  with    portal  vein    infection, 

157 
tropical  abscess  and,  differentiation,  149 
of  spleen  as  cause  of  portal  pyaemia,  70 
porto-pyaemic,  67 
pyscmic,  156 

single,  as  cause  of  tropical  abscess,  125 
secondary,  due  to  infection  from  large  single 

abscess,  159 
single,  120.     See  also  Tropical  abscess. 
subphrenic,  differentiation  from  hydatid  cysts 
of  liver,  405 
from  tropical  abscess,  148 
tropical,  120._    See  also  Tropical  abscess. 
tuberculous,  in  liver,  344 
Acanthosis  nigricans,  252 
Accessory  livers,  3 
lobes,  minute,  3 
Acclimatisation  as  disposing  factor  in  tropical 

abscess,  127 
Acholuric  jaundice,  228,  529 
Achroo-amyloid  liver,  433 
Actinomycosis  of  gall-bladder,  616 
of  liver,  381 

clinical  picture,  384 
diagnosis,  389 
frequency,  381 
method  of  origin,  381 
morVjid  anatomy,  382 
prognosis,  384 
treatment,  384 
Acute  atrophy  of  liver,  564.     See  also  Acute  yel- 
low atrophy. 
yellow  atrophy,  564 
age  in,  565 

alcoholic  excess  as  cause,  567 
blood  in,  577 

chloroform  narcosis  as  cause,  567 
clinical  picture,  574 
course,  574 
definition,  564 
diagnosis,  578 
differential  diagnosis,  578 
differentiation  from  icterus  gravis,  578 

from  phosphorus  poisoning,  578 
duration,  574 


Acute  yellow  atrophy,  etiology,  564 
first  stage,  onset  of,  575 
frequency,  564 
gastro-intestinal  tract  in,  573 
heart  in,  573 
histology,  570 
kidneys  in,  573 
liver  dulness  in,  576 
mental  disturbance  as  cause,  565 
micro-organisms  in,  573 
morbid  anatomy,  568 
nervous  system  in,  573 
onset,  575 
pancreas  in,  573 
pathogeny,  573 

phosphorus  poisoning  as  cause,  567 
pre-existing  hepatic  disease  as  cause,  567 
pregnancy  as  cause,  565 
prognosis,  579 
regenerative  changes  in,  571 
second  stage,  onset  of,  575 
sex  in,  565 
size  of  liver  in,  568 
spleen  in,  573 
syphilis  as  cause,  566 
termination,  578 
treatment,  579 
urine  in,  577 
weight  of  liver  in,  568 
Addison's  disease,  differentiation  from  pigment- 
ary cirrhosis  of  hsemochromatosis,  304 
Adenitis,  syphilitic,  as  cause  of  jaundice,  542 
Adenoma,  cystic,  of  gaU-bladder,  618 
of  liver,  452 
acinous,  453 

derived  from  bile-ducts,  454 
histology,  462 
multiple,  455 

cirrhosis  and,  relation,  456 
clinical  aspect,  459 
derived  from  bile-ducts,  455 
microscopic  appearances  in,  459 
morbid  anatomy,  458 
nature  of,  457 
secondary  changes  in,  459 
secondary  changes  in,  462 
single,  453 

derived  from  bile-ducts,  454 
solitary,  derived  from  liver-cells,  453 
morbid  anatomy,  454 
Adipose  ascites  in  cirrhosis,  245 
Albuminuria  as  symptom  of  cirrhosis,  232 
hepatogenous,  510 
in  malignant  disease  of  liver,  510 
Alcohol  as  cause  of  cirrhosis,  182 
Alcoholic  cirrhosis,  178 
hypertrophic,  198 
drinks  as  cause  of  cirrhosis,  182 
excess  as  cause  of  acute  yellow  atrophy,  567_ 
Alcoholism  as  cause  of  hypertrophic  biliary  cir- 
rhosis, 309 
as  disposing  factor  in  tropical  abscess,  128 
Alimentary  canal,  diseases  of,  acute  cholecys- 
titis from,  592 
canal  in  hypertrophic  biliary  cirrhosis,  315_ 
micro-organisms  from,  as  cause  of  cirrhosis, 
190 
Alveolar  hydatid  of  liver,  419.     See  also  Multi- 

locular  hydatid  of  liver. 
Ama-ba  as  cause  of  tropical  abscess,  133 
Amoebic  abscess,  histological  appearances  in, 132 
Ampulla  of  N'ater,  bile-containing  cyst  in  com- 
munication with,  652 
carcinoma  of,  697 


773 


774 


INDEX. 


Ampulla  of  Vater,  carcinoma  of,  diagnosis,  701 
diarrhoea  in,  701 

differentiation  from  jaundice,  701 
etiology,  700 

imitating  cholelithiasis,  702 
morbid  anatomy,  699 
signs,  701 
symptoms,  701 
treatment,  702 
gall-stones  in,  inflammatory  effects,  756 
mechanical  effects,  741 
Amyloid  disease  of  liver,  430 
Anaemia  in  jaundice,  534 

splenic,   ascites  due  to,  differentiation    from 
ascites  in  cirrhosis,  253 
chronic,    differentiation    from    pigmentary 
cirrhosis  of  hEemochromatosis,  304 
gumma  of  liver  resembling,  363 
differentiation  from  cirrhosis,  287 
hamatemesis  due  to,  differentiation  from 
hsematemesis  in  cirrhosis,  270 
Anaemic  infarcts,  morbid  anatomy,  103 

traumatism  as  cause,  107 
Anatomical  abnormalities  of  liver,  1 
Aneurysm  as  cause  of  portal  thrombosis,  57 
of  abdominal  aorta  as  cause  of  jaundice,  550 
of   hepatic  artery,  43.     See  also  Hepatic  an- 
eurysm. 
of   superior  mesenteric   artery   as   cause   of 
jaundice,  550 
Angina    pectoris,    differentiation    from    biliary 

colic,  733 
Angiocholitis,  672 
Angioma  of  liver,  460 
clinical  aspect,  464 
morbid  anatomy,  461 
pathogeny,  463 
prognosis,  465 
treatment,  465 
Annular  cirrhosis,  178 
Aorta,   abdominal,   aneurysm  of,   as   cause  of 

jaundice,  550 
Appendicitis  and  acute  catarrhal  cholecystitis, 
598 
as  cause  of  portal  pyaemia,  68 
differentiation  from  acute  catarrhal  cholecys- 
titis, 600 
from  biliary  colic,  731 
in  suppurative  cholecystitis,  608 
Appendicular  liver,  68,  158 

lobe  of  liver,  12 
Arsenic  as  cause  of  cirrhosis,  185 
Arteries,  gastric,  erosions  of,  hsematemesis  due 
to,  differentiation  from  haematemesis  in  cir- 
rhosis, 269 
i^.rteriosclerosis,  hepatic,  46 

in  cirrhosis,  222 
Artery,  hepatic,  diseases  of,  43.     See  also  He- 
patic artery. 
mesenteric,  superior,  aneurysm  of,  as  cause  of 
jaundice,  550 
Arthritis  in  hypertrophic  biliary  cirrhosis,  320 

in  tropical  abscess,  137 
Arthritism,  39,  187 

Ascaris  lumbricoides  as  cause  of  jaundice,  539 
in  bile-ducts,  676 
clinical  aspects,  677 
treatment,  676 
Ascites,  adipose,  in  cirrhosis,  245 
chyliform,  in  cirrhosis,  245 
chylous,  in  cirrhosis,  244 
definition,  240 
derivation,  240 
differentiation  from  hydatid  cysts  of  liver,  407 

from  tropical  abscess,  152 
fatty,  in  cirrhosis,  245 
hemorrhagic,  in  cirrhosis,  245 
in  carcinoma  of  gall-bladder,  632 
in  cirrhosis,  240 
bad  effects,  255 
cardiac  failure  as  cause,  243 
causes,  240 

concomitant  inflammation  of  peritoneum  as 
cause,  242 
perihepatitis  as  cause,  243 
continuous  drainage  in,  256 
differentiation  from  abdominal  cysts,  250 
tumors,  249 


Ascites  in  cirrhosis,  differentiation  from  ascites 
due  to  acute  peritonitis,  250 
due  to  chronic  peritonitis,  250 
due  to  lardaceous  disease  of  liver,  252 
due  to  malignant  disease  of  liver,  252 
due  to  nodules  of  malignant  disease, 

251 
due  to  other  causes,  255 
due  to  ovarian  papilloma,  253 
due  to  renal  disease,  253 
due  to  splenic  ansemia,  253 
due  to  syphilitic  disease  of  liver,  252 
due  to  thrombosis  of  portal  vein,  252 
due  to  tricuspid  regurgitation,  253 
due  to  tuberculous  peritonitis,  251 
from  encysted  peritonitis,  249 
from  hydatid  cysts,  250 
from  obesity,  250 

from  other  abdominal  conditions,  248 
from  ovarian  cyst,  248 
from  parovarian  cyst,  248 
from  pregnant  uterus  with  hydrops  am- 
nii,  250 
diuretics  in,  261 
effects,  248 
epiplopexy  for,  258 
frequency,  240 

relation  between  weight  of  liver  and,  240 
large  trocar  in,  256 
obstructions  to  passage  of  blood  through 

cirrhotic  liver  as  cause,  241 
onset,  243 

paracentesis  in,  advisability,  254 
indications,  255 
method  of  performing,  255 
physical  signs,  246 
prognosis,  254 
purgatives  in,  262 
restriction  of  fluid  in,  262 
symptoms,  248 
toxic  nature,  241 
treatment,  254 

by  vascular  peritoneal  adhesions,  257 
in  malignant  disease  of  liver,  505,  507 
in  portal  pyaemia,  76 

thrombosis,  62 
in  prognosis  of  cirrhosis,  292 
milky,  in  cirrhosis,  245 
non-fatty,  in  cirrhosis,  245 
Ascitic  fluid  in  cirrhosis,  bacteriology,  245 
character  of  cells  in,  244 
characters,  244 
tension,  246 
Aspiration  in  tropical  abscess,  154 
Asystole,  hepatic,  85 
Atrophic  biliary  cirrhosis,  307 
cirrhosis,  178 

sclerosing  cholecystitis,  615 
Atrophy,  acute  yellow,  564.     See  also  Acute  yel- 
low atrophy. 
cyanotic,  of  liver,  85 


Bacillus  coli  as  cause  of  acute  cholecystitis,  593 
in  production  of  cholelithiasis,  704 
tubercle,  paths  of  reaching  liver,    337.     See 

also  Tubercle  bacillus. 
typhoid,  as  cause  of  acute  cholecystitis,  593 
entrance  into  gall-bladder,  594 
by  common  bile-duct,  595 
by  hepatic  vein,  595 
by  portal  vein,  595 
in  production  of  cholelithiasis,  704,  705 
Bacterial  toxines  as  cause  of  cirrhosis,  186 
Balantidium  coli  in  bile-ducts,  680 
Banti's  disease,   hypertrophic  biliary  cirrhosis 
and,  differentiation,  324 
relation,  314 
Bile,  escape  of,  from  fistula  of  operation  wound, 
_  in  tropical  abscess,  147 
pigment,  436 

stagnation  of,  as  cause  of  cholelithiasis,  706 
Bile-containing    cyst    in    communication    with 

ampulla  of  Vater,  652 
Bile-ducts,  abnormalities  of,  639 
casts  of,  718 
congenital  obliteration  of,  639 

association  witli  malformations,  640 


INDEX. 


775 


Bile-ducts,  congenital  obliteration  of,  bibliog- 
raphy, 650 
bUe-ducts  in,  645 
cirrhosis  associated  with,  641,  642 
clinical  picture,  647 
definition,  639 
diagnosis,  648 
differential  diagnosis,  648 
differentiation  from  syphilitic  disease  of 

liver,  649 
duration,  648 
etiology,  640 
faeces  in,  647 
frequency,  640 
gall-bladder  in,  645 
haemorrhage  in,  647 
heredity  in,  640 
jaundice  in,  647 
liver  in,  644 
morbid  anatomy,  644 
nomenclature,   640 
pathogeny,  641 
prognosis,  648 
sex  in,  641 
spleen  in,  647 
syphilis  as  cause,  641 
treatment,  649 
urine  in,  647 
diseases  of,  639 
extra-hepatic, chronic  catarrhal  cholangitis  of, 

670 
intra-hepatic,   small,  chronic  catarrhal  cho- 
_  langitis  of,  672 

ligature  of,  in  production  of  obstructive  bili- 
ary cirrhosis,  326 
,  newly  formed,  in  cirrhosis,  196,  205 
Biliary  cirrhosis,  306 
atrophic,  307 
hypertrophic,  306.    See  also  Hypertrophic 

biliary  cirrhosis. 
obstructive,  326.     See  also  Obstructive  bil- 
iary cirrhosis. 
colic,  723.     See  also  Colic,  biliary. 
fistula,  756.     See  also  Fistula,  biliary. 
obstruction,  cysts  due  to,  441 
effects  on  liver,  329 
Bilious  typhoid,  584 
Biliousness,  40 
Bilirubin  gall-stones,  mixed,  717 

in  jaundice,  536 
Bilirubin-calcium  gall-stones,  pure,  718 
Black  disease  in  cirrhosis,  272 

jaundice,  532 
Blood  as  symptom  of  cirrhosis,  234 
in  acute  yellow  atrophy,  577 
in  hypertrophic  biliary  cirrhosis,  321 
in  malignant  disease  of  liver,  509 
in  portal  pyaemia,  77 
in  Weil's  disease,  586 

obstruction   to,   through  cirrhotic  liver,   as- 
cites due  to,  241 
Breast,   carcinoma   of,   as  cause   of  secondary 

malignant  disease  of  liver,  496 
Breath,  offensive,  as  symptom  of  cirrhosis,  229 
Bright's  disease  as  cause  of  cholelithiasis,  712 
Bronchitis  in  cirrhosis,  281 
Bronchobiliary  fistula,  760 
diagnosis,  761 
prognosis,  761 
signs,  761 
symptoms,  761 
treatment,  761 
Bruits,  venous,  as  symptom  of  cirrhosis,  238 
Budd's  cirrhosis,  187 


Cachexia  in  malignant  disease  of  liver,  503 
Calcification  of  liver,  437 
primary,  437 
secondary,  437 

of  portal  vein,  81 
Calcium  carbonate  gall-stones,  718 
Calculi,  703.     See  also  Gall-stones. 

intra-hepatic,  721 

pancreatic,  as  cause  of  jaimdice,  5.50 
Cammidge's  test  for  jaundice  due  to  pancreatic 

disease,  548 
Canaliculi  in  cirrhosis,  p.seudobile,  196,  205 


CanalicuH  in  hypertrophic  biliary  cirrhosis,  314 

in  obstructive  biliary  cirrhosis,  331 
Cancer  du  pylore  pancreatico-biliaire,  698 

en  amande,  471 
Caput  medusae,  211 
Carbohydrate  food  in  cirrhosis,  296 
Carcinoma  in  cirrhosis,  224 

of  ampuUa  of  Vater,  697.     See  also  Ampulla 

of  Vater,  carcinoma  of. 
of  bile-ducts,  differentiation  from  carcinoma 

of  gall-bladder,  635 
of  breast  as  cause  of  secondary  malignant 

disease  of  liver,  496 
of  colon   as   cause   of   secondary   malignant 

disease  of  liver,  496 
of  duodenum  as  cause  of  jaundice,  544 
of  gall-bladder,  620 
age  in,  630 
as  cause   of  secondary  malignant  disease 

of  liver,  496 
ascites  in,  632 

behaviour  and  appearance,  623 
clinical  picture,  630 
complications,  633 
diagnosis,  634 
differential  diagnosis,  634 
differentiation  from  carcinoma  of  bile-ducts, 
635 
of  pancreas,  635 
of  stomach,  635 
of  transverse  colon,  635 
from   faecal  accumulation  in  transverse 

colon,  636 
from  floating  kidney,  636 
from  gall-stones,  634 
from  malignant  disease   of  larger  bile- 
ducts,  695 
of  liver,  635 
from  syphilitic  disease  of  liver,  635 
duration,  633 
dyspepsia  in,  632 
etiology,  627 
extension  by  continuity,  624 

by  fistulae,  625 
haemorrhage  in,  624 
histology,  621 
jaundice  in,  631 
liver  in,  626 
morbid  anatomy,  620 
oedema  of  legs  in,  632 
pressure  effects,  625 
prognosis,  636 
relation  to  gall-stones,  627 
secondary  growths  in,  626 
sex  in,  629 
situation,  623 
starting-point,  622 
treatment,  636 
of  larger  bile-ducts,  683.     See  also  Malignant 

disease  of  larger  bile-ducts. 
of  liver,  differentiation  from  cirrhosis,  287 
from  hydatid  cysts,  403 
diffuse,  471 

primary,  degenerative  changes  in,  480 
developing  in  cirrhotic  liver,  473 
extension  into  hepatic  vein,  480 

into  portal  or  hepatic  veins,  480 
gall-stones  in,  480 
infiltrating,  471 
massive,  471 
melanotic,  478 
morbid  anatomy,  474 
multiple,  472 
nodular,  472 
pathology,  479 
secondary  growths  in,  475 

frequency,  480 
varieties,  470 
secondary,  frequency  of,  485 
starting-point,  479 
of  oesophagus  as  cause  of  secondary  malig- 
nant disease  of  liver,  497 
of  pancreas,   differentiation  from  carcinoma 
of  gall-bladder,  635 
from  malignant  disease    of    larger    bile- 
ducts,  693 
of  stomach  as  cause  of  jaundice,  543 
of  portal  pya;mia,  69 


776 


INDEX. 


Carcinoma  of  stomach  as  cause  of  portal  throm.- 
bosis,  55 
differentiation  from^  carcinoma  of  gall-blad- 
der, 635 
hsematemesis   due  to,   differentiation  from 
hffimatemesis  in  cirrhosis,  269 
of     transverse     colon,     differentiation     from 

carcinoma  of  gall-bladder,  635 
primary,  with  cirrhosis,  473 
clinical  aspects,  478 
Cardiac  cirrhosis,  88 

failure,  ascites  in  cirrhosis  from,  243 
lesions  as  cause  of  nutmeg  liver,  85 
liver,  85 
Casts  of  bile-ducts,  718 

Catarrhal  cholangitis,  acute,  655.     See  also  Ca- 
tarrhal jaundice. 
chronic,  670 

of  extra-hepatic  ducts,  670 
clinical  aspect,  671 
diagnosis,  671 
treatment,  671 
of  small  intra-hepatic  bUe-ducts,  672 
cholecystitis,    acute,    597.     See    also    Chole- 
cystitis, acute  catarrhal. 
chronic,      613.       See      also      Cholecystitis, 
chronic  catarrhal. 
jaundice,  540,  655 
causation,  655 
clinical  picture,  657 
definition,  655 
diagnosis,  660 

differentiation    from    hypertrophic    biliary 
cirrhosis,  323 
from    malignant  disease    of  larger    bile- 
ducts,  695 
from  Weil's  disease,  587 
duration,  659 
effects,  659 
frequency,  657 
in  newborn,  560 

treatment,  560 
morbid  anatomy,  657 
prognosis,  661 
symptoms,  premonitory,  657 

when  disease  is  fully  developed,  658 
treatment,  661 
Cavernoma  of  liver,  461 

Cells,  character  of,  in  ascitic  fluid  in  cirrhosis,  244 
liver,    hyperplasia    of,    in    treatment    of   cir- 
rhosis, 299 
in  cirrhosis,  206,  207 
solitary  adenoma  derived  from,  453 
Cerebral  abscess  complicating  tropical  abscess, 

146 
Children,  cirrhosis  in,  332 
clinical  features,  333 
hypertrophic  biliary  cirrhosis  in,  334 
in  India,  cirrhosis  in,  335 
Chill  on  liver,  109 
Chlorides  in  cirrhosis,  232 

Chloroform  narcosis  as  cause  of  acute  yellow 
p  atrophy,  567 

Cholagogues  in  cholelithiasis,  765 
Cholangitis,    catarrhal,    acute,    655.     See    also 
Catarrhal  jaundice. 
chronic,    670.     See   also   Catarrhal  cholan- 
gitis, chronic. 
jaundice  from,  540 
suppurative,  663 
bacteriology,  665 
clinical  picture,  668 
complications,  668 
diagnosis,  669 

differential,  669 
differentiation  from  portal  pysemia,  78 
diseases  which  dispose  to,  664 
duration,  669 
etiology,  663 

microscopic  appearances,  667 
morbid  anatomy,  655 
prognosis,  670 
treatment,  670 
tuberculous,  340 
Cholecystitis,  acute,  591 

Bacillus  coli  as  cause,  593 
bacteriology,  595 
catarrhal,  597 


Cholecystitis,  acute  catarrhal,  appendicitis  and, 
598 
clinical  features,  598 
diagnosis,  600 

differentiation  from  appendicitis,  600 
from  biliary  colic,  600 
from  suppurative  cholecystitis,  600 
jaundice  in,  599 
liver  in,  599 
morbid  anatomy,  597 
pain  in,  598 
prognosis,  601 
Riedel's  lobe  in,  599 
signs,  598 
symptoms,  598 
treatment,  601 
causes,  591 
disposing,  591 
exciting,  592 
chronic  cholecystitis  from,  602 
diseases  of  alimentary  canal  as  cause,  592 
empyema  of  gall-bladder  from,  601 
forms  of,  596 

heemic  infections  as  cause,  592 
hydrops  of  gall-bladder  from,  601 
microbic  infection  as  cause,  592 
sequels,  601 

serous  distension  of  gall-bladder  from,  601 
traumatism  as  cause,  596 
typhoidal  infection  as  cause,  593 
ulceration  of  gall-bladder  from,  602 
atrophic  sclerosing,  615 
chronic  catarrhal,  613 
causes,  613 
clinical  features,  614 
microscopic  appearances,  613 
morbid  anatomy,  613 
treatment,  614 
from  acute  cholecystitis,  602 
croupous,  603 
differentiation  from  biliary  colic,  730 

from  hydatid  cysts  of  liver,  403 
fibrinous,  603 
from  gall-stones,  747 
gangrenous,  611 

clinical  features,  612 
diagnosis,  612 
frequency,  612 
morbid  anatomy,  61 2 
treatment,  612 
membranous,  603 
clinical  features,  604 
microscopic  appearances,  604 
treatment,  604 
phlegmonous,  610 
clinical  features,  610 
diagnosis,  610 
frequency,  610 
jaundice  in,  610 
morbid  anatomy,  610 
prognosis,  611 
treatment,  611 
suppurative,  604 
appendicitis  in,  608 
clinical  picture,  605 
complications,  607 
diagnosis,  608 
differential  diagnosis,  608 
differentiation  from  acute  catarrhal  chole- 
cystitis, 600 
jaundice  in,  606 
morbid  anatomy,  605 
pain  in,  606 
prognosis,  609 
pulse  in,  606 
results,  607 
Riedel's  lobe  in,  606 
spleen  in,  607 
symptoms,  605,  606 
treatment,  609 
toxic,  596 
Cholecystocolic  fistula,  759 
Cholecystoduodenal  fistula,  758 
Choledochoduodenal  fistula,  758 
Cholelithiasis,  703.     See  also  Gall-stones. 
age  in,  715 

anxiety  and  worry  as  cause,  709 
biliary  colic  in,  723.     See  also  Colic,  biliary. 


INDEX. 


777 


Cholelithiasis,  Bright's  disease  as  cause,  712 
carcinoma  of  ampuUa  of  Vater  imitating,  702 
causes,  703 
disposing,  706 
exciting,  703 
immediate,  703 
cholagogues  in,  765 
cirrhosis  as  cause,  712 
clinical  picture,  722 
colon  bacillus  in  production  of,  704 
constipation  as  cause,  709 
diabetes  as  cause,  711 
diet  as  cause,  708 

in  treatment,  769 
foreign  bodies  as  cause,  707 
frequency,  714 

geographical  distribution,  715 
Gl^nard's  disease  as  cause,  710 
heart  disease  as  cause,  710 
hereditary  influences,  713 
in  early  life,  716 
in  insane,  713 
indigestion  as  cause,  709 
leptothricial,  706 
malignant  disease  as  cause,  712 
microbic  origin,  704 
myxoedema  as  cause,  712 
occupation  as  cause,  714 
pregnancy  as  cause,  709 
pulmonary  disease  as  cause,  711 
race  in,  715 

relation  of  various  factors  and  diseases  to,  708 
sex  in,  716 

stagnation  of  bile  as  cause,  706 
toxsemia  in  production  of,  706 
treatment,  763 
diet,  769 
general,  764 
prophylaxis,  763 
spa,  768 
surgical,  770 
to  dissolve  calciili,  767 
to  prevent  catarrhal  inflammation,  766 

stagnation  of  bile,  764 
to  remove  catarrhal  inflammation  of  bili- 
ary and  intestinal  tracts,  766 
typhoid  bacillus  in  production  of,  704,  705 
uterine  fibroma  and,  713 
visceroptosis  as  cause,  710 
worry  and  anxiety  as  cause,  709 
Cholemic  family,  309 
Cholera  as  cause  of  cirrhosis,  188 
Cholesterin  gall-stones,  717 

amorphous  and  crystaUine,  718 
laminated,  717 
mixed,  717 
pure,  717 
in  jaundice,  537 
Chylif  orm  ascites  in  cirrhosis,  245 
Chylous  ascites  in  cirrhosis,  244 
Cicatrices,  syphilitic,  of  liver,  355 

gumma  combined  with,  356 
Circulation,  micro-organisms  in,  producing  poi- 
sons, as  cause  of  cirrhosis,  193 
poisons  in,  as  cause  of  cirrhosis,  192 
Circulatory  system  in  jaundice,  534 
Cirrhose  biliare  splenomegalique,  318 
Cirrhoses  biliares  anicteriques,  308 
Cirrhosis,  174 

adipose  ascites  in,  245 
age  in,  179,201 
albuminuria  as  symptom,  232 
alcohol  as  cause,  182 
alcoholic,  178 

drinks  as  cause,  182 
hypertrophic,  l98 
annular,  178 

anthracotica,  185,  301,  436 
arsenic  as  cause,  185 
arteriosclerosis  in,  222 
as  cause  of  cholelithiasis,  712 

of  portal  thrombosis,  54 
ascites  in,  240.     See  also  Ascites  in  cirrhosis, 
ascitic  fluid  in,  bacteriology,  245 
character  of  cells  in,  244 
characters.  244 
ten.sion,  246 
stage,  225 


Cirrhosis,  associated  lesions,  221 

with  congenital  obliteration  of  bile-ducts, 

641,  642 
with  tuberculosis  elsewhere  than  liver,  346 
of  liver,  345 
atrophic,  178 
biliary,  307 
bacterial  toxines  as  cause,  186 
bile-ducts  in,  208 
bUiary,  306 
atrophic,  307 
hypersplenomegalic,  318 
hypertrophic,  306.     See  also  Hypertrophic 

biliary  cirrhosis. 
obstructive,  326.     See  also  Obstructive  bili- 
ary cirrhosis. 
black  disease  in,  272 
blood  as  symptom,  234 
bronchitis  in,  281 
Budd's,  187 

carbohydrate  food  in,  296 
carcinoma  with,  224,  478 
clinical  aspects,  478 
carcinomatosa,  473 
cardiac,  88 
chlorides  in,  232 
cholera  as  cause,  188 
chronic  peritonitis  in,  222,  284 
chyliform  ascites  in,  245 
chylous  ascites  in,  244 

classification  according  to  methods  by  which 
induced,  174 
anatomical,  175,  176 
clinical,  176 
clinical  course,  224 
clubbing  of  fingers  in,  228 
coma  in,  277 
common,  178 
comparison  of  main  forms  with  some  forms 

of  kidney  disease,  178 
complications,  281 
in  prognosis,  293 
congenital,  333 
constipation  in,  as  symptom,  230 

treatment,  297 
convulsions  in,  278 
cysts  in,  441 

debility  as  symptom,  228 
definition,  178 
delirium  in,  277 

tremens  in,  277 
diagnosis,  285 

differential,  285 
diaphragm  in,  morbid  appearances,  220 
diarrhoea  in,  as  symptom,  230 

treatment,  297 
diet  in,  295 

differential  diagnosis,  285 
differentiation  from  carcinoma  of  liver,  287 
from  chronic  venous  engorgement,  286 
from  enlargements  of  liver,  286 
from  hydatid  cyst  of  liver,  287 
from  hypertrophic  biliary  cirrhosis,  322 

with  jaundice,  285 
from  intestinal  obstruction,  288 
from  intra-hepatic  suppuration,  288 
from  leukaemia,  287 
from  malarial  enlargement,  286 
from  malignant  disease,  514  . 

from  portal  obstruction  due  to  syphilitic 
disease  of  liver,  360 
pyaemia,  79 
from  splenic  anaemia,  287 
from  syphilitic  disease  of  liver,  287 
from  typhoid  fever,  288  .  . 

from  universal  chronic  perihepatitis,  172 
dilatation  of  communications  between  portal 
vein  and  general  systemic 
veins  in,  209 
bad  effects  and  results,  213 
diseases  of  heart  in,  223 
drugs  in,  296 
duration,  278 
dyspepsia  in,  as  symptom,  229 

treatment,  297 
dyspeptic,  184 
early  stage,  225 
engorgement  of  portal  vein  in,  treatment,  298 


778 


INDEX. 


Cirrhosis,  enlargement  of  liver  in,  differentia- 
tion from  hydatid  cysts,  403 
in  prognosis,  291 
of  spleen  in,  cause,  216 
in  prognosis,  291 

epistaxis  in,  274 

etiology,  179 

facial  aspect  in,  227 

false  hamoptysis  in,  273 

fatty  ascites  in,  245 

fever  in  prognosis,  293 

fibrosis  of,  nature  of,  195 

flush  area  of,  227 

functional  activity  of  kidneys  in  prognosis, 
293 

gall-bladder  in,  208 

gall-stones  in,. 208 

general      communications     between      retro- 
peritoneal veins  in,  209 

geographical  distribution,  180 

glycosuria  as  symptom,  232 

gout  in,  284 

gumma  of  liver  imitating,  359 
of  liver  in,  356 

hffimatemesis    Ln,    262.       See    also    Hamat- 
emesis  in  cirrhosis. 


See  also  Hemorrhage 
See  also  HcEinorrhage 


hsematuria  in,  274 
hsemoptysis    in,   273. 

in  cirrhosis. 
hgemorrhage  in,   273. 

in  cirrhosis. 
hsemorrhagic  ascites  in,  245 
heart  in,  223 
hemorrhoids  in,  273 
hepatic  artery  in,  214  ; 

pain  as  sjTnptom,  237 
heredity  as  cause,  181 
histology,  202 

hiTJerplasia  of  liver  cells  in  treatment,  299 
hj'persplenomegalic  biliary,  318 
hj-pertrophic  biliary,   306.     See  also  Hyper- 
trophic biliary  cirrhosis. 
in  children,  332 

clinical  features,  333 

in  India,  335 
intestine  in,  morbid  appearances,  219 
jaundice  as  s\Tnptoni,  228 
kidneys  in,  223 

morbid  appearances,  220 
Laennec's,  178 
late  stage,  225 
latency,  226 
lead  as  cause,  186 

liver  and  spleen  in,  relation  between  size  of, 
217 

cells  in,  206,  207 

substance  in  treatment,  298 

symptoms,  236 
malarial,  305 
maligna,  473 
melsena,  272 

treatment,   273 
menorrhagia  in,  275 
mental  disturbance  in,  276 
method  of  death,  279 
metrorrhagia  in,  275 

micro-organisms    from   alimentary    canal   as 
cause,   190 

in  circulation  producing  poisons  as  cause, 
193 
milky  ascites  in,  245 
minor  signs  and  symptoms,  227 
mixed,  176 
monolobular,  176 
morbid  anatomy,  197 

appearances  in  liver  in,  199 
multilobular,   176,   178 

parasj-philitic,    378.     See    also    Parasyph- 
ilitic  multilobular  cirrhosis. 
multiple  adenoma  and,  relationship,  456 
naphthol  as  cause,  186 
nervous  symptoms,  276 
newly  formed  bile-ducts  in,  196,  205 
non-fatty  ascites  in,  245 
nutrition  in  prognosis,  291 
obstructive  biliary,   326.     See  also  Obstruc- 
tive biliary  cirrhosis. 
occupation  as  cause,  180 


Cirrhosis,  oedema  of  feet  as  symptom,  239 

of  legs  in  prognosis,  293 
oesophagus  in,  morbid  appearances,  218 
offensive  breath  as  sjinptom,  229 
pain  in,  treatment,  297 

palliative  and  symptomatic  treatment,  297 
pancreas  in,  morbid  appearances,  219 
paralysis  in,  278 
parasyphUitic    multilobular,    378.     See    also 

Parasyphiliiic  multilobular  cirrhosis. 
pathogeny,   181 
pericellular,  176 

of  hereditarj'  syphilis,  333 
peripheral  neuritis  in,  283 
peritonitis  in,  222,  284 

of  liver  in  prognosis,  291 
pigmentary,  of  heemochromatosis,  300.     See 

also     Pigmentary    cirrhosis    of    hemochro- 
matosis. 
pigmented,  299 
piles  in,  273 

pleurisy  with  effusion  in,  282 
poisons  in  circulation  as  cause,  192 

manufactured  in  intestine  as  cause,  186 
in  spleen  as  cause,  189 

other  than  alcohol  as  cause,  184 
portal,  178.     See  also  Cirrhosis. 

vein  in,  209 
primary  carcinoma  ■with,  473 
clinical  aspects,  478 

sarcoma  with,  482 
prognosis,  289 

age  in,  291 

ascites  in,  292 

complications  in,  293 

effect  of  treatment  in,  290 

enlargement  of  liver  in,  291 
of  spleen  in,  291 

fever  in,  293 

functional  activity  of  kidneys  in,  293 

general  nutrition  iii,  291 

hffimatemesis  in,  292 

hsemorrhage  in,  292 

cedema  of  legs  in,  293 

period  of  disease  in,  290 

size  of  liver  in,  291 
pruritus  in,  276 

pseudobile  canaliculi  in,  196,  205 
pulmonary  tuberculosis  in,  221 
relation  between  size  of  liver  and  spleen  in, 

217 
renal  disease  in,  223,  284 
respiration  as  symptom,  235 
saliva  in,  229 
sarcoma  with,  482 
secondary  infections  in,  284 
sex  in,  180 
signs,  minor,  227 
size  and  weight  of  liver  in,  197 

of  liver  in  prognosis,  291 
skin  in,  227 

small  intestine  in,  morbid  appearances,  219 
spa  treatment,  296 
spleen  in,  214,  238 

enlargement  of,  cause,  216 

liver  and,  relation  between  size  of,  217 

microscopic  appearances,  216 

morbid  appearances,  215 
stomach  in,  morbid  appearances,  218 
symptomatic  and  palliative  treatment,  297 
symptoms,  227 

temperature  as  sjTnptom,  235 
terminal  infections  in,  284 
termination,  279 
thrombosis  in,  285 
treatment,  294 

carbohydrate  food  in,  296 

diet  in,  295 

drugs  in,  296 

effect  of,  on  prognosis,  290 

hvperplasia  of  liver  cells  in,  299 

spa,  296 

symptomatic  and  palliative,  297 

to    prevent    and    remove    factors    which 
favour  morbid  changes  in  liver,  294 

to  promote  compensatory  mechanisms,  299 
tuberculosis  associated  with,  elsewhere  than 

liver,  346 


INDEX. 


779 


Cirrhosis,  tuberculosis  in,  221,  281 
of  liver  associated  with,  345 
tuberculous  peritonitis  in,  222 
typhoid  fever  as  cause,  188 
umbilical  vein,  189 
urea  in,  231 
urine  in,  230 

urotoxic  coeflBcient  as  symptom,  233 
venous,  178 

bruits  as  symptom,  238 
vomiting  in,  treatment,  297 
wasting  as  symptom,  229 
weight  and  size  of  liver  in,  197 
Climate  as  disposing  factor  in  tropical  abscess, 

126 
Cloudy  swelling  of  liver,  5 
Clubbing  of  fingers  in  cirrhosis,  228 

in  hypertrophic  biliary  cirrhosis,  319 
Coefficient,  urotoxic,  as  symptom  of  cirrhosis, 

233 
Colic,  biliary,  723 

acute,  treatment,  734 
complications,  729 
diagnosis,  729 
differential  diagnosis,  730 
differentiation  from  acute  catarrhal  chole- 
cystitis, 600 
dyspepsia,  731 
pancreatitis,  732 
from  angina  pectoris,  733 
from  appendicitis,  731 
from  cholecystitis,  730 
from  colitis,  731 
from  duodenal  ulcer,  730,  731 
from  enteralgia,  732 
from  floating  kidney,  730 
from  hepatalgia,  732 
from  hepatic  crises  in  tabes,  732 
from  hyperchlorhydria,  731 
from  intestinal  sand,  731 
from  lead  colic,  732 
from  lumbago,  733 

from    neuralgia    of    abdominal    sympa- 
thetic, 732 
of  liver,  732 
from  renal  colic,  730 
from  ulcer  of  stomach,  730 
jaundice  in,  728 
onset,   724 
pain  in,  724 
prognosis,  733 
signs,  724 
symptoms,  724 
termination,  729 
treatment,   733 
surgical,   735 
lead,  differentiation  from  biliary  colic,  732 
renal,  differentiation  from  biliary  colic,  730 
Colitis,  differentiation  froni  biliary  colic,  73 1_ 
Colon  baciUus  in  production  of  cholelithiasis, 
704 
carcinoma  of,  as  cause  of  secondary  malig- 
nant disease  of  liver,  496 
transverse,      carcinoma     of,      differentiation 
from  carcinoma  of  gall-bladder,  635 
fajcal     accumulation     in,      differentiation 
from   carcinoma   of   gall-bladder, 
636 
from  malignant  disease  of  liver,  520 
Coma  in  cirrhosis,  277 

Common  cirrhosis,  178.     See  also  Cirrhosis. 
Congenital  cirrhosis,  333 

diaphragmatic  hernia,  displacement  of  liver 

from,  17 
ectopia  of  liver,  16 
malpositions  of  liver,  16 

obliteration    of    bile-ducts,    639.     See    also 
Bile-ducts,  congenital  obliteration  of. 
Congestion  of  liver,  acute,  109 
clinical  picture,  110 
duration,  111 
morbid  anatomy,   110 
prophylaxis,  112 
treatment.    111 
Conglomerate  gall-stones,  718 
Constipation  as  cause  of  cholelithiasis,  709 
of  jaundice,  551 
as  symptom  of  cirrhosis,  2.30 


Constipation  in  cirrhosis,  treatment,  297 

in  portal  pyaemia,  76 
Convulsions  in  cirrhosis,  278 
Corset  liver,  8 
Courvoisier's  law,  694 
Crises,  hepatic,  in  tabes,   differentiation  from 

biliary  colic,  732 
Croupous  cholecystitis,  603 
Cutaneous  biliary  fistula,  757 
Cyanotic  atrophy  of  liver,  85 
Cystic  adenoma  of  gall-bladder,  618 

disease  of  kidneys,  association  of  cystic  dis- 
ease of  liver  with,  446 
of  liver,  445 
age  in,  446 

association  with  cystic  disease  of  kid- 
neys, 446 
clinical  picture,  451 
degenerative  theories,  450 
developmental  theory,  450 
frequency,   445 
in  infants,  445 
inflammatory  theory,  449 
microscopic  appearances,  447 
morbid  anatomy,  446 
new  formation  theory,  450 
pathology,   449 
sex  in,  446 
treatment,   452 
duct,   gall-stones  in,   distended  gaU-bladder 
from,  737 
mechanical  effects,  737 
infiamrctation  in,  from  gall-stones,  750 
tumors  of  bile-ducts,  651 
clinical  features,  652 
prognosis,  652 
treatment,   652 
Cysts,   abdominal,   differentiation  from  ascites 
in  cirrhosis,  250 
bile-containing,      in      communication      with 

ampulla  of  Vater,  652 
due  to  biliary  obstruction,  441 
hydatid,     differentiation     from     ascites     in 
cirrhosis,  250 
of  bile-ducts,  682 
of  gall-bladder,  616 
of  liver,    389.     See   also   Hydatid  cysts   of 

liver. 
suppurating,  as  cause  of  tropical  abscess, 
125 
differentiation  from  tropical  abscess,  148 
in  cirrhosis,  441 
of  gall-bladder,  618     _ 

ovarian,     differentiation     from     ascites     in 
cirrhosis,  248 
from  hydatid  cysts  of  liver,  407 
pancreatic,  as  cause  of  jaundice,  548 

differentiation     from      hydatid     cysts     of 
liver,  406 
from  tropical  abscess,   150 
parasitic,  of  liver,  441 
parovarian,    differentiation    from    ascites    in 

cirrhosis,  248 
peripancreatic,   differentiation   from  hydatid 

cysts  of  liver,  406 
pseudo-formation  of,  in  secondary  malignant 

disease  of  liver,  489 
simple,  of  liver,  441,  442 
clinical  features,  443 
diagnosis,  444 

differentiation  from  hydatid  cysts,  402 
microscopic  appearances,  443 
mode  of  formation,  442 
morbid  anatomy,  442 
treatment,  444 


Debility  as  symptom  of  cirrhosis,  228 
Deformities,  acquired,  of  liver,  8 
Delirium  in  cirrhosis,  277 

tremens  in  cirrhosis,  277 
Diabfete  bronzd,  220,  232,  300 
Diabetes  as  cause  of  cholelithiasis,  711 
Diaphragm,  morbid  appearances,  in  cirrhosis, 

220 
Diaphragmatic  furrows,  10 

hernia,  congenital,  displaced  liver  from,  17 
displaced  liver  in,  17 


780 


INDEX. 


Diaphragmatic  sulci,  10 
Diarrhcea  as  symptom  of  cirrhosis,  230 
in  carcinoma  of  ampulla  of  Vater,  701 
in  cirrhosis,  treatment,  297 
in  portal  pyEemia,  76 
thrombosis,   63 
Diet  as  cause  of  cholelithiasis,  708 

as  disposing  factor  in  tropical  abscess,  128 
in  hypertrophic  biliary  cirrhosis,  325 
Dilatation,    cylindrical,    of   common   bile-duct, 
from  gall-stones  in  common  bile-duct,  741 
of  bile-ducts,  651 

saccvdar,    of   common   bile-duct,    from   gall- 
stones in  common  bUe-duct,  741 
Dipping  for  liver,  248 
Discoloration,  postmortem,  of  liver,  5 
Dislocation  of  liver,  22 
Displaced  liver,  16 

abdominal  conditions  leading  to,  19 

acquired,  17  _ 

backwards,  abdominal  conditions  causing, 

21 
differentiation  from  malignant  disease,  519 
downwards,  abdominal  conditions  causing, 

19 
forwards,  abdominal  conditions  causing,  20 
from  congenital  diaphragmatic  hernia,  17 
from  effusion  into  right  pleural  cavity,  18 
from  emphysema  of  lung,  19 
from  malignant  disease  of  lung,  19 
from  pericardial  effusion,  19 
from  pneumonia,  19 
from  tight  lacing,  IS 
in  diaphragm.atic  hernia,  17 
in  rickets,  18 
in  spinal  curvature,  18 
thoracic  conditions  giving  rise  to,  18 
upwards,  abdominal  conditions  causing,  20 
Distoma  in  bile-ducts,  677 
clinical  aspects,  677 
morbid  anatomy,  677 
Distomum  conjunctivum  in  bile-ducts,  677 
hepaticum  in  bile-ducts,  677 
in  gall-bladder,  616 
lanceolatum  in  bile-ducts,  677 
sinense  in  bile-ducts,  677 
Diuretics  in  ascites  due  to  cirrhosis,  261 
Diverticulum    of    Vater,    carcinoma    of,     697. 

See  also  Ampulla  of  Vater,  carcinoma  of. 
Double  gall-bladder,  589 
Drainage,  continuous,  in  ascites  due  to  cirrhosis, 

256 
Drugs  in  cirrhosis,  296 
Duodenal  fistula,  757 

Duodenum,  carcinoma  of,  as  cause  of  jaundice, 
544 
lesions  of,  as  cause  of  jaundice,  544 
rupture  into,  in  tropical  abscess,  145 
ulcer  of,  as  cause  of  hgematemesis  in  cirrhosis, 
266 
of  jaundice,  544 
of  portal  pyaemia,  266 
differentiation  from  biliary  colic,  730,  731 
Dwarfing  of  left  lobe  of  liver,  ,3 
Dysentery  as  cause  of  tropical  abscess,  120 
Dyspepsia,  acute,   differentiation  from  biliary 
colic,  731 
as  symptom  of  cirrhosis,  229 
in  carcinoma  of  gall-bladder,  632 
in  cirrhosis,  treatment,  297 
Dyspeptic  cirrhosis,  184 


Eclampsia,     puerperal,     as    cause    of    portal 

thrombosis,  57 
Ectopia,  congenital,  16 
Electrolysis  in  hydatid  cysts  of  liver,  409 
Embolism  of  hepatic  artery,  45 
as  cause  of  infarcts,  106 
veins,  51 

of  portal  vein,  80 

as  cause  of  infarcts,  105 

retrograde,  as  cause  of  infarcts,  106 
Embryoma  of  liver,  467 
Emotional   jaundice,   spasm   of  muscular  coat 

of  bile-ducts  as  cause,  541 
Emphysema  of  lung,  displaced  liver  from,  19 
Emphysematous  liver,  5 


Empyenia   of  gall-bladder   from   acute   chole- 
cystitis, 601 
Endarteritis  obliterans  as  cause  of  infarcts,  106 
Endocarditis,    infective,    portal    pyaemia   and, 

differentiation,  78 
Endophlebitis  of  hepatic  veins,  50 
of  portal  vein,  80 
chronic,  80 
England,  occurrence  of  tropical  abscess  in,  127 
Engorgement  of    liver,  chronic  venous,  differ- 
entiation from  malignant  disease,  518 
of  portal  vein  in  cirrhosis,  treatment,  298 
Enlargement  of  gall-bladder  in  jaundice,  535 
of  glands  in  portal  fissure  as  cause  of  jaundice 

542 
of  hepatic  artery,  46 

of  liver,  differentiation  of  cirrhosis  from,  286 
gummatous,  differentiation  from  hydatid 

cysts,  404 
in  cirrhosis,   differentiation  from  hydatid 

cysts,  404 
in  prognosis  of  cirrhosis,  291 
malarial,  differentiation  from  cirrhosis,  286 
painless,      differentiation     from     hydatid 
cysts,  404 
of  spleen  in  cirrhosis,  cause,  216 
in  portal  pyaemia,  76 

thrombosis,  62 
in  prognosis  of  cirrhosis,  291 
Enteralgia,  differentiation  from  bUiary  colic,  732 
Epiplopexy  in  ascites  due  to  cirrhosis,  258 
Epistaxis  in  cirrhosis,  274 
Epithelioma  trab^culaire,  475 
Extra-hepatic  bile-ducts,  malignant  disease  of, 
683.     See    also    Malignant   disease   of   larger 
bile-ducts. 


Facets  on  gall-stones,  722 
Facial  aspect  in  cirrhosis,  227 
Fsecal  accumulation  in  transverse  colon,  differ- 
entiation from  carcinoma  of  gall- 
bladder, 636 
from  malignant  disease  of  liver,  520 
Faeces  in  congenital  obliteration  of  bUe-ducts, 
647 
in  jaundice,  533 
Farre's  tubercles,  487 
Fatty  ascites  in  cirrhosis,  245 
liver,  423 

clinical  picture,  427 
diagnosis,  429 
etiology,  423 
histology,  426 
morbid  anatomy,  425 
prognosis,  429 
signs,  427 
symptoms,  428 
treatment,  429 
tumors  of  gall-bladder,  619       _ 
Feet,  oedema  of,  as  symptom  of  cirrhosis,  239 
in  malignant  disease  of  liver,  511 
in  tropical  abscess,  141 
Feigned  jaundice,  538 
Fibrinous  cholecystitis,  603 
Fibroma  of  bile-ducts,  682 
of  gall-bladder,  618 
of  liver,  466 
Fibromyoma,  uterine,  gall-stones  and,  713 
Fibrosis  of  cirrhosis,  nature  of,  195 

sporadic,  176 
Fingers,  clubbing  of,  in  cirrhosis,  228- 

in  hypertrophic  biliary  cirrhosis,  319 
hippocratic,  228 
Fissure,  portal,  lymphatic  glands  in,  83 
Fistula  between  bile-ducts  themselves,  761 
biliary  and  gastro-intestinal  tracts,  757 

tract  and  small  intestine,  760 
gall-bladder  and  kidneys,  762 
and  portal  vein,  762 
and  urinary  bladder,  762 
pericardium  and  biliary  tract,  762 
biliary,  756 

cutaneous,  757 
external,  757 
gastric,  758 
bronchobiliary,      760.     See     also     Broncho- 
biliary  fistula. 


INDEX. 


781 


Fistula,  cholecystocolic,  759 
cholecystoduodenal,  758 
choledochoduodenal,  758 
duodenal,  757 

in  extension  of  carcinoma  of  gall-bladder,  625 
Floating  kidney  as  cause  of  jaundice,  546 
differentiation  from  biliary  colic,  730 
from  carcinoma  of  gall-bladder,  636 
lobe  of  liver,  12 
Fluid,  restriction  of,  in  ascites  due  to  cirrhosis, 

262 
Flush  area  of  cirrhosis,  227 
Foaming  liver,  5 

etiology,  6 
Foreign  bodies  as  cause  of  cholelithiasis,  707 
in  bile-ducts  as  cause  of  jaundice,  539 
in    mesenteric    veins   as   cause    of    portal 
pyajmia,  69 
Fracture,  spontaneous,   of  gaU-stones  in  gall- 
bladder, 722 
Functional  disease  of  liver,  36 

treatment,  41 
Furrows,  diaphragmatic,  of  liver,  10 


Gall-bladder,  abnormalities  of,  589 
in  size  and  shape,  590 
absence  of,  589 
dilated,  tropical  abscess  and,  differentiation, 

152 
diseases  of,  589 

distended,  from  calculi  in  cystic  duct,  737 
double,  589 

effect  of  tight  lacing  on,  14 
in  cirrhosis,  208 

in  congenital  obliteration  of  bile-ducts,  645 
in  jaundice,  553 

in  malignant  disease  of  larger  bile-ducts,  689 
inflammatory    thickening    around,    differen- 
tiation from  malignant  disease  of  liver,  520 
malposition  of,  589 
Gall-stones,  703.     See  also  Cholelithiasis. 
as  cause  of  jaundice  in  newborn,  561 
of  portal  pyaemia,  71 
of  suppurative  pylephlebitis,  756 
biliary  fistula  from,  756.     See  also  Fistula, 
biliary. 
gastric  fistula  from,  758 
bilirubin,  mixed,  717 
bilirubin-calcium,  pure,  718 
bronohobiliary  fistula  from,  760.     See    also 

Bronchobiliary  fistula. 
calcium  carbonate,  718 
cause  of  passage  out  of  gall-bladder,  723 
cholecystitis  from,  747 
cholecystocolic  fistula  from,  759 
cholecystoduodenal  fistula  from,  758 
choledochoduodenal  fistula  from,  758 
cholesterin,  717 

amorphous  and  crystalline,  718 
laminated,  717 
mixed,  717 
pure,  717 
classification,  717 

colic  from,  723.     See  also  Colic,  biliary. 
common,  717 
conglomerate,  718 

differentiation  from  carcinoma  of  gall-blad- 
der, 634 
from  malignant  disease  of  larger  bile-ducts, 
694 
duodenal  fistula  from,  757 
facets  on,  722 

fistula  between  bUe-ducts  themselves  from, 
.761 
biliary      and     ''gastro-intestinal     tracts 
from,  757 
tract  and  small  intestine  from;  760 
gall-bladder  and  kidneys  from,  762 
and  portal  vein  from,  762 
and  urinary  bladder  from,  762 
pericardium  and  biliary  tract  from,  762 
of  duodenum  from,  757 
foreign  bodies  in,  718 
gumma  of  liver  resembling,  363 
hemorrhage  of  gall-bladder  from,  747 
hour-glass  contraction  of  gall-bladder  from, 
747 


Gall-stones  in  ampulla  of  Vater,  inflammatory 
effects,  756 
mechanical  effects,  741 
in  cirrhosis,  208 

in  common  bile-duct,  cylindrical  dilatation 
from,  741 
differentiation   from   malignant   disease 

of  liver,  519 
intermittent    hepatic    fever   from,    750. 

See  also  Intermittent  hepatic  fever. 
mechanical  effects,  739,  741 
number,  740 
pancreatitis  from,  755 
saccular  dilatation  from,  741 
situation,  739 
in  cystic  duct,  mechanical  effects,  737 
in  gall-bladder,  formation  of,  mode  of,  718 
time  required,  719 
mechanical  effects,  735 
number,  719 
shape,  719 
situation,  720 
size,  719 

spontaneous  fracture  of,  722 
in  primary  carcinoma  of  liver,  480 
infective  changes  set  up  by,  746 
inflammation  and  infective  changes  in  com- 
mon bile-duct  from,  750 
in  cystic  duct  from,  750 
inflammatory  and  infective  changes  in  gall- 
bladder from,  746 
changes  set  up  by,  746 
intestinal   obstruction  from,   742.     See  also 

Intestinal  obstruction  from  gall-stones. 
mechanical  effects,  735 

in  ampulla  of  Vater,  741 
in  common  bile-duct,  739 
in  cystic  duct,  737 
in  gall-bladder,  735 
passage  of,  into  intestines,  results,  760 
perforation  of  gall-bladder  from,  748 

into  general  cavity  of  peritoneum,  748 
into  localised  pocket  of  peritoneum  cut 
off  byadhesions,  748 
pericholecystic  adhesions  from,  749 
relation  of  carcinoma  of  gall-bladder  to,  627 
of  malignant   disease   of  larger  bile-ducts 
to,  684 
removal  of,  768 
rupture  and  perforation  of  gall-bladder  into 

peritoneum  from,  762 
scars  of  gall-bladder  from,  747 
ulceration  of  gall-bladder  from,  into  liver,  748 
of  hepatic  artery  from,  762 
Gangrene     of     gall-bladder,      611.     See     also 

Cholecystitis,  gangrenous. 
Gangrenous   cholecystitis,  611.     See  also  Cho- 
lecystitis, gangrenous. 
pancreatitis  as  cause  of  portal  pysemia,  70 
Gastric  arteries,  erosions  of,  hsematemesis  diie 
to,    differentiation    from    hcematemesis   in 
cirrhosis,  269 
disturbances  as  symptoms  of  malignant  dis- 
ease of  liver,  .512 
fistula,  biliary,  758 

veins,  varicose,  as  cause  of  ha?matemesis  in 
cirrhosis,  268 
Gastritis  as  cause  of  hiematemesis  in  cirrhosis, 

265 
Gastro-intestinal   symptoms   of  portal  throm- 
bosis, 62 
tract  in  acute  yellow  atrophy,  573 
Gastroptosis  as  cause  of  jaundice,  550 
Gin-drinker's  liver,  178 

Glands   in    portal   fissure,   enlargement   of,   as 
cause  of  jaundice,  542 
lymphatic,  in  hypertrophic  biliary  cirrhosis, 
315 
in  portal  fissure,  83 
morbid  conditions  of,  83 
mesenteric,  suppurating,  as  cause  of  portal 

pyaemia,  70 
suprarenal,    as    site    of    primary    malignant 
disease  in  secondary  malignant  disease 
of  liver,  500 
new  growths  of,  as  cause  of  jaundice,  545 
tumors  of,  differentiation  from  malignant 
disease  of  liver,  520 


782 


INDEX. 


GMnard's  disease  as  cause  of  cholelithiasis,  710 
Glycosuria  as  symptom  of  cirrhosis,  232 
Gout  in  cirrhosis,  284 
Granular  liver,  200 
Gum,  yellow,  5.57 
Gumma  of  liver,  350 
age  in,  357 
association    with    lardaceous    change    in 

hver,  356 
causes,  357 

predisposing,  357 
clinical  manifestations,  358 
diagnosis,  364 
frequency,  356 
imitating  cirrhosis,  359 

hepatic  tumors,  361 
in  cirrhosis,  356 
method  of  formation,  350 
microscopic  appearances,  352 
number,   355 
predisposing  causes,  357 
prognosis,  364 

resembling  chronic  splenic  ansemia,  363 
gall-stones,  363 

hypertrophic  biliary  cirrhosis,  363 
lardaceous  disease,  360 
perihepatitis,  360 
simple  chronic  peritonitis,  360 
retrogressive  changes  in,  354 
striation,  355 
structure,  350 

syphilitic  cicatrices  combined  with,  356 
differentiation    from    universal    chronic 
perihepatitis,  173 
treatment,   365 
surgical,   366 
with  fever  resembling  hepatic  suppuration, 
362 
of  portal  fissure  as  cause  of  jaundice,  543 
Gummatous  enlargement  of  liver,   differentia- 
tion from  hydatid  cysts,  404 
inflammation  as  cause  of  portal  thrombosis, 
57 


H^MATEMEsis  in  cirrhosis,  262 

differentiation   from  hsematemesis   due  to 
carcinoma  of  stomach,  269 
due  to  erosions  of  gastric  arteries,  269 
due  to  gastric  ulcer,  269 
due  to  other  causes,  268 
due  to  splenic  ansemia,  270 
duodenal  ulcer  as  cause,  266 
etiology,  265 
frequency,  263 
gastric  ulcer  as  cause,  266 
gastritis  as  cause,  265 
hemorrhage  from  pharynx  as  cause,  268 
minute  erosions  of  gastric  mucous  mem- 
brane as  cause,  265 
prognosis,  270 
treatment,  270 

varicose  gastric  veins  as  cause,  268 
oesophageal  veins  as  cause,  266 
in  prognosis  of  cirrhosis,  292 
Hsematogenous  jaundice,  527,  528 
Hsematoidin  in  liver,  436 
Hsematuria  in  cirrhosis,  274 
Hsemic  infections,  acute  cholecystitis  from,  592 
Hsemochromatosis,  pigmentary  cirrhosis  of,  300. 
See  also  Pigmentary  cirrhosis  of  hcemochroma- 
fosis. 
Hffimohepatogenous  jaundice,  530 

differentiation  from  jaundice,  531 
Haemophoeic  jaundice,  529 
Hajmopty.sis,  false,  in  cirrhosis,  273 

in  cirrhosis,  273 
Hemorrhage  from  bowel  in  cirrhosis,  272 

from  pharynx  as  cause   of  haematemesis  in 

cirrhosis,  268 
in  carcinoma  of  gall-bladder,  624 
in  cirrhosis,  273 
from  larynx,  273 
from  lungs,  274 
from  nose,  274 
general,  275 
treatment,   276 
in  congenital  obliteration  of  bile-ducts,  647 


Haemorrhage  in  hypertrophic  biliary  cirrhosis, 
319 
in  jaundice,  537 

in  malignant  disease  of  liver,  505 
in  prognosis  of  cirrhosis,  292 
of  gall-bladder  from  gall-stones,   747 
Haemorrhagic  ascites  in  cirrhosis,  245 

infarct,  traumatism  as  cause,  116 
Haemosiderin  in  liver,  435 

Perl's  test  for,  436 
Heart,  diseases  of,  in  cirrhosis,  223 
in  acute  yellow  atrophy,  573 
in  hypertrophic  biliary  cirrhosis,  320 
Heart-disease  as  cause  of  cholelithiasis,  710 
Hemorrhoids  in  cirrhosis,  27.3 
Hepatalgia,   differentiation   from  biliary  colic, 

732 
Hepatic  abscess,  120.     See  also  Abscess. 

and   portal    vein    thrombosis,    combined,    as 

cause  of  infarcts,  106 
aneurysm,  age  and  sex  in,  43 
as  cause  of  jaundice,  550 
causation,  43 
diagnosis,  45 
differentiation     from     hydatid     cysts     of 

artery,  404 
symptoms,  44 
treatment,  45 
artery,   aneurysm  of,   43.     See  also   Hepatic 
aneurysm. 
arteriosclerosis  of,  46 
diseases  of,  43 
embolism  of,  45 

as  cause  of  infarcts,  106 
enlargement  of,  46 
in  cirrhosis,  214 
thrombosis  of,  45 

tubercle  bacilli  in  liver  through,  337 
ulceration  of,  from  gall-stones,  762 
asystole,  85 

fever,  intermittent,  750.     See  also  Intermit- 
tent hepatic  fever. 
hypernephroma,  479 
pain  as  symptom  of  cirrhosis,  237 

of  malignant  disease  of  liver,  512 
suppuration,  portal  pyaemia  and,  differentia- 
tion, 78 
veins,  chronic  periphlebitis  of,  50 
diseases  of,  47 
embolism  of,  51 
endophlebitis  of,  50 

entrance  of  typhoid  bacilli  into  gall-blad- 
der by,   595 
extension  of  primary  carcinoma  into,  480 
obstruction    of,   by  new-growth,   as  cause 

of  infarcts,  105 
rupture  into,  in  liydatid  cysts  of  liver,  417 

in  tropical  abscess,  145 
stricture  of,  48 

symptoms,  50 
suppurative  phlebitis  of,  51 
thrombosis  of,  47 
diagnosis,  48 
treatment,  48 
Hepatism,  26,  39 
Hepatitis,  acute,  114 
diagnosis,  118 

differentiation  from  tropical  abscess,  151 
morbid  anatomy,  114 
symptomatology,  117 
treatment,  118 
interstitial,  chronic,  178 
nodular,  455 
Hepatocele,  16 

Hepatogenous  albuminuria,  510 
Hepatoma,  456 
Hepatomphalos,  1 6 
Hepatoptosis,  22 
age  in,  23 

as  cause  of  jaundice,  5.50 
associated  conditions  in,  26 
complications,  28 
diagnosis,  32 

differential,  32 
etiology,  24 

exciting,  26 
frequency,  23 
history,  22 


INDEX. 


783 


Hepatoptosis,  neurasthenia  and,  26 
onset,  29 
partial,   12 
physical  signs,  28 
sex  in,  23 
symptoms,  29 

absence  of,  32 
total,  existence  of,  22 

forms  of,  27 
treatment,  33 
visceroptosis  and,  26 
with  anteversion,  27 
Hereditary  jaundice  in  newborn,  562 

syphilis,  pericellular  cirrhosis  of,  333 
Herpetism,  39 

Hernia,    diaphragmatic,    congenital,    displaced 
liver  from,  17 
displaced  liver  in,  17 
Hiccough  in  portal  pycemia,  76 
Hippocratic  fingers,  228 
Hobnailed  liver,  178 
Hodgkin's  disease,  386 
clinical  evidence,  388 
differentiation  from  tropical  abscess,  152 
microscopic  appearances,  386 
morbid  anatomy,  386 
prognosis,  388 
treatment,   388  _ 
Hour-glass    contraction    of    gall-bladder    from 

gall-stones,  747 
Hydatid  cysts,  differentiation  from  ascites  in 
cirrhosis,  250 
of  bile-ducts,  682 
of  gall-bladder,  616 
of  liver,  389 
ages  in,  397 
alveolar,    419.      See    also    Multilocular 

hydatid  of  liver. 
clinical  picture,  397 
condition  of  remainder  of  liver  in,  394 
death  of,  changes  following,  393 
diagnosis,  401 

by    examination    of    fluid    from    ex- 
ploratory puncture,  402 
differential,  402 
differentiation  from  aneurysm  of  hepatic 
artery,  404 
from  ascites,  407 
from  carcinoma,  403 
from  cholecystitis,  403 
from  cirrhosis,  287 
from  conditions  in  anterior  abdominal 

wall,  403 
from  gummatous  enlargement,  404 
from  hydatid  cysts  of  pleural  cavity, 

405 
from  large  cirrhotic  liver,  403 
from  malignant  disease,  402,  516 
from  ovarian  cysts,  407 
from  painless  enlargement,  404 
from  pancreatic  cysts,  406 
from  peripancreatic  cysts,  406 
from  renal  growths,  406 
from  simple  cysts,  402 
from  subphrenic  abscess,  404 
from  suppuration,  404 
from  suprarenal  growths,  407 
duration,  407 
electrolysis  in,  409 

embedded  in  substance   of  liver,   diag- 
nosis, 403 
etiology,  395 
age,  397 

geographical  distribution,  395 
method  of  infection,  396 
sex,  397 
frequency,  395 

geographical  distribution  in,  395 
injection  of  antiseptic  fluids  into  interior 

of  cysts  in,  409 
method  of  infection  in  cause  of,  396 
multilocular,  419.    See  also  Multilocular 

hydatid  of  liver. 
number,  391 
physical  signs,  398 
prognosis,  407 

projecting    downwards    into    abdomen, 
diagnosis,  405 


Hydatid    cysts     projecting    downwards    from 
anterior  surface,  diagnosis,  402 
upwards  into  thorax,  diagnosis,  404 
rupture  in,   412.     See   also   Rupture  in 

hydatid  cysts  of  liver. 
sex  in,  397 
situation,  391 
size,  391 
spontaneous  death,  391 

causes,  392 
sterile,  390 
structure,  390 

suppurating,  as  cause  of  tropical  abscess, 
.  125 
differentiation  from  tropical  abscess, 
148 
suppuration  in,  418 

mechanism,  418 
symptoms,  397 
tapping  in,  409 

accidents  and  bad   effects   following, 
410 
treatment,  409 
electrolysis,  409 
injection     of     antiseptic     fluids     into 

cyst,  409 
prophylaxis,  411 
surgical,  411 
tapping,  409 

accidents  and  bad  effects  following, 
410 
with      jaundice,      differentiation     from 
hypertrophic  biliary  cirrhosis,  323 
of     pleural     cavity,     differentiation    from 
hydatid  cysts  of  liver,  405 
thrill,  399 
Hydrops  of  gall-bladder  from  acute  cholecys- 
titis, 601 
Hypersemia  phlegmasique,  305 
Hvperchlorhydria,  differentiation  from  biliary 

colic,  731 
Hypernephroma,  hepatic,  479 
Hyperplasia  of  liver,  nodular,  455 

of  liver-cells  in  treatment  of  cirrhosis,  299 
Hypersplenomegalic  biliary  cirrhosis,  318 
Hypertrophic  alcoholic  cirrhosis,  198 
biliary  cirrhosis,  306 
age  in,  309 

alcoholism  as  cause,  .309 
alimentary  canal  in,  31.5 
arthritis  in,  320 
asplenomegalic  form,  307 
bacterial  origin,  312 
Banti's  disease  and,  differentiation,  324 

relation,  314 
blood  in,  321 
clinical  picture,  316 
clubbing  of  fingers  in,  319 
course,  316 
definition,  306 
diagnosis,  322 

differential,  322 
diet  in,  325 

differentiation  from  Banti's  disease,  324 
from  chronic  infectious  jaundice,  323 

jaundice,  323 
from    hydatid     cysts    in     liver    with 

jaundice,  323 
from  malaria,  323 
from  malignant  disease,  515 
of  larger  bile-ducts,  695 
from  obstructive  jaundice,  323 
from   pigmentary  cirrhosis  of  ha;mo- 

chromatosis,  304,  323 
from  portal  cirrhosis,  322 
from  syphilitic  disease  of  liver  with 

chronic  jaundice,  323 
from  Weil's  disease,  323 
duration,  324 
etiology,  309 
age  in,  .309 
heredity  in,  309 
malaria  in,  310 
sex  in,  .309 
forms,  307 

gumma  of  liver  resembling,  363 
hfflmorrhages  in,  319 
heart  in,  320 


784 


INDEX. 


Hypertrophic  biliary   cirrhosis,  hepatomegalic 
form,  307 

frequency,  308 
heredity  in,  309 
history,  306 

hypersplenomegalic  form,  307 
in  children,  334 
infective  origin,  310 
jaundice  in,  318 
kidneys  in,  316 
liver  in,  312,  317 

microscopic  appearances,  313 
IjTnphatic  glands  in,  315 
malaria  in  etiology  of,  310 
metasplenomegalic  form,  307 
morbid  anatomy,  312 
nervous  system  in,  320 
onset,  316 
ordinary  form,  307 
pancreas  in,  316 
physical  development  in,  319 

signs,  317 
presplenomegalic  form,  307 
prognosis,  324 
pseudobile  canaliculi  in,  314 
pulse  in,  320 

respiratory  system  in,  321 
sex  in,  309 
signs,  physical,  317 
spleen  in,  315,  318 
splenomegalic  form,  307 
symptoms,  317 
termination,  322 
treatment,  325 

diet  in,  325 

surgical,  326 
urine  in,  321 
with      jaundice,      differentiation     from 

cirrhosis,  285 


Iced  liver,  86.  97,  98,  164 
Icterus  gravis,  563 

differentiation  from  acute  yellow  atrophy, 
578 
Idiopathic  jaundice,  557.     See  also  Jaundice, 

idiopathic. 
India,  cirrhosis  in  children  in,  335 
Indigestion  as  cause  of  cholelithiasis,  709 
Infarcts  in  liver,  102 

ansemic,  morbid  anatomy,  103 

traumatism  as  cause,  107 
combined  portal  and  hepatic  vein  throm- 
bosis as  cause,  106         _ 
embolism  and   thrombosis  of  portal  vein 
as  cause,  105 
of  hepatic  artery  as  cause,  106 
endarteritis  obUterans  as  cause,  106 
etiologj^  104 

hsemorrhagic,  traumatism  as  cause,  106 
morbid  anatomy,  102 
obstruction  of  portal  or  hepatic  veins  by 

new-growth  as  cause,  105 
pathology,  107 

retrograde  embolism  as  cause,  106 
traumatism  as  cause,  106 
Infections,  secondary,  in  cirrhosis,  284 
Infectious  jaundice,  583 
mild,  in  newborn,  560 

treatment,  560 
severe,  in  newborn,  561 

due  to  general  infections,  561 
due  to  umbiUcal  infection,  561 
epidemic  forms,  561 
Infective    endocarditis,    portal    pyaemia    and, 
differentiation,  78 
jaundice,  584 
Infiltration,  leucocythcemic,  of  liver,  439 

leukEcmic,  of  liver,  439.     See  also  Leuhcemic 
infiltration  of  liver. 
Inflammation  from  adjacent  parts  as  cause  of 
tropical  abscess,  124 
gummatous,  as  cause  of  portal  thrombosis, 

57 
of     peritoneum,     concomitant,     ascites     in 

cirrhosis  due  to,  242 
syphilitic,  of  portal  vein,  as  cause  of  portal 
thrombosis,  54 


Inflammatory  conditions  causing  portal  throm- 
bosis, 52 
Insane,  cholelithiasis  in,  713 
Intermittent  hepatic  fever,  750 
clinical  features,  752 
complications,  752 
diagnosis,  753 

differentiation  from  malignant  disease, 
519 
from  tropical  abscess,  519 
prognosis,  753 
symptoms,  752 
treatment,  753 
surgical,  754 
Interstitial  hepatitis,  chronic,  178 

pancreatitis,  chronic,  as  cause  of  jaundice, 
549 
Intestinal  lithiasis,  differentiation  from  biliary 
colic,  731 
obstruction,    differentiation    from    cirrhosis, 
288 
from  gaU-stones,  742 
age  in,  744 

clinical  picture,  744  • 

diagnosis,  745 
duration,  745 

entrance  of  calculus  into  intestine,  742 
frequency,  742 
prognosis,  745 
sex  in,  744 
site,  744 
treatment,  745 
ulceration  as  cause  of  portal  pyEemia,  69 
Intestines,  hsemorrhage  from,  in  cirrhosis,  272 
in  pigmentary  cirrhosis  of  hsemochromatosis 

302 
in  portal  thrombosis,  61 
passage  of  gaU-stones  into,  results  of,  760 
poisons  manufactured  in,  as  cause  of  cirrhosis, 

186 
rupture  into,  in  hydatid  cysts  of  liver,  417 

in  tropical  abscess,  145 
small,  morbid  appearances,  in  cirrhosis,  219 
strangulation     of,     complicating    tropical 
abscess,  147 
Intra-abdominal  malignant  disease  as  cause  of 

portal  thrombosis,  55 
Intra-hepatic    bile-ducts,     small,     chronic    ca- 
tarrhal cholangitis  of,  672 
calculi,  721 
jaundice,  530 

differentiation  from  jaundice,  531 
pericholangitis,  673 

suppuration,    differentiation    from    cirrhosis, 
288 
from  malignant  disease,  517 
tumors  as  cause  of  jaundice,  541 
Intra-thoracic  conditions,  portal  pyaemia  and, 

differentiation,  78 
Iodine  stain  for  lardaceous  disease  of  liver,  431 


Jaundice,  526 

acholuric,  228,  529 

anaemia  in,  534 

aneurysm  of  abdominal  aorta  as  cause,  550 

of  hepatic  artery  as  cause,  550 

of  superior  mesenteric  artery  as  cause,  550 
as  symptom  of  cirrhosis,  228 
Ascaris  lumbricoides  as  cause,  539 
bilirubin  in,  536 
black,  532 

calculus  of  pancreas  as  cause,  550 
carcinoma  of  duodenum  as  cause,  544 

of  stomach  as  cause,  543   • 
catarrhal,    540,    655.      See    also    Catarrhal 

jaundice. 
cholangitis  as  cause,  540 
cholesterin  in,  537 

chronic,    differentiation    from    hypertrophic 
biliary  cirrhosis,  323 

interstitial  pancreatitis  as  cause,  549 

prognosis,  554 
circulatory  system  in,  534 
classification,  530 
constipation  as  cause,  551 
cysts  of  pancreas  as  cause,  548 
definition,  526 


INDEX. 


785 


Jaundice,  diagnosis,  538 
age  in,  552 

degree  and  intensity  in,  552 
differential,  539 
duration  and  progress  in,  552 
family  tendency  in,  552 
general  remarks  on,  551 
occuri-ence  of  pain  in,  552 
onset  in,  552 
sex  in,  552 
differential  diagnosis,  539 
differentiation  from  carcinoma  of  ampulla  of 
Vater,  701 
from  hypertrophic  biliary  cirrhosis,  323 
from  toxa»mic  jaundice,  531 
due  to  changes  in  walls  of  larger  ducts,  540 
due  to  obstruction  inside  lumen  of  duct,  539 
due  to  polycholia,  527,  528 
due  to  pressure  on  bile-duels  from  without, 

541 
due  to  suppression  of  bile-secreting  function 

of  liver,  527,  529 
duodenal  lesions  a?  cause,  544 
emotional,   spasm  of  muscular  coat  of  bile- 
ducts  as  cause,  541 
enlargement  of  gall-bladder  in,  535 

of  glands  in  portal  fissure  as  cause,  542 
etymology,  52G 
faeces  in,  533 
feigned,  538 

floating  kidney  as  cause,  546 
foreign  bodies  in  bUe-ducts  as  cause,  539 
gall-bladder  in,  553 
gastroptosis  as  cause,  550 
gumma  in  portal  fissure  as  cause,  543 
hsematogenous,  527,  528 
haernohepatogenous,  530 

differentiation  from  jaundice,  531 
hsemophopic,  .529 
hjEmorrhage  in,  537 
hepatoptosis  as  cause,  550 
hereditary,  in  newb.orn,  562 
idiopathic,   557 

clinical  characters,  559 
diagnosis,  .559 
etiology,  557 
frequency,  558 
morbid  anatomy,  558 
prognosis.  560 
in  acute  catarrhal  cholecystitis,  599 
in  biliary  colic,  728 
in  carcinoma  of  gaU-bladder;  631 
in  congenital  obliteration  of  bile-ducts,  647 
in  hypertrophic  oiliary  cirrhosis,  318 
in  malignant  disease  of  larger  bile-ducts,  691 

of  liver,  505,  506 
in  newborn,  557 

due  to  obstruction  or  organic  change,  561 
gall-stones  as  cause,  561 
hereditarv,  .562 
mild  forms.  557 
infectious,  560 
treatment,  560 
severe  forms,  560 
infectious,  561 

due  to  general  infections,  561 
due  to  umbilical  infections,  561 
epidemic  forms,  561 
in  phlegmonous  cholecystitis,  610 
in  portal  pyscmia,  75 

thrombosis,  63 
in  secondary  stage  of  syphilis  of  liver,  348 
clinical  features,  349 
diagnosis,  349 
onset,  349 
prognosis,  349 
.sex,  .349 
treatment,   349 
in  suppurative  cholecystitis,  606 
in  tropical  .ibscess,  138 
infectious,  .583 

chronic,  hypertrophic  biliary  cirrhosi.s  and, 

differentiation,  323 
mild,  in  newborn,  560 

treatment,  560 
severe,  in  newborn,  561 

due  to  general  infections,  561 
due  to  umbilical  infection,  561 

50 


Jaundice  in  severe  affections,  epidemic  forms, 
561 
infective,  584 
intra-hepatic,  530 

differentiation  from  jaundice,  531 
tumors  as  cause,  541 
liver  in,  535,  .553 
malignant,  56.3 

differentiation  from  acute  yellow  atrophj', 

578 
disease  of  pancreas  as  cause,  547 
new-growths  of  bile-duct  as  cause,  540 

of  kidneys  and  suprarenal  body  as  cause, 
545 
of  phosphorus  poisoning,  580 
clinical  manifestations,  .581 
diagnosis,  .583 
frequency,   580 
morbid  anatomy,  580 
pathogeny,  581 
prognosis,  583 
treatment,   583 
urine  in,  582 
ovarian  tumors  as  cause,  .551 
pancreatic  calculus  as  cause,  550 
cysts  as  cause,  550 
lesions  as  cause,  546 
parasites  as  cause,  539 
pathology,  527 
perigastritis  as  cause,  543 
peritoneal  adhesions  as  cause,  545 
physiological,     557.       See     also     Jaundice, 

idiopathic. 
pregnancy  as  cause,  551 
primary  growths  of  bile-ducts  as  cause,  540 
progno.sis,  554 
pruritus  in,  536 

treatment,   556 
respiration  in,  535 

retroperitoneal  tumors  as  cause,  546 
round-worms  as  cause,  539 
secretions  in,  534 
signs,  532 

simple,  5.57.     See  also  Jaundice,  idiopathic. 
spleen  in,  535 

stomach-lesions  as  cause,  543 
stricture  of  bile-ducts  as  cause,  540 
symptoms,  535 

due    to    absence    of    bile    from    intestinal 

tract,  538 
due  to  bile  in  circulation,  535 
due  to  poisons  other  than  bile  in  circula- 
tion, 537 
syphilitic  adenitis  as  cause,  542 
temperature  in,  535 
toxa^mic,  530 

differentiation  from  jaundice,  531 
treatment,   55.5 
palliative,  556 
symptomatic,  556 
ulcer  of  duodenum  as  cause,  544 

of  stomach  as  cause,  543 
urine  in,  532 
urobihu  in,  231,  529 
xanthop.sia  in.  536 
yellow  vision  in,  .536 

Kidneys,  cystic  disease  of,  association  of  cystic 
disease  of  liver  with,  446 
floating,  as  cause  of  jaundice,  546 

differentiation  from  biliary  colic,  730 
from  carcinoma  of  gall-bladder,  636 
functional  activity  of,  in  prognosis  of  cirrho- 
sis, 293 
in  acute  yellow  atrophy,  573 
in  cirrhosis,  223 

in  congenital  syphilis  of  liver,  372 
in  hyi)ortro|)hic  biliary  cirrhosis,  316 
in  universal  chronic  perihepatitis,  170 
morbid  ai^pearances,  in  cirrhosis,  220 
new-growths  of,  as  cause  of  jaundice,  545 
pelvis  (if,  rupture  into,  in  tropical  abscess,  145 
tumor     of,     differentiation    from    malignant 
disease  of  liver,  519 

Lacing,  tight,  displaced  liver  from,  IS 
effect  of,  on  gall-bladder,  15 


786 


INDEX. 


Laennec's  cirrhosis,  178 
Laminated  cholesterin  gall-stones,  717 
Lardaceous    change    in    liver,    association    of 
gumma  of  liver  with,  356 
disease  of  liver,  367,  430 

ascites     due     to,     differentiation     from 

ascites  in  cirrhosis,  252 
clinical  picture,  433 
diagnosis,  433 
differentiation   from   malignant   disease, 

515 
etiology,  430 
frequency,  430 

gumma  of  liver  resembling,  360 
iodine  stain  for,  431 
microscopic  examination,  432 
morbid  anatomy,  431 
pathogeny,  431 
prognosis,  434 
signs,  433 

staining  reactions,  432 
symptoms,  433 
treatment,  435 
Larynx,  hemorrhage  from,  in  cirrhosis,  273 
Le  foie  corde,  27 
Le  foie  en  gourde  de  pelerin,  27 
Lead  as  cause  of  cirrhosis,  186 

colic,  differentiation  from  biliary  colic,  732 
Legs,  oedema  of,  in  carcinoma  of  gall-bladder, 
632 
in  prognosis  of  cirrhosis,  293 
Leptothricial  cholelithiasis,  706 
Leuoocythaemic  infiltration  of  liver,  439 
Leukgemia,  differentiation  from  cirrhosis,  287 
Leuksemic  infiltration  of  liver,  439   • 
clinical  features,  440 
diagnosis,  440 

microscopic  appearances,  439 
morbid  anatomy,  439 
prognosis,  440 
treatment,  440 
Ligature    of    bile-ducts    in    production    of    ob- 
structive biliary  cirrhosis,  326 
Linguiform  lobe  of  liver,  12 
Lipoma  of  liver,  466 
Lithiemia  in  liver,  39 

Murchison's  theory,  39    _ 
Lithiasis,  intestinal,  differentiation  from  biliary 

colic,  731 
Liver,  abnormal  lobulation  of,  1 
accessory,  3 

acquired  deformities  of,  8 

and    lung,    passive    engorgement    in,    com- 
parison of,  89 
and    spleen,    relation    between    size    of,    in 

cirrhosis,  217 
appendicular  lobe  of,  12 

cells,  hyperplasia  of,  in  treatment  of  cirrhosis, 
299 
in  cirrhosis,  206,  207 
solitary  adenoma  derived  from,  453 
morbid  anatomy,  454 
chronic  venous  engorgement  of,  85.    See  also 

Nutmeg  liver. 
displaced,  16.     See  also  Displaced  liver. 
dulness  in  acute  yellow  atrophy,  576 
effects  of  biliary  obstruction  on,  329 

of  tuberculosis  elsewhere  in  body  on,  344 
factors   responsible   for   normal   position   of, 

24 
floating  lobe  of,  12 
functional  diseases  of,  36 

treatment,  41 
in  acute  catarrhal  cholecystitis,  599 
in  carcinoma  of  gall-bladder,  626 
in  congenital  obliteration  of  bile-ducts,  644 

syphilis  of  liver,  368 
in  hypertrophic  biliary  cirrhosis,  312,  317 

microscopic  appearances,  313 
in  jaundice,  535,  553 
in  malignant  disease  of  larger  bile-ducts,  690 

of  liver,  504 
in  nutmeg  liver,  92 
■  in  obstructive  biliary  cirrhosis,  330 
in  portal  pyaemia,  72,  76 

thrombosis,  59 
in  universal  chronic  perihepatitis,  169 
left  lobe,  dwarfing  of,  3 


Liver,  linguiform  lobe  of,  12 
malpositions  of,  congenital,  16 
minute  accessory  lobes,  3 
morbid  appearances  in,  in  cirrhosis,  199 
pathological     appearances     of,    in     tropical 

abscess,  130 
paths  by  which  tubercle  bacillus  reach,  337. 

See  also  Tubercle  bacillus. 
poisons  conveyed  to,  by  portal  vein,  182 
postmortem  appearances,  5 

discoloration  of,  5 
right  and  left  lobes,   alteration  in   relative 

size  of,  1 
size  of,  in  cirrhosis,  197 
substance  in  treatment  of  cirrhosis,  298 
symptoms  of  cirrhosis,  236 
tongue-like  lobes  of,  12 
transposition  of,  16 
weight  of,  in  cirrhosis,  197 

incidence  of  ascites  and,  relation  between, 
240 
Lumbago,  differentiation  from  bUiary  cohc,  733 
Lungs  and  liver,  passive  engorgement  in,  com- 
parison of,  89 
emphysema  of,  displaced  liver  from,  19 
hffimorrhage  from,  in  cirrhosis,  274 
in  portal  pysemia,  74 
in  tropical  abscess,  135,  139 
lesions  of,  as  cause  of  nutmeg  liver,  85 
malignant  disease  of,  displaced  liver  from,  19 
rupture  into,  in  hydatid  cysts  of  liver,  414 
in  tropical  abscess,  14.3 
Lymphadenoma  affecting  liver,  386.     See  also 

Hodgkin's  disease. 
Lymphangioma  of  liver,  465 
Lymphatic     glands     in     hypertrophic     bUiary 
cirrhosis,  315 
in  portal  fissure,  83 
morbid  conditions  of,  83 
vessels,  morbid  conditions  of,  83 

tubercle  bacilli  in  liver  through,  337 


Malaria    as    cause    of    hypertrophic    biliary 
cirrhosis,  310 
as  disposing  factor  in  tropical  abscess,  128 
hypertrophic    biliary    cirrhosis    and,    differ- 
entiation, 323 
tropical  abscess  and,  differentiation,  151 
Malarial  cirrhosis,  305 

enlargement    of    liver,    differentiation    from 

cirrhosis,  286 
infection,  portal  pysemia  and,  differentiation, 

78 
pigmentation  of  cirrhotic  liver,  305 
Malformations,  congenital  obliteration  of  bile- 
ducts  associated  with,  640 
Malignant  disease  as  cause  of  cholelithiasis,  712 
intra-abdominal,  as  cause  of  portal  throm- 
bosis, 55 
nodules  of,  ascites  due  to,  differentiation 

from  ascites  in  cirrhosis,  251 
of   gall-bladder,    primary,    620.      See    also 
Carcinoma  of  gall-bladder. 
secondary,  637 
of  larger  bile-ducts,  683 
age  in,  685 
appearance,  685 
behaviour,  687 
bile-ducts  in,  689 
clinical  picture,  690 
complications,  692 
diagnosis,  693 
differential,  693 
naked-eye,  687 
differentiation     from     carcinoma     of 
pancreas,  693 
from  catarrhal  jaundice,  695 
from  hypertrophic  biliary  cirrhosis, 

695 
from  malignant  disease  of  liver,  695 
from   primary  malignant  disease  of 
gall-bladder,  695 
etiology,  684 
frequency,  683 
gall-bladder  in,  689 
jaundice  in,  691 
liver  in,  690 


INDEX. 


787 


Malignant  disease  of  larger  bile-ducts,  micro- 
scopic appearances,  688 
morbid  anatomy,  685 
onset,  690 

relation  to  gall-stones,  684 
secondary  growths  in,  690 
sex  in,  684 
situation,  685 
symptoms,  691 
treatment,  696 
surgical,  696,  697 
of  liver,  468 
age  in,  468 
albuminuria  in,  510 
as  cause  of  portal  thrombosis,  55 
ascites  in,  505,  507 

due  to,  differentiation  from  ascites  in 
cirrhosis,  252 
blood  in,  509 
cachexia  in,  503 
clinical  features,  501 
diagnosis,  514 
differential  diagnosis,  514 
differentiation  from  carcinoma  of  gall- 
bladder, 635 
from  chronic  venous  engorgement,  518 
from  cirrhosis,  514 
from  fcecal  accumulation  in  transverse 

colon,  520 
from  gall-stone  in  common  bile-duct, 

519 
from  hydatid  cyst,  402,  516 
from    hypertrophic    biliary    cirrhosis, 

515 
from  inflammatory  thickening  around 

gall-bladder,  520 
from  intermittent  hepatic  fever,  519 
from  intra-hepatic  suppuration,  517 
from  lardaceous  liver,  515 
from     malignant     disease     of    larger 

bile-ducts,  695 
from  multilocular  hydatid,  517 
from  portal  pysemia,  79 
from  pregnancy,  520 
from  renal  tumor,  519 
from  sjTJhilitic  disease,  515 
from  tumors  of  suprarenal  body,  520 
from  universal  chronic   perihepatitis, 

173 
from  wandering  liver,  519 
duration,  513 
fever  in,  503 

gastric  disturbances  as  symptom,  512 
hsemorrhages  in,  505 
hepatic  pain  as  symptom,  512 
jaundice  in,  505,  506 
liver  in,  504 
melanuria  in,  511 
oedema  of  feet  in,  511 
peripheral  neuritis  as  symptom,  513 
physical  signs,  501 
primary,  468 

condition  of  remainder  of  liver  in,  484 
differentiation  from  secondary  malig- 
nant disease,  520 
etiology,  470 
frequency,  468 

ratio    between    frequency    of    sec- 
ondary malignant  disease  and,  485 
morbid  anatomy,  470 
sex  in,  468 

situation  of  growth,  470 
prognosis,  522 
pruritus  as  symptom,  513 
secondary,  485 
age  in,  486 

carcinoma  of  breast  as  cause,  496 
of  colon  as  cause,  496 
of  oesophagus  as  cause,  497 
condition  of  remainder  of  liver  in,  491 
degenerative  changes  in,  488 
differentiation    from    primary    malig- 
nant disease,  520 
direct  invasion  by  growth  in,  495 
formation  of  pseudo-cysts  in,  489 
frequency,  485 

ratio  V^etween  frequency  of  primary 
malignant  disease  and,  485 


Malignant  disease  of  liver,  secondary,  growths 
in,  effects  of,  490 
histology,  490 

metastasis  in,  methods  of,  493 
morbid  anatomy,  486 
primary  carcinoma  of  gall-bladder  as 
cause,  496 
growths  in,  situation  of,  495 
secondary   growths  in,   due   to   retro- 
grade embolism,  494 
sex  in,  485 
stomach  as  site  of  primary  growth, 

495 
suprarenal  glands  as  site  of  primary 

malignant  disease,  500 
umbilic'ation  in,  489 
symptoms,  512 

thoracic  signs  and  symptoms,  512 
treatment,  523 
medical.  523 
operative,  524 
urine  in,  509 
venous  hum  in,  505 
of  lung,  displaced  liver  from,  19 
of  pancreas  as  cause  of  jaundice,  547 
of  portal  thrombosis,  56 
jaundice,  563 

differentiation  from  acute  yellow  atrophy, 
578 
Malpositions,  congenital,  of  liver,  16 

of  gaU-bladder,  589 
Melcena  in  cirrhosis,  272 

treatment,   273 
Melanotic  sarcoma,  primarj',  of  liver,  483 
Melanuria  in  malignant  disease  of  liver,  511 
Membranous  cholecystitis,  603 
Menorrhagia,  in  cirrhosis,  275 
Mental  disturbance  as  cause  of  acute  yellow 
atrophy,  565 
in  cirrhosis,  276 
Mesenteric  artery,   superior,   aneurysm   of,   as 
cause  of  jaundice,  550 
glands,     suppurating,     as    cause    of    portal 

pyaemia,  70 
veins,  foreign  bodies  in,   as  cause  of  portal 
pyamia,  69 
Mesentery,  layers  of,  suppuration  between,  as 

cause  of  portal  pyeemia,  70 
Metastasis,  methods  of,  in  secondary  malignant 

disease  of  liver,  493 
Metrorrhagia  in  cirrhosis,  275 
Miliary  tuberculosis  of  liver,  339 
histology,  339 
morbid  anatomy,  338 
signs  and  sjonptoms,  340 
Milky  ascites  in  cirrhosis,  245 
Mixed  bilirubin  gaU-stones,  717 
cholesterin  gall-stones,  717 
cirrhosis,  176 
Monolobular  cirrhosis,  176 
Movable  liver,  22 
Multilobular  cirrhosis,  176,  178 
Multilocular  hydatid  of  liver,  clinical  features, 
421 
course,  422 
diagnosis,  422 
differentiation  from  malignant  disease, 

517 
duration,  422 
frequency,  419 
histology,  421 
history,  419 
morbid  anatomy,  421 
nature,  420 
prognosis,  422 
treatment,  422 
Murchison's  theory  of  lithrrmia,  39 
Muscle,  rectus,  suppuration  in,  tropical  abscess 

and,  differentiation,  150 
Myxa:>dema  as  cause  of  cholelithiasis,  712 
Myxoma  of  liver,  465 


NjEvus  of  liver,  461 
Naphthol  as  cause  of  cirrhosis,  186 
Narcosis,  chloroform,  as  cause  of  acute  yellow 
atrophy,  567 


788 


INDEX. 


Nervous  symptoms  of  cirrhosis,  276 
system  in  acute  yellow  atrophy,  573 
system    in     hypertrophic     biliary    cirrhosis, 
320 
Neuralgia  of  abdominal  sympathetic,  differen- 
tiation from  biliary  colic,  732 
of  liver,  differentiation  from  biliary  colic,  732 
Neurasthenia,  hepatoptosis  and,  26 
Neuritis,  peripheral,  as  symptom  of  malignant 
disease  of  liver,  513 
in  cirrhosis,  283 
Newborn,  cystic  disease  of  liver  in,  445 

jaundice  in,  567.    See  also  Jaundice  in  new- 
horn. 
New-growths,      obstruction      of      portal      and 
hepatic   veins    by,    as    cause    of    infarcts, 
105 
of  bile-ducts  as  cause  of  jaundice,  540 
of  kidneys  as  cause  of  jaundice,  545 
of    suprarenal    body    as    cause    of    jaundice, 

545 
tropical  abscess  and,  differentiation,  151 
Nodular  hepatitis,  455 
hyperplasia  of  liver,  455 
primary  carcinoma  of  liver,  472 
sarcoma  of  liver,  481 
Nodules  of  malignant   disease,  ascites  due  to, 

differentiation  from  ascites  in  cirrhosis,  251 
Nose,  hemorrhage  from,  in  cirrhosis,  274 
Nutmeg  liver,  85 

cardiac  lesions  as  cause,  85 

clinical  picture,  91 

complications,  94 

course,  95 

diagnosis,  95 

differentiation  from  cirrhosis,  287 

from  malignant  disease,  518 
etiology,  85 
liver  in,  92 

lung  lesions  as  cause,  85 
microscopic  appearances,  89 
morbid  anatomy,  86 
pancreas  in,  91 
physical  signs,  92 
size  of,  86 
spleen  in,  91 
symptoms,  91 
termination,  95 
treatment,  95 
urine  in,  94 


Obesity,  differentiation  from  ascites  in  cirrho- 
sis, 250 
Obliteration,    congenital,    of    bile-ducts,    639. 

See  also  Bile-ducts,  congenital  obliteration  of. 
Obstructive  biliary  cirrhosis,  326 
clinical  features,  331 
effects  on  liver,  329 
frequency,  328 
history,  326 
ligature  of  bile-ducts  on  production  of, 

326 
liver  in,  330 
morbid  anatomy,  330 
pancreas  in,  331 
pseudobile  canaliculi  in,  331 
spleen  in,  331 
treatment,  332 
jaundice,  532.     See  also  Jaundice. 
Ochronosis,  304 

CEdepaa  of  feet  as  symptom  of  cirrhosis,  239 
in  malignant  disease  of  liver,  511 
in  tropical  abscess,  141 
of  legs  in  carcinoma  of  gall-bladder,  632 
in  prognosis  of  cirrhosis,  293 
(Esophageal  yeiris,   varicose,   as  cause  of  hse- 

matemesis  in  cirrhosis,  266 
ffisopha^us,  carcinoma  of,  as  cause  of  secondary 
malignant  disease  of  liver,  497 
morbid  appearances,  in  cirrhosis,  218 
Opsiuria,  94 

Ovarian   cyst,   differentiation   from   ascites  in 
cirrhosis,  248 
from  hydatid  cyst  of  liver,  407 
papilloma,    ascites    due    to,    differentiation 

from  ascites  in  cirrhosis,  253 
tumors  as  cause  of  jaundice,  551 


Pancreas,  calculus  of,  as  cause  of  jaundice,  550 
carcinoma  of,  differentiation  from  carcinoma 
of  gall-bladder,  635 
from   malignant   disease   of  larger  bile- 
ducts,  693 
in  acute  yellow  atrophy,  573 
in  hypertrophic  biliary  cirrhosis,  316 
in  nutmeg  liver,  91 
in  obstructive  biliary  cirrhosis,  331 
in  pigmentary  cirrhosis  of  hsemochromatosis, 

302 
in  portal  pyaemia,  74 
lesions  of,  as  cause  of  jaundice,  546 
malignant  disease  of,  as  cause  of  jaundice,  547 

of  portal  thrombosis,  56 

morbid  appearances,  in  cirrhosis,  219 

Pancreatic  cysts  as  cause  of  jaundice,  548 

differentiation  from  hydatid  cysts  of  liver, 
406 
from  tropical  abscess,  150 
Pancreatitis,  acute,  differentiation  from  biliary 
cohc,  732 
from  tropical  abscess,  150 
chronic,  as  cause  of  portal  thrombosis,  56 

interstitial,  as  cause  of  jaundice,  549 
from  gall-stones  in  common  bile-ducts,  755 
gangrenous,  as  cause  of  portal  pyEemia,  70 
suppurative,  as  cause  of  portal  pysemia,  70 
Papilloma  of  bile-ducts,  681 
of  gall-bladder,  617 

ovarian,  ascites  due  to,  differentiation  from 
ascites  in  cirrhosis,  253 
Paracentesis   in    ascites    due    to    cirrhosis,    ad- 
visability of,  254 
indications  for,  255 
method  of  performing,  255 
Paralysis  in  cirrhosis,  278 
Paramcecium  coli  in  bUe-ducts,  680 
Parasites  as  cause  of  jaundice,  539 

in  portal  vein,  82 
Parasitic  affections  of  bde-ducts,  677 
of  gall-bladder,  616 
cysts  of  liver,  441 
Parasyphilitic  affections  of  liver,  366 
multilobular  cirrhosis,  378 
clinical  features,  379 
diagnosis,  379 
prognosis,  380 
treatment,  380 
Parovarian    cyst,    differentiation    from    ascites 

in  cirrhosis,  248 
Pelvic  conditions  as  cause  of  portal  pysemia,  70 
Pelvis  of  right  kidney,  rupture  into,  in  tropical 

abscess,  145 
Pentastoma  constrictum  in  bile-ducts,  679 
Perforation  of  gall-bladder  from  gall-stones,  748 
into  general  cavity  of  peritoneum,  748 
into  localised  pocket  of  peritoneum  cut 
off  by  adhesions,  748 
Pericardial  effusion,  displaced  liver  from,  19 
Pericarditic  pseudo-cirrhosis,  97 

mechanism  of  morbid  processes,  100 
microscopic  appearances,  98 
morbid  anatomy,  98 
prognosis  and  results,  101 
Pericardium,  rupture  into,  in  hydatid  cysts  of 
liver,  414 
in  tropical  abscess,  144 
Pericellular  cirrhosis,  176 

of  hereditary  syphilis,  333 
Pericholangitis,  673 
acute,  673 
chronic,  673 
intra-hepatic,  673 
tuberculous,  340 
Pericholecystic  adhesions  frorn  gall-stones,  749 
Perigastritis  as  cause  of  jaundice,  543 
Perihepatitis,  160 
acute,  160 

causation,  160 
diagnosis,  162 
morbid  anatomy,  161 
signs,  162 
symptoms,  162 
treatment,  162 
chronic,  162 

deforming,   164 
hyaline,  164 


INDEX. 


789 


Perihepatitis,  chronic,  local,  162 
treatment,  163 
concomitant,  ascites  in  cirrhosis  due  to,  243 
diffuse  chronic  hyperplastic,  164 
gumma  of  liver  resembling,  360 
universal  chronic,  97,  164 
age  in,  171 

associated     with     chronic     perihepatitis 
associated  with  arteriosclerosis  and 
granular  kidneys,  166 
with   varjdng   degrees   of   chronic   in- 
flammation of   pericardium    and 
pleura,  164 
clinical  picture,  171 
C9urse,  171 
diagnosis,  172 

diflferential,  172 
differentiation  from  chronic  tuberculous 
peritonitis,  173 
from  cirrhosis,  172 
from  malignant  disease  of  liver,  173 
from  syphilitic  gummata,  173 
heredity'  in,  171 
history,  164 
kidneys  in,  170 
liver  in,  169 
morbid  anatomy,  169 
onset,  171 
pathogeny,  164 
peritoneum  in,  170 
prognosis,  173 
sex  in,  171 
signs,  171 
spleen  in,  170 
symptoms,  171 
treatment,  173 
urine  in,  172 
Peripancreatic  cysts,  differentiation  from  hyda- 
tid cysts  of  liver,  406 
Peripheral  neuritis  as  symptom  of  malignant 
disease  of  liver,  513 
in  cirrhosis,  283 
Periphlebitis,  chronic,  of  hepatic  veins,  50 
Peritoneal    adhesions    as    cause    of     jaundice, 
545 
vascular,  surgical  treatment  of  ascites  due 
to  cirrhosis  by,  25 1 
ca\'itv,    rupture    into,    in    hvdatid    cysts    of 
liver,  412 
Peritoneum  iri  universal  chronic  perihepatitis, 
.    170         . 
inflammation    of,    concomitant,    ascites    in 

cirrhosis  due  to,  242 
rupture  and  perforation  of  gall-bladder  into, 

from  gall-stones,  762 
rupture  into,  in  tropical  abscess,  144 
secondary    infection    of,    after    rupture    in 
hydatid  cysts  of  liver,  413 
Peritonismus,  413 

Peritonitis,  acute,  ascites  due  to,  differentiation 
from  ascites  in  cirrhosis,  250 
chronic,  as  cause  of  portal  thrombosis,  56 
ascites  due  to,  differentiation  from  ascites 

in  cirrhosis,  250 
in  cirrhosis,  222,  284 
simple,  gumma  of  liver  resembling,  360 
encysted,     differentiation    from    ascites    in 

cirrhosis,  249 
in  portal  pya?mia,  74 

tuberculous,    ascites    due    to,    differentiation 
from  ascites  in  cirrhosis,  251 
chronic,     differentiation     from     universal 

chronic  perihepatitis,  173 
in  cirrhosis,  222 
Perl's  test  for  ha;mosiderin  in  liver,  436 
Phantom  tumor,   tropical  abscess  and,   differ- 
entiation, 150 
Pharynx,     hsjcmorrhage     from,     as     cause     of 

ha>matemesis  in  cirrhosis,  268 
Phlebitis,  suppurative,  of  hepatic,  veins,  51 
Phlebosclerosis,    chronic,    as    cause    of    portal 

thrombosis,  53 
Phlegmonous     cholecystitis,      610.     See     also 

Cholecystitis,  phlei/moitous. 
Phosphorus  poi.soning  as  cause  of  acute  yellow 
atrophy,  567 
differentiation  from  acute  yellow  atrophv, 
578 


Phosphorus  poisoning,  jaundice  of,  580.      See 

also  Jaundice  of  phosphorus  poisoning. 
Physiological  jaundice,  557.    See  also  Jaundice. 

idiopathic. 
Pigment,  bile,  436 

Pigmentary  cirrhosis  of  hsemochromatosis,  300 
age  in,  302 
diagnosis,  303 

differential,  304 
differentiation  from  Addison's  disease, 
304 
from  chronic  splenic  anaemia,  304 
from    hypertrophic    biliary    cirrhosis, 
304,  323 
etiologv,  300 
history,  300 
intestines  in,  302 
morbid  anatomy,  .302 
pancreas  in,  .302 
prognosis,  304 
sex  in,  302 
spleen  in,  302 
symptoms,  302 
treatment,  304 
Pigmentation,  malarial,  of  cirrhotic  liver,  305 
of  liver,  435 
extrinsic,  436 
intrinsic,  435 
Pigmented  cirrhosis,  299 
Piles  in  cirrhosis,  273 
Pleura  in  portal  pysemia,  74 
in  tropical  abscess,  134 
rupture  into,  in  hydatid  cysts  of  liver,  414 
in  tropical  abscess,  144 
Pleural  cavity,  hydatid  cj-sts  of,  differentiation 
_  from  hydatid  cysts  of  liver,  405 
right,  effusion  into,  displaced  liver  from,  18 
effusion,  tropical  abscess  and,  differentiation, 
152 
Pleurisy  with  effusion  in  cirrhosis,  282 
Pneumonia,  displaced  liver  from,  19 
Poisoning,  phosphorus,  as  cause  of  acute  yellow 
atrophy,  567 
differentiation  from  acute  yellow  atrophy, 

578 
jaundice   of,    580.      See   also   Jaundice   of 
phosphorus  poisoning. 
Poisons  conveyed  to  liver  by  portal  vein,  182 
in  circulation  as  cause  of  cirrhosis,  192 
manufactured  in  intestine  as  cause  of  cirrho- 
sis, 186 
in  spleen  as  cause  of  cirrhosis,  189 
other  than  alcohol  as  cause  of  cirrhosis,  184_ 
produced  in  liver  by  micro-organisms  in  cir- 
culation, as  cause  of  cirrhosis,  193 
Polycholia,  jaundice  from,  527,  528 
Portal  and  hepatic  vein  thrombosis  combined, 
as  cause  of  infarcts,  106 
cirrhosis,  178.     See  also  Cirrhosis. 
fissure,  gumma  in,  as  cause  of  jaundice,  543 

lymphatic  glands  in,  83 
obstruction  due  to  syphilitic  disease  of  liver, 

differentiation  from  cirrhosis,  360  * 

pj'Eemia,  67,  74 

abscess  of  spleen  as  cause,  70 

age  in,  72 

appendicitis  as  cause;  68 

ascites  in,  76 

bacteriology,  74 

blood  in,  77 

carcinoma  of  stomach  as  cause,  69 

causation,  67 

clinical  picture, -75 

constipation  in,  76 

course,  75 

diagnosis,  77 

differential,  77 
diarrha>a  in,  76 

differentiation  from  hepatic  suppuration,  78 
from  infective  endocarditis,  78 
from  intra-tlioracic  conditions,  78 
from  malarial  infection,  78 
from  malignant  disease  of  liver,  79 
from  suppurative  cholangitis,  78 
from  tropical  abscess,  77,  149 
from  typhoid  fever,  78 
duodenal  ulcer  as  cause,  69 
duration,  75 


790 


INDEX. 


Portal  pyaemia,  etiology,  72 

foreign  bodies  in  mesenteric  veins  as  cause, 

69 
gall-stones  as  cause,  71,  756 
gangrenous  pancreatitis  as  cause,  70 
hiccough  in,  76 
histology,  73 

intestinal  ulceration  as  cause,  69 
jaundice  in,  75 
liver  in,  72,  76 
morbid  anatomy,  72 
onset,  75 
pancreas  in,  74 
pelvic  conditions  as  cause,  70 
peritonitis  in,  74 
pleura  in,  74 
prognosis,  79 
rigors  in,  75 
sex  in,  72 
signs,  75 
spleen  in,  74 

enlargement  of,  76 
suppurating  mesenteric  glands  as  cause,  70 
suppuration  between  layers  of  mesentery 

as  cause,  70 
suppurative  pancreatitis  as  cause,  70 
termination,  77 
thoracic  signs,  76 
treatment,  79 

tympanitic  distension  of  abdomen  in,  76 
ulcer  of  stomach  in,  76 

as  cause,  69 
urine  in,  77 
vomiting  in,  76 
thrombosis,  52 
age  in,  58 

aneurysm  as  cause,  57 
as  cause  of  infarcts,  105 
ascites  in,  62 

due   to,  differentiation   from   ascites   in 
cirrhosis,  252 
carcinoma  of  stomach  as  cause,  55 
causation,  52 
chronic  pancreatitis  as  cause,  56 

peritonitis  as  cause,  56 
_  phlebosclerosis  as  cause,  53 
cirrhosis  as  cause,  54 
clinical  picture,  61 
diagnosis,  64 
diarrhoea  in,  63 
dilatation  of  superficial   abdominal  veins 

_  in,  63 
disease  of  portal  vein  as  cause,  53 
distribution  of,  on  portal  vein,  58 
gastro-intestinal  symptoms,  62 
gummatous  inflammation  as  cause,  57 
inflammatory  conditions  causing,  52 
intestines  in,  61 
intra-abdominal     malignant     disease     as 

cause,  55 
jaundice  in,  63 
liver  in,  59 
malignant  disease  of  liver  as  cause,  55 

of  pancreas  as  cause,  56 
morbid  anatomy,  59 
onset,  61 

pressure  on  portal  vein  as  cause,  55 
prognosis,  65 

puerperal  eclampsia  as  cause,  57 
sex  in,  58 
signs,  62 
spleen  in,  61 

enlargement  of,  62 
symptonas,  62 
syphilitic  inflammation  of  portal  vein  as 

cause,  54 
traumatism  as  cause,  57 
treatment,  65 

ulcer  of  stomach  as  cause,  53 
urine  in,  63 
vein,  calcification  of,  81 

chronic  endophlebitis  of,  80 
disease  of,  as  cause  of  portal  thrombosis,  53 
distribution  of  thrombosis  on,  58 
embolism  of,  80 

as  cause  of  infarcts,  105 
endophlebitis  of,  80 
engorgement  of,  in  cirrhosis,  treatment,  298 


Portal  vein,   entrance    of    typhoid  baciUi  into 
gaU-bladder  through,  595 
extension  of  primary  carcinoma  into,  480 
in  cirrhosis,  209 
infection,    multiple   abscess   in   connexion 

with,  157 
obstruction  of,  by  new-growth,   as  cause 

of  infarcts,  105 
parasites  in,  82 

poisons  conveyed  to  liver  by,  182 
pressure  on,  as  cause  of  portal  thrombosis, 

55 
rupture  into,  in  tropical  abscess,  146 
syphilitic    inflammation    of,    as    cause    of 

portal  thrombosis,  54 
thrombosis  of,  52.     See  also  Portal  throm- 
bosis. 
tubercle  bacilli  in  liver  through,  337 
Porto-pyeemic  liver  abscess,  67 
Postmortem  appearances  of  liver,  4 

discoloration  of  liver,  5 
Pregnancy  as  cause  of  acute  yellow  atrophy,  565 
of  cholelithiasis,  709 
_  of  jaundice,  551 
differentiation    from    malignant    disease    of 
liver,  520 
Pregnant   uterus   with   hydrops   amnii,    differ- 
entiation from  ascites  in  cirrhosis,  250 
Prolapse  of  liver,  22 

Pruritus  as  symptom  of  malignant  disease  of 
liver,  513 
in  cirrhosis,  276 
in  jaundice,  536 
treatment,  556 
Pseudobile  canaliculi  in_  cirrhosis,  196,  205 
in  hypertrophic  biliary  cirrhosis,  314 
in  obstructive  biliary  cirrhosis,  331 
Pseudo-cirrhosis,    pericarditic,    97.      See    also 

Pericarditic  pseudo-cirrhosis. 
Pseudo-cysts,     formation     of,     in     secondary 

malignant  disease  of  liver,  489 
Pseudo-tuberculosis  after  rupture  in  hydatid 

cysts  of  liver,  414 
Psorospermosis  of  bile-ducts,  678 

clinical  aspect,  679 
Puerperal  eclampsia  as  cause  of  portal  throm- 
bosis, 57 
Pulmonary  disease  as  cause  of  cholelithiasis,  711 

tuberculosis  in  cirrhosis,  221 
Pulse  in  hypertrophic  biliary  cirrhosis,  320 
Purgatives  in  ascites  due  to  cirrhosis,  262 
Pyaemia,  portal,  67.    See  also  Portal  pycemia. 
Pj'aemic  abscess,  156 

single,  as  cause  of  tropical  abscess,  125 
Pylephlebitis  adhaesiva,  52 

suppurative,  67.    See  also  Portal  pycemia. 
Pylethrombosis,  52 


Rectus  muscle,  suppuration  in,  differentiation 

from  tropical  abscess,  150 
Recurrent  hepatic  fever,  750.     See  also  Inter- 
mittent hepatic  fever. 
Regurgitation,    tricuspid,    ascites   due   to,    dif- 
ferentiation from  ascites  in  cirrhosis,  253 
Renal  colic,  differentiation  from  bUiary  colic, 
730 
disease,  ascites  due  to,  differentiation  from 
ascites  in  cirrhosis,  253 
in  cirrhosis,  223,  284 
growths,  differentiation  from  hydatid  cysts 
of  liver,  406 
Respiration  as  symptom  of  cirrhosis,  235 

in  jaundice,  535 
Respiratory    system    in    hypertrophic    biliary 

cirrhosis,  321 
Retroperitoneal  tumors  as  cause  of  jaundice, 
546 
veins,   general   communications  between,   in 
cirrhosis,  209 
Rickets,  displaced  liver  in,  18 
Riedel's  lobe,  12 

in  acute  catarrhal  cholecystitis,  599 
in  suppurative  cholecystitis,  606 
Rigors  in  portal  pyrcmia,  75 
Round-worms  as  cause  of  jaundice,  539 
Rupture  and  perforation   of  gall-bladder  into 
peritoneum  from  gall-stones,  762 


INDEX. 


791 


Rupture  in  tij-datid  cysts  of  liver,  412 
into  bile-ducts,  41.5 
into  hepatic  veins,  417 
into  intestines,  417 
into  lung,  414 
into  pericardium,  414 
into  peritoneal  cavity,  412 
into  pleura,  414 
into  stomach,  417 
into  vena  cava,  inferior,  417 
pseudo-tuberciilosis  after,  414 
secondarv    infection    of    peritoneum 
from,  413 
in  tropical  abscess,  142 

externally  onto  surface  of  body,  146 

into  bile-ducts,   145 

into  duodenum,  145 

into  gall-bladder,  145 

into  hepatic  veins,  145 

into  inferior  vena  cava,  145 

into  intestines,  145 

into  lung,  143  _ 

into  pelvis  of  right  kidney,  145 

into  pericardium,  144 

into  peritoneum,  144 

into  pleura,  144 

into  portal  vein,  146 

into  stomach,  145 


SAxrvA  in  cirrhosis,  229 

Sand,    intestinal,    differentiation    from   biliary 

colic,  731 
Sarcoma  of  liver,  melanotic,  497 

primary,  arising  in  cirrhotic  liver,  482 
diffuse,  482 
infiltrating,  482 
massive,  481 
melanotic,  483 
multiple,  481 
nodular,  481 
starting-place,  484 
with  cirrhosis,  482 
secondary,  497 

frequency,  485 
varieties,  481 
Scars  of  gall-bladder  from  gall-stones,  747 
Schnurleber,  27 

Sclerosing  cholecystitis,  atrophic,  615 
Secretions  in  jaundice,  534 
Serositis,  multiple,  97 

Single  abscess,  120.    See  al.so  Tropical  abscess. 
pysemic  abscess  as  cause  of  tropical  abscess, 
125 
Skiagraphy  in  tropical  abscess,  140 
Skin  in  cirrhosis,  227 
Solitary  tubercle  of  liver,  342 

clinical  aspect,  343 
Spa  treatment  in  cirrhosis,  296 
Spasm  of  muscular  coat  of  bile-ducts  as  cause 

of  emotional  jaundice,  541 
Spinal  curvature,  displaced  liver  in,  18 
Spleen,  abscess  of,  as  cause  of  portal  pyEemia,  70 
and  liver,  relation  between  size  of,  in  cirrho- 
sis, 217 
enlargement  of,  in  cirrhosis,  cause,  216 
in  portal  pyaemia,  76 

thrombosis,  62 
in  prognosis  of  cirrhosis,  291 
in  acute  yellow  atrophy,  573 
in  cirrhosis,  214,  238 

microscopic  appearances,  216 
morbid  appearances,  215 
in  congenital  obliteration  of  bile-ducts,  647 

syphilis  of  liver,  372 
in  hypertrophic  biliary  cirrhosis,  315,  318 
in  jaundice,  .535 
in  nutmeg  liver,  91 
in  obstructive  biliary  cirrhosis,  331 
in  pigmentary  cirrhosis  of  hajmochromatosis, 

302 
in  portal  pyaemia,  74 

thrombosis,  61 
in  suppurative  cholecystitis,  607 
in  tropical  abscess,  141 
in  universal  chronic  perihepatitis,  170 
poi-sons  manufactured  in,  as  cause  of  cirrho- 
sis, 189 


Splenic  antemia,  ascites  due  to,  differentiation 
from  ascites  in  cirrhosis,  253 
chronic,    differentiation    from    pigmentary 
cirrhosis  of  hoemochromatosis,  304 
gumma  of  liver  resembling,  363 
differentiation  from  cirrhosis,  287 
hsematemesis  due  to,  differentiation  from 
hcematemesis  in  cirrhosis,  270 
Sporadic  fibrosis,  176 

Stagnation  of  bile  as  cause  of  cholelithiasis,  706 
Stain,  iodine,  for  lardaceous  disease  of  liver,  431 
Staining    reactions    in    lardaceous    disease    of 

liver,  432 
Sterile  hydatid  cysts  of  liver,  390 
Stomach  as  site  of  primary  growth  in  secondary 
malignant  disease  of  liver,  495 
carcinoma  of,  as  cause  of  jamidice,  543 
of  portal  pysemia,  69 
thrombosis,  55 
differentiation    from    carcinoma    of    gall- 
bladder, 635 
haematemesis  due  to,  differentiation  from 
hsematemesis  in  cirrhosis,  269 
lesions  of,  as  cause  of  jaundice,  543 
morbid  appearances,  in  cirrhosis,  218 
rupture  into,  in  hydatid  cysts  of  liver,  417 

in  tropical  abscess,  145 
ulcer  of,  as  cause  of  haematemesis  in  cirrhosis 
266 
of  portal  pyfemia,  69 
thrombosis,  53 
differentiation  from  biliary  colic,  730 
haematemesis  due  to,  differentiation  from 

hsematemesis  in  cirrhosis,  269 
jaundice  from,  .543 
in  portal  pyaemia,  76 
Strangulation  of  small  intestine  complicating 

tropical  abscess,  147 
Stricture  of  bile-ducts,  653 
as  cause  of  jaundice,  540 
diagnosis,  654 
frequency,  653 
symptoms,  654 
treatment,  654 
of  hepatic  veins,  48 
symptoms,  50 
Subphrenic  abscess,  differentiation  from  hyda- 
tid cysts  of  liver,  404 
from  tropical  abscess,  148 
Sugar-iced  liver,  169 
Sulci,  diaphragmatic,  10 

Suppurating  hydatid  cyst  as  cause  of  tropical 
abscess,  125 
tropical  abscess  and,  differentiation,  148 
mesenteric  glands  as  cause  of  portal  pyaemia, 
70 
Suppuration  between  layers   of  mesentery  as 
cause  of  portal  pyaemia,  70 
hepatic,  as  cause  of  portal  pyaemia,  70 
differentiation  from  hydatid  cysts,  404 

from  portal  pyaemia,  78 
gumma  of  liver  with  fever  resembling,  362 
in  hydatid  cysts  of  liver,  418 

niechanism,  418 
in  rectus  muscle,  tropical  abscess  and,  differ- 
entiation, 150 
intra-hepatic,  differentiation  from  cirrhosis, 
288 
from  malignant  disease,  517 
Suppurative  cholangitis,   663.     See   also   Clio- 
langitis,  suppurative. 
cholecystitis,    604.      See    also    Cholecystitis, 

suppurative. 
pancreatitis  as  cause  of  portal  pyaemia,  70 
phlebitis  of  hepatic  veins,  51 
pjdephlebitis,  67.    See  also  Portal  pyceinia. 
Suprarenal  glands  as  site  of  primary  malignant 
disease  in  secondary  malignant  disease 
of  liver,  500 
new-growths  of,  as  cau.se  of  jaundice,  545 
tumors  of,  differentiation  from  malignant 
disease  of  liver,  520 
growths,  differentiation    from  hydatid  cysts 
of  liver,  406 
Swelling,  cloudy,  of  liver,  5 
Syphilis,  acquired,  of  liver,  hepatic  lesions  in, 
347 
as  cause  of  acute  yellow  atrophy,  566 


792 


INDEX, 


Syphilis  as  cause  of  cpngenital  obliteration  of 
bile-ducts,   641 
congenital,  delayed,  of  liver,  375.  _  See  also 
Tardive  hereditary  syphilis  of  liver. 
of  liver,  367 

clinical  features,  373 

diagnosis,  374 

frequency,  367 

hepatic  manifestations  of,  367 

history,  367 

kidneys  in,  372 

liver  in,  368 

microscopic  appearances,  369 
microscopic  appearances,  369 
morbid  anatomj^  368 
prognosis,  374 
spleen  in,  372 
treatment,  375 
hereditary,  pericellular  cirrhosis  of,  333 
of  liver,  347 
history,  347 

secondary  stage,  jaundice  in,  348.  See  also 
Jaundice  in  secondary  stage  of  syphilis 
of  liver.  * 

tertiary  lesions,  350.     See  also  Gumma  of 
liver. 
Syphilitic  adenitis  as  cause  of  jaundice,  542 
cicatrices  of  liver,  355 

gumma  combined  with,  356 
disease  of  liver,  ascites  due  to,  differentiation 
from  ascites  in  cirrhosis,  252 
differentiation  from   carcinoma   of  gall- 
bladder, 635 
from  cirrhosis,  287 
from   congenital   obliteration   of  bUe- 

ducts,  649 
from  malignant  disease,  515 
from  tropical  abscess,  152 
with    chronic    jaundice,     differentiation 
from    hypertrophic    biliary    cirrhosis, 
323 
gummata  of  liver,   differentiation  from  uni- 
versal chronic  perihepatitis,  173 
inilaramation    of    portal    vem    as    cause    of 
portal  thrombosis,  54 


Tabes,  hepatic  crises  in,   differentiation  from 

biliary  colic,  732 
Taenia  echinococcus,  390 
Tapping  in  hydatid  cysts  of  liver,  409 

accidents   and   bad   effects   following, 
410 
Tardive  hereditary  syphilis  of  liver,  375 
clinical  features,  367 
description,  375 
diagnosis,  377 
history,  375 
incidence,  37.5 
morbid  anatomy,  376 
prognosis,  378 
treatment,  378 
Teratoma  of  liver,  467 
Tertiary  lesions  of  syphilis  in  liver,  350.     See 

also  Gumma  of  liver. 
Test,    Cammidge's,    for   jaundice    due   to   pan- 
creatic disease,  548 
Thoracic    conditions    giving    rise   to   displaced 
_  liver,  18 
signs  and  symptoms  of  malignant  disease  of 
liver,  512 
of  portal  pvffimia,  76 
Thrm,  hydatid,  399 

Thrombosis,  combined  portal  and  hepatic  vein, 
as  cause  of  infarcts,  106 
in  cirrhosis,  285 
of  hepatic- artery,  45 
veins,  47 

diagnosis,  48 
treatment,  48 
of   inferior  vena  cava  complicating  tropical 

abscess,  147 
of  portal   vein,   52.     See  also   Portal  throm- 
bosis. 
Tight-laced  liver,  8 

clinical  features,  11 
treatment,  11 
Tight  lacing,  displaced  liver  from,  18 


Tight  lacing,  effect  on  gall-bladder,  15 
Tongue-like  lobes  of  liver,  12 
anatomy,  13 
diagnosis,  14 
frequency,  13 
physical  signs,  14 
symptoms,  14 
treatment,  14 
Torpid  liver,  40 

Toxaemia  in  production  of  cholelithiasis,  706 
Toxaemic  jaundice,  530 

differentiation  from  jaundice,  531 
Toxic  cholecystitis,  596 

Toxines,  bacterial,  in  cause  of  cirrhosis,  186 
Transposition  of  liver,  16 

Traumatism  as  cause  of  acute  cholecystitis,  696 
of  anaemic  infarcts,  107 
of  haemorrhagic  infarct,  106 
of  infarcts,  106 
of  portal  thrombosis,  57 
of  tropical  abscess,  123 
Tricuspid  regurgitation,  ascites  due  to,  differ- 
entiation from  ascites  in  cirrhosis,  253 
Trocar  in  ascites  due  to  cirrhosis,  256 
Tropical  abscess,  120 
abdomen  in,  140 

acclimatisation  as  disposing  factor,  127 
age  as  disposing  factor,  129 
alcoholism  as  disposing  factor,  128 
amosba  as  cause,  133 
appetite  in,  137 
arthritis  in,  137 
aspiration  in,  154 
bacteriology,   133 
ballottement  in,  141 
blood  in,  138 

cerebral  abscess  complicating,  146 
climate  as  disposing  factor,  126 
clinical  picture,  135 
complications,  146 
contents,  133 
cough  in,  136 
course,  141 
crepitation  in,  141 
decubitus  in,  138 
diagnosis,  147 

differential,  148 
diet  as  disposing  factor,  128 
differentiation  from  acute  hepatitis,  151 
pancreatitis,  150 
from  ascites,  152 
from  dUated  gall-bladder,  152 
from  intermittent  hepatic  fever,  150 
from  IjTnphadenoma,  152 
from  malaria,  151 
from  multiple  abscess,  149 
from  new-growth,  151 
from  pancreatic  cyst,  150 
from  phantom  tumor,  150 
from  pleural  effusion,  152 
from  portal  pyaemia,  77 
from  subphrenic  abscess,  148 
from  suppurating  hydatid  cysts,  148 
from  suppuration  in  rectus  muscle,  150 
from  suppurative  pylephlebitis,  149 
from  syphilitic  disease,  152 
from  tuberculosis,  153 
from  typhoid  fever,  151 
digestive  symptoms,  137 
disposing  factors,  126 
duration,  141 
dysentery  as  cause,  120 
escape   of  bile  from  fistula  of    operation 

wound  in,  147 
etiology,  120 
facial  aspect  in,  138 
fever  in,  135 
flatulence  in,  137 
friction  in,  141 

geographical  distribution,  126 
hepatic  dulness  in,  141 
inflammation     from     adjacent     parts     as 

cause,  124 
jaundice  in,  138 
latency  in,   135 
lungs  in,  13.5,  1.39 
malaria  as  disposing  factor,  128 
morbid  anatomy,  129 


INDEX. 


793 


Tropical  abscess,  nervous  symptoms,  137 
number,   130 

occurrence  in  England,  127 
onset,  135 
pain  in,  136 

painful  suocussion  in,  140 
pathological  appearances  of  liver  in,  130 
physical  signs,  137 
pleura  in,  134 
prognosis,  153 
pulse  in,  138 

race  as  disposing  factor  in,  127 
respiration  in,  139 

rigidity  of  upper  ijart  of  right  rectus  mus- 
cle in,  140 
rigors  in,  136 

rupture  in,  142.    See  also  Rupture  in  tropi- 
cal abscess. 
secondary  abscesses  due  to  infection  from, 

159 
sex  as  disposing  factor,  128 
shape,  130 

shoulder  pain  in,  136 
single  pysemic  abscess  as  cause,  125 
situation,  129 
size,  130 

skiagraphy  in,  140 
spleen  in,  141 

strangulation    of    small    intestine    compli- 
cating, 147 
suppurating  hydatid  cyst  as  cause,  125 
sweating  in,  135 
symptoms,   135 
tenderness  in,  136 
termination,  142 

thronabqsis    of   inferior    vena    cava    com- 
plicating, 147 
traumatism  as  cause,  123 
treatment,    154 
typhoid  fever  as  cause,  124 
urine  in.  141 
vomiting  in,  137 
wasting  in,  137 

yellow  fever  as  disposing  factor,  128 
liver,   111 
Tubercle  bacillus,  paths  of  reaching  liver,  337 
by  common  bOe-duet,  337 
by  hepatic  artery,  337 
by  lymphatics,  337 
by  portal  vein,  337 
by  umbilical  vein,  337 
solitary,  of  liver,  342 
clinical  aspect,  343 
Tuberculosis,      differentiation     from     tropical 
abscess,  153 
elsewhere    than    liver,    cirrhosis    associated 
with,  346 
effects  on  liver,  344 
in  cirrhosis,  221,  281 
miliary,    of    liver,    338.      See    also    Miliary 

tuberculosis  of  liver. 
of  bile-ducts,  336 
of  liver,  336 

cirrhosis  associated  with,  345 
forms,  338 
local,  340 
pulmonary,  in  cirrhosis,  221 
Tuberculous  abscess  in  liver,  344 
cavities  in  liver,  340 
cholangitis,  340 

disease  of  liver  involving  bile-ducts,  340 
clinical  features,  342 
etiology,  340 
histology,  342 
incidence,  340 
macroscopic  diagnosis,  341 
morbid  appearance,  341 
perichola,ngitis,  340 

peritonitis,    ascites    due    to,    differentiation 
from  ascites  in  cirrhosis,  251 
chronic,     differentiation     from     universal 

chronic  perihepatitis,  173 
in  cirrhosis,  222 
Tumors,    abdominal,    differentiation    from   as- 
cites in  cirrhosis,  249 
cystic,  of  bile-ducts,  651 
clinical  features,  652 
prognosis,  652 


Tumors,  cystic,  of  bile-ducts,  treatment,  652 
fatty,  of  gall-bladder,  619 
hepatic,  gumrna  of  liver  imitating,  361 
innocent,  of  bile-ducts,  681 

of  gall-bladder,  617 
of    kidney,    differentiation    from    malignant 

disease  of  liver,  519 
of    suprarenal    body,     differentiation    from 

malignant  disease  of  liver,  520 
phantom,   differentiation   from   tropical   ab- 
scess, 150 
retroperitoneal,  as  cause  of  jaundice,  546 
Tympanitic  distension  of    abdomen  in  portal 

pyaemia,  76 
Typhoid   bacillus,  entrance  into   gall-bladder, 
594 
by  common  bile-duct,  595 
by  hepatic  vein,  595  * 

by  portal  vein,  595 
in  production  of  cholelithiasis,  704,  705 
fever  as  cause  of  acute  cholecystitis,  593 
of  cirrhosis,  188 
of  tropical  abscess,  124 
bilious,  584 

differentiation  from  cirrhosis,  288 
from  portal  pyaemia,  87 
from  tropical  abscess,  151 
from  Weil's  disease,  587 


Ulcer,    duodenal,    as    cause    of   haematemesis 
in  cirrhosis,  266 
of  jaundice,  544 
of  portal  pysemia,  69 
differentiation  from  biliary  colic,  730,  731 
of    stomach    as    cause    of    haematemesis    in 
cirrhosis,  266 
of  portal  pyasmia,  69 
thrombosis,  53 
differentiation  from  biliary  colic,  730 
haematemesis  due  to,  differentiation  from 

haematemesis  in  cirrhosis,  269 
in  portal  pyaemia,  76 
jaundice  from,  543 
Ulceration,     intestinal,     as     cause     of    portal 
pyaemia,  69 
of  gall-bladder  from  acute  cholecystitis,  602 

into  liver,  from  gall-stones,  748 
of  hepatic  artery  from  gall-stones,  762 
Umbilical  vein  cirrhosis,  189 

tubercle  bacilli  in  liver  through,  337 
Umbilication  in  secondary  malignant  disease 

of  liver,  489 
Universal  chronic  perihepatitis,  164.     See  also 

Perihepatitis,  universal  chronic. 
Urobilin  jaundice,  231,  529 
Urotoxic  coefficient  as  symptom  of  cirrhosis, 

233 
Uterine  fibromyoma  and  gall-stones,  713 
Uterus,  pregnant,  with  hydrops  amnii,  differ- 
entiation from  ascites  in  cirrhosis,  250 


Varicose    gastric  veins  as   cause  of    haemat- 
emesis in  cirrhosis,  268 
oesophageal  veins  as  cause  of  hcematemesis 
in  cirrhosis,  266 
Vascular  symptoms  of  cirrhosis,  233 
Vater's  ampulla,  carcinoma  of,  697.     See  also 

Ampulla  of  Voter,  carcinoma  of. 
Vein,  portal.     See  also  Portal  vein. 

umbilical,  tubercle  bacLUi  in  liver  through, 
.337 
Veins,  abdominal,  superficial,  dilatation  of,  in 
portal  thrombosis,  63 
hepatic,   diseases  of,   47.     See  also  Hepatic 

veins. 
mesenteric,   foreign   bodies   in,    as   cause    of 

portal  pyffimia,  69 
retroperitoneal,  general  communications  be- 
tween, in  cirrhosis,  209 
varicose  gastric,  as  cause  of  haematemesis  in 
cirrhosis,  268 
oesophageal,  as  cause  of  hajmatemesis  in 
cirrhosis,  266 
Vena  cava,  inferior,  rupture  into,  in  hydatid 
cysts  of  liver,  417 
in  tropical  abscess,  145 


794 


INDEX. 


Vena  cava,  thrombosis  of,  complicating  tropical 

abscess,  147 
Venous  bruits  as  symptom  of  cirrliosis,  238 

cirrhosis,  178 

engorgement,  chronic,  of  liver,  85.     See  also 
Nutmeg  liver. 

hum  in  raalignant  disease  of  liver,  505 
Visceroptosis  as  cause  of  cholelithiasis,  710 

hepatoptosis  and,  26 
Vision,  yellow,  in  jaundice,  636 
Vomiting  in  cirrhosis,  treatment,  297 

in  portal  pysemia,  76 


Wandering  liver,  21 

differentiation  from  malignant  disease,  519 
Washing  as  symptom  of  cirrhosis,  229 
Waxy  disease  of  liver,  430 
Weil's  disease,  584 

bacteriology,  585 

blood  in,  586 

diagnosis,  586 

differentiation    from    catarrhal    jaundice, 
587 
from  hypertrophic  biliary  cirrhosis,  323 


Weil's    disease,    differentiation    from    typhoid 
fever,  687 

etiology,  585 

morbid  anatomy,  585 

prognosis,  687 

symptoms,  586 

treatment,  587 

urine  in,  686 
Whisky-drinker's  liver,  178 
Winckel's  disease,  562 
Worms,  round-,  as  cause  of  jaundice,  639 

Xanthopsia  in  jaundice,  536 

Yellow  atrophy,  acute,  564.     See  also  Acute 
yellow  atrophy. 
fever  as  disposing  factor  in  tropical  abscess, 

128 
gum,  557_ 
vision  in  jaundice,  536 

ZUCKERGUSSLEBER,  97,  98,  164,  169 


SAUNDERS'  BOOKS 


on 


Skin,  Genito-Urinary 
Diseases,  Chemistry,  and 
Eye,  Ear,  Nose,  and  Throat 

W.  B.  SAUNDERS   COMPANY 

925  WALNUT  STREET  PHILADELPHIA 

9,  HENRIETTA   STREET.   COVENT  GARDEN.  LONDON 


MECHANICAL    EXCELLENCE 

|kTOT  alone  for  their  literary  excellence  have  the  Saunders  publi- 
^  ^  cations  become  a  standard  on  both  sides  of  the  Atlantic :  their 
mechanical  perfection  is  as  universally  commended  as  is  their  sci- 
entific superiority.  The  most  painstaking  attention  is  bestowed 
upon  all  the  details  that  enter  into  the  mechanical  production  of  a 
book,  and  medical  journals,  both  at  home  and  abroad,  in  reviewing 
the  Saunders  publications,  seldom  fail  to  speak  of  this  distinguishing 
feature.  The  attainment  of  this  perfection  is  due  to  the  fact  that  the 
firm  has  its  own  Art  Department,  in  which  photographs  and  drawings 
of  a  very  high  order  of  merit  are  produced.  This  department  is  of 
decided  value  to  authors,  in  enabling  them  to  procure  the  services  of 
artists  specially  skilled  in  the  various  methods  of  illustrating  medical 
publications. 

A  Complete  Catalogue  of  our  Publications  will  be  Sent  upon  Request 


SAUNDERS'    BOOKS   ON 


StelwaglonV 
Diseases  of  the  Skin 


A  Treatise  on  Diseases  of  the  Skin.  For  Advanced  Students  and 
Practitioners.  By  Henry  W.  Stelwagon,  M.  D.,  Ph.D.,  Professor  of 
Dermatology  in  the  Jefferson  Medical  College,  Philadelphia.  Hand- 
some octavo  volume  of  1135  pages,  with  258  text-cuts  and  32  full- 
page  colored  lithographic  and  half-tone  plates.  Cloth,  $6.00  net ; 
Sheep  or  Half  Morocco,  $7.50  net. 

JUST       ISSUED  — NEW      (5th)       EDITION 
FIVE    LARGE    EDITIONS    IN   FIVE  YEARS 


The  demand  for  five  editions  of  this  work  in  a  period  of  five  years,  and  the 
many  gratifying  review  notices  indicate  beyond  a  doubt  the  practical  character  of 
the  book.  In  preparing  the  work  the  predominant  aim  kept  in  view  was  to  sup- 
ply the  physician  with  a  treatise  written  on  plain  and  practical  lines,  giving  abun- 
dant helpful  case  illustrations.  In  this  edition  the  section  on  Tropical  Skin 
Diseases  has  been  very  thoroughly  revised  and  a  number  of  unusual  illustrations 
added.      It  is  the  most"  up-to-date  work  on  skin  diseases  published. 


John  T.  Bowen,  M.D., 

Assistant  Professor  of  Dermatology,  Harvard  University  Medical  School,  Boston. 

"  It  gives  me  great  pleasure  to  endorse  Dr.  Stelwagon's  book.  The  clearness  of  description 
is  a  marked  feature.  It  is  also  very  carefully  compiled.  It  is  one  of  the  best  text-books  yet 
published  and  a  credit  to  American  dermatology." 

George  T.  Elliot.  M.  D., 

Professor  of  Dermatology,  Cornell  University. 
"It  is  a  book  that  I  recommend  to  my  class  at  Cornell,  because  for  conservative  judgment, 
for  accurate  observation,  and  for  a  thorough  appreciation  of  the  essential  position  of  dermatol- 
ogy, I  think  it  holds  first  place." 

Boston  Medical  and  Surgical  Journal 

"We  can  cordially  recommend  Dr.  Stelwagon's  book  to  the  profession  as  the  best  text- 
book on  dermatology,  for  the  advanced  student  and  general  practitioner,  that  has  been  brought 
strictly  up  to  date.  .  .  .  The  photographic  illustrations  are  numerous,  and  many  of  them  are 
of  great  excellence." 


DISEASES   OF   THE  EYE. 


DeSchweinitz*s 
Diseases  of  the  Eye 

Just  Issued — The  New  (5th)  Edition,  Enlarged 

Diseases  of  the  Eye :  A  Handbook  of  Ophthalmic  Practice. 
By  G.  E.  DeSchweinitz,  M.D.,  Professor  of  Ophthalmology  in  the  Uni- 
versity of  Pennsylvania,  Philadelphia,  etc.  Handsome  octavo  of  894 
pages,  313  text-illustrations,  and  6  chromo-lithographic  plates.  Cloth, 
^5.00  net;  Sheep  or  Half  Morocco,  ^6.50  net. 

WITH  313  TEXT-ILLUSTRATIONS  AND  6  COLORED  PLATES 

For  this  new  edition  the  text  has  been  very  thoroughly  revised,  and  the  work 
enlarged  by  the  addition  of  new  matter  to  the  extent  of  some  one  hundred  pages. 
There  have  been  added,  amongst  other  subjects,  chapters  on  the  following  :  X-Ray 
Treatment  of  Epithelioma,  Xeroderma  Pigmentosum  ;  Purulent  Conjunctivitis  of 
Young  Girls  ;  Jequiritol  and  Jequiritol  Serum  ;  X-ray  Treatment  of  Trachoma  ; 
Infected  Marginal  Ulcer  ;  Keratitis  Punctata  Syphilitica  ;  Uveitis  and  Its  Varieties  ; 
Eye-  ground  Lesions  of  Hereditary  Syphihs  ;  Macular  Atrophy  of  the  Retina  ; 
Worth's  Amblyoscope  ;  Stovain,  Alypin  ;  Motais'  Operation  for  Ptosis  ;  Kuhnt- 
Miiller's  Operation  for  Ectropion;  Haab's  Method  for  Foreign  Bodies;  and 
Sweet's  X-Ray  Method  of  Locahzing  Foreign  Bodies.  Other  chapters  have  been 
rewritten.     The  excellence  of  the  illustrative  feature  has  been  maintained. 


PERSONAL  AND   PRESS  OPINIONS 


Samuel  Theobald,  M.D.. 

Clinical  Professor  of  Ophthalmology,  Johns  Hopkins  University ,  Baltimore. 
"  It  is  a  work  that  I  have  held  in  high  esteem,  and  is  one  of  the  two,  or  three  books  upon 
the  eye  which  I  have  been  in  the  habit  of  recommending  to  my  students  in  the  Johns  Hopkins 
Medical  School." 

W.  Franklin  Coleman,  M.  D., 

Professor  of  Diseases  of  the  Eye,  Postgraduate  Medical  School,  Chicago. 
"I  am  very  much  pleased  with  deSchweinitz's  work  and  will  recommend  it  to  the  members 
of  my  class  as  a  most  reliable,  complete,  and  up  to  date  text-book." 

British  Medical  Journal 

"A  clearly  written,  comprehensive  manual.  One  wliich  we  can  commend  to  students  as  a 
reliable  text-book,  written  with  an  evident  knowledge  of  the  wants  of  those  entering  upon  the 
study  of  this  special  branch  of  medical  science." 


SAUNDERS'    BOOKS   ON 


GET  /ft  •  THE  NEW 

THE  BEST  J\  m  6  r  1  C  S^  H  STANDARD 

Illustrated   Dictionary 

Just  Issued — New  (4th)  Edition 


The  American  Illustrated  Medical  Dictionary.  A  new  and  com- 
plete dictionary  of  the  terms  used  in  Medicine,  Surgery,  Dentistry, 
Pharmacy,  Chemistry,  and  kindred  branches ;  with  over  loo  new  and 
elaborate  tables  and  many  handsome  illustrations.  By  W.  A.  Newman 
DoRLAND,  M.  D.,  Editor  of  "  The  American  Pocket  Medical  Diction- 
ary." Large  octavo,  nearly  840  pages,  bound  in  full  flexible  leather. 
Price,  ^4.50  net;  with  thumb  index,  ;^5.oo  net. 

WITH   2000   NEW  TERMS 

In  this  edition  the  book  has  been  subjected  to  a  thorough  revision.  The 
author  has  also  added  upward  of  two  thousand  important  new  terms  that  have 
appeared  in  medical  literature  during  the  past  few  months. 

Howard  A.  Kelly,  M.  D., 

Professor  of  Gynecology,  Johns  Hopkins  Universiiy ,  Baltimore. 

"  Dr.  Borland's  Dictionary  is  admirable.  It  is  so  well  gotten  up  and  of  such  convenient 
size.     No  errors  have  been  found  in  my  use  of  it." 

Theobald's  Prevalent  Eye  Diseases 


Prevalent  Diseases  of  the  Eye.  By  Samuel  Theobald,  M.  D,, 
Clioical  Professor  of  Ophthalmology  and  Otology,  Johns  Hopkins 
University.  Octavo  of  550 pages,  with  219  text-cuts  and  several  colored 
plates.     Cloth,  $a,.^o  net ;  Half  Morocco,  ^6.00  net. 

JUST  READY— FOR  THE  PRACTITIONER 

With  few  exceptions  all  the  works  on  diseases  of  the  eye,  although  written 
ostensibly  for  the  general  practitioner,  are  in  reality  adapted  only  to  the  specialist ; 
but  Dr.  Theobald  in  his  book  has  described  very  clearly  and  in  detail  those  condi- 
tions, the  diagnosis  and  treatment  of  which  come  within  the  province  of  the  general 
practitioner.  The  therapeutic  suggestions  are  concise,  unequivocal,  and  specific. 
It  is  the  one  work  on  the  Eye  written  particularly  for  the  general  practitioner. 

Charles  A.  Oliver.  M.D.. 

Clinical  Professor  of  Ophthabnology,   Woman's  Medical  College  of  Pennsylvania. 

"  I  feel  I  can  conscientiously  recommend  it,  not  only  to  the  general  physician  and  medical 
student,  for  whom  it  is  primarily  written,  but  also  to  the  experienced  ophthalmologist.  Most 
surely  Dr.  Theobald  has  accomplished  his  purpose." 


CHEMISTRY  AND  EYE,   EAR,   NOSE,  AND   THROAT.  5 

Wells*  Chemical  Pathology 

Chemical  Pathology.     Being  a  Discussion  of  General  Pathology 

from    the    Standpoint  of    the   Chemical  Processes  Involved.       By  H. 

Gideon  Wells,  Ph.D.,  M.D.,  Assistant  Professor  of  Pathology  in  the 

University  of  Chicago.     Octavo  of  549  pages.     Cloth,  ^3.25  net;     Half 

Morocco,  ^4.75  net. 

JUST   ISSUED 

Dr.  Wells  here  concisely  pi'esents  the  latest  work  systematically  considering  the 
subject  of  general  pathology  from  the  standpoint  of  the  chemical  processes 
involved.  It  is  written  for  the  physician,  for  those  engaged  in  research  in  pathol- 
ogy and  physiologic  chemistry,  and  for  the  medical  student.  In  the  introductory 
chapter  are  discussed  the  chemistry  and  physics  of  the  animal  cell,  giving  the 
essential  facts  of  ionization,  diffusion,  osmotic  pressure,  etc.,  and  the  relation  of 
these  facts  to  cellular  activities.  Special  chapters  are  devoted  to  Diabetes  and  to 
Uric-acid  Metabolism  and  Gout. 

Wm.  H.  Welch,  M.  D.,  Professor  of  Pathology,  fohns  Hopkins  University. 

"  The  work  fills  a  real  need  in  the  English  literature  of  a  very  important  subject,  and  I  shall 
be  glad  to  recommend  it  to  my  students." 


American  Text-Book  of 
Eye,  Ear,  Nose,  and  Throat 

American  Text=Book  of   Diseases  of   the   Eye,    Ear,  Nose,   and 

Throat.  Edited  by  G.  E.  de  Schweinitz,  M.  D.,  Professor  of  Ophthal- 
mology in  the  University  of  Pennsylvania  ;  and  B.  Alexander  Randall, 
M.  D.,  Clinical  Professor  of  Diseases  of  the  Ear  in  the  University  of 
Pennsylvania.  Imperial  octavo,  125 1  pages,  with  766  illustrations,  59 
of  them  in  colors.    Cloth,  ^7.00  net ;  Sheep  or  Half  Morocco,  $8.50  net. 

This  work  is  essentially  a  text-book  on  the  one  hand,  and,  on  the  other,  a 
volume  of  reference  to  which  the  practitioner  may  turn  and  find  a  series  of  articles 
written  by  representative  authorities  on  the  subjects  portrayed  by  them.  There- 
fore, the  practical  side  of  the  question  has  been  brought  into  prominence.  Par- 
ticular emphasis  has  been  laid  on  the  most  approved  methods  of  treatment. 

Americ&n  Journal  of  the  Medic&l  Sciences 

"  The  different  articles  are  complete,  forceful,  and,  if  one  may  be  permitted  to  use  the  term, 
'snappy,'  in  decided  contrast  to  some  of  the  labored  but  not  more  learned  descriptions  which 
have  appeared  in  the  larger  systems  of  ophthalmology." 


SAUNDERS'    BOOKS    ON 


Brtihl,  Politzer,  anb  Smith's 
Otology 


Atlas  and  Epitome  of  Otology.  By  Gustav  Bruhl,  M.  D.,  of 
Berlin,  with   the   collaboration    of  Professor   Dr.  A.   Politzer,  of 

Vienna.  Edited,  with  additions,  by  S.  MacCuen  Smith,  M.D.,  Pro- 
fessor of  Otology  in  the  Jefferson  Medical  College,  Philadelphia. 
With  244  colored  figures  on  39  Hthographic  plates,  99  text  illustra- 
tions, and  292  pages  of  text.  Cloth,  ^3.00  net.  In  Saunders'  Hand- 
Atlas  Series. 

INCLUDING  ANATOMY  AND  PHYSIOLOGY 

The  work  is  both  didactic  and  clinical  in  its  teaching.  A  special  feature  is 
the  very  complete  exposition  of  the  minute  anatomy  of  the  ear,  a  working  knowl- 
edge of  which  is  so  essential  to  an  intelligent  conception  of  the  science  of  otology. 
The  association  of  Professor  Politzer  and  the  use  of  so  many  valuable  specimens 
from  his  notably  rich  collection  especially  enhance  the  value  of  the  treatise.  The 
work  contains  everything  of  importance  in  the  elementary  study  of  otology. 

Clarence  J.  Blake,  M.  D., 

Professor  of  Otology  in  Harvard  University  Medical  School,  Boston. 

"  The  most  complete  work  of  its  kind  as  yet  published,  and  one  commending  itself  to  both 
the  student  and  the  teacher  in  the  character  and  scope  of  its  illustrations." 


Haab  and  deSch"weinitz*s 
Operative  Ophthalmology 

Atlas  and  Epitome  of    Operative    Ophthalmology.       By  Dr.  O. 

Haab,  of  Zurich.  Edited,  with  additions,  by  G.  E.  de  Schweinitz, 
M.  D.,  Professor  of  Ophthalmology  in  the  University  of  Pennsylvania. 
With  30  colored  lithographic  plates,  1 54  text-cuts,  and  375  pages  of 
text.     In  Saunders'  Hand-Atlas  Series.     Cloth,  $3.50  net. 

RECENTLY   ISSUED 

Dr.  Haab's  Atlas  of  Operative  Ophthalmology  will  be  found  as  beautiful  and 
as  practical  as  his  two  former  atlases.  The  work  represents  the  author' s  thirty 
years'  experience  in  eye  work.  The  various  operative  interventions  are  described 
with  all  the  precision  and  clearness  that  such  an  experience  brings.  Recognizing 
the  fact  that  mere  verbal  descriptions  are  frequently  insufficient  to  give  a  clear 
idea  of  operative  procedures,  Dr.  Haab  has  taken  particular  care  to  illustrate 
plainly  the  different  parts  of  the  operations. 

Johns  Hopkins  Hospital  Bulletin 

"  The  descriptions  of  the  various  operations  are  so  clear  and  full  that  the  volume  can  well 
hold  place  with  more  pretentious  text-books." 


DISEASES   OF   THE  EYE. 


Haab  and  DeSchweinitz's 
External  Diseases  qf  the  Eye 


Atlas  and  Epitome  of  External  Diseases  of  the  Eye.     By  Dr.  O. 

Haab,  of  Zurich.  Edited,  with  additions,  by  G.  E.  deSchweinitz, 
M.  D.,  Professor  of  Ophthalmology,  University  of  Pennsylvania.  With 
98  colored  illustrations  on  48  lithographic  plates  and  232  pages  of 
text.     Cloth,  33.00  net.     In  Saunders'  Hand-Atlas  Scries. 

SECOND   REVISED    EDITION— RECENTLY   ISSUED 

Conditions  attending  diseases  of  the  external  eye,  which  are  often  socompHcated, 
have  probably  never  been  more  clearly  and  comprehensively  expounded  than  in 
the  forelying  work,  in  which  the  pictorial  most  happily  supplements  the  verbal 
description.     The  price  of  the  book  is  remarkably  low. 

The  Medical  Record,  New  York 

"  The  work  is  excellently  suited  to  the  student  of  ophthalmology  and  to  the  practising 
physician.     It  cannot  fail  to  attain  a  well-deserved  popularity." 

Haab  and  DeSchweinitzV 
Ophthalmoscopy 


Atlas  and  Epitome  of  Ophthalmoscopy  and  Ophthalmoscopic 
Diagnosis.  By  Dr.  O.  Haab,  of  Ziirich.  From  the  Tliird  Revised 
and  Enlarged  German  Edition.  Edited,  with  additions,  by  G.  E. 
deSchweinitz,  M.  D.,  Professor  of  Ophthalmology,  University  of 
Pennsylvania.  With  152  colored  lithographic  illustrations  and  85 
pages  of  text.     Cloth,  $3.00  net.     In  Saunders'  Hand-Atlas  Series. 

The  great  value  of  Prof.  Haab's  Atlas  of  Ophthalmoscopy  and  Ophthalmo- 
scopic Diagnosis  has  been  fully  established  and  entirely  justified  an  English 
translation.  Not  only  is  the  student  made  acquainted  with  carefully  prepared 
ophthalmoscopic  drawings  done  into  well-executed  lithographs  of  the  most  im- 
portant fundus  changes,  but,  in  many  instances,  plates  of  the  microscopic  lesions 
are  added.     The  whole  furnishes  a  manual  of  the  greatest  possible  service. 

The  Lancet,  London 

"We  recommend  it  as  a  work  that  should  be  in  the  ophthalmic  wards  or  in  the  library  of 
every  hospital  into  which  ophthalmic  cases  are  received." 


SAUNDERS'    BOOKS     ON 


Barnhill  and  Wales'  Otology 

A  Text=Book  of  Modern  Otology.  By  John  F.  Barnhill,  M.  D., 
Professor  of  Otology,  Laryngology,  and  Rhinology,  and  Earnest  deW. 
Wales,  M.  D.,  Associate  Professor  of  Otology,  Laryngology,  and 
Rhinology,  State  College  of  Physicians  and  Surgeons,  Indianapolis. 
Octavo  of  600  pages,  with  300  original  illustrations. 

JUST  READY 

The  authors,  in  writing  this  work,  kept  ever  in  mind  the  needs  of  the  physician 
engaged  in  general  practice.  It  represents  the  results  of  personal  experience  as 
practitioners  and  teachers,  influenced  by  the  instruction  given  by  such  authorities 
as  Sheppard,  Dundas  Grant,  Percy  Jakins,  Jansen,  and  Alt.  Much  space  is  de- 
voted to  prophylaxis,  diagnosis,  and  treatment,  both  medical  and  surgical.  Great 
pains  have  been  taken  with  the  illustrations,  in  order  to  have  them  as  practical  and 
as  helpful  as  possible,  and  at  the  same  time  highly  artistic.  A  large  number  rep- 
resent the  best  work  of  Mr.  H.  F.  Aiken. 

Grunwald  and  Grayson  on  Larynx 

Atlas    and    Epitome   of    Diseases    of    the    Larynx.     By   Dr.    L. 

Grtjnwald,  of  Munich.  Edited,  with  additions,  by  Charles  P.  Gray- 
son, M.  D.,  Clinical  Professor  of  Laryngology  and  Rhinology,  Univer- 
sity of  Pennsylvania.  With  107  colored  figures  on  44  plates,  25  text- 
cuts,  and  103  pages  of  text.  Cloth,  ^2.50  net.  In  Saunders'  Hand-Atlas 
Series. 

British  Medical  Journal 

"Excels  everything  we  have  hitherto  seen  in  the  way  of  colored  illustrations  of  diseases  of  the 
larynx.  .  .  .  Not  only  valuable  for  the  teaching  of  laryngology,  it  will  prove  of  the  greatest 
help  to  those  who  are  perfecting  themselves  by  private  study." 


Saxe*s  Urinalysis 


Examination  of  the  Urine.  By  G.  A.  De  Santos  Saxe,  M.  D., 
Pathologist  to  Columbus  Hospital,  New  York  City.  i2mo  of  391 
pages,  fully  illustrated.     Flexible  leather,  ^1.50  net. 

RECENTLY  ISSUED 

This  work  is  intended  as  an  aid  in   diagnosis,    by  interpreting  the  clinical 
significance  of  the  chemic  and   microscopic   urinary  findings. 

Francis  Carter  Wood,    M.  D., 

Adjunct  Professor  of  Clinical  Pathology,    Columbia    University. 

"It  seems  to  me  to  be  one  of  the  best  of  the  smaller  works  on  this  subject ;  it  is  indeed,  better 

than  a  good  many  of  the  larger  ones." 


NOSE,    THROAT,   AND   EAR. 


Cradle's 
Nose,  Pharynx,  and  Ear 

Diseases  of  the  Nose,  Pharynx,  and  Ear.  By  Henry  Gradle, 
M.  D.,  Professor  of  Ophthalmology  and  Otology,  Northwestern  Uni- 
versity Medical  School,  Chicago.  Handsome  octavo  of  547  pages, 
illustrated,  including  two  full-page  plates  in  colors.     Cloth,  ;^3.50  net. 

INCLUDING  TOPOGRAPHIC  ANATOMY 

This  volume  presents  diseases  of  the  Nose,  Pharynx,  and  Ear  as  the  author 
has  seen  them  during  an  experience  of  nearly  twenty-five  years.  In  it  are 
answered  in  detail  those  questions  regarding  the  course  and  outcome  of  diseases 
which  cause  the  less  experienced  observer  the  most  anxiety  in  an  individual  case. 
Topographic  anatomy  has  been  accorded  liberal  space. 

Pennsylvania  Medical  Journal 

"This  is  the  most  practical  volume  on  the  nose,  pharynx,  and  ear  that  has  appeared 
recently.  ...  It  is  exactly  what  the  less  experienced  observer  needs,  as  it  avoids  the  confusion 
incident  to  a  categorical  statement  of  everybody's  opinion." 

Kyle's 
Diseases  of  Nose  anb  Throat 


Diseases  of  the  Nose  and  Throat.  By  D.  Braden  Kyle,  M,  D., 
Professor  of  Laryngology  in  the  Jefferson  Medical  College,  Phila- 
delphia; Consulting  Laryngologist,  Rhinologist,  and  Otologist,  St. 
Agnes'  Hospital.  Octavo,  669  pages;  over  184  illustrations,  and  26 
lithographic  plates   in  colors.     Cloth,  ;^4.oo  net. 

JUST  ISSUED— THE  NEW  (4th)  EDITION 

Four  large  editions  of  this  excellent  work  fully  testify  to  its  practical 
value.  In  this  edition  the  author  has  revised  the  text  thoroughly,  bringing 
it  absolutely  down  to  date.  With  the  practical  purpose  of  the  book  in  mind,  ex- 
tended consideration  has  been  given  to  treatment,  each  disease  being  considered  in 
full,  and  definite  courses  being  laid  down  to  meet  special  conditions  and  symptoms. 

Dudley  S.  Reynolds.  M.  D., 

Fortnerly  Professor  of  Ophthalmology  and  Otology,  Hospital  College  of  Medicine,  Louisville. 
"  It  is  an  important  addition  to  the  text-books  now  in  use,  and  is  better  adapted  to  the  uses 
of  the  student  than  any  other  work  with  which  I  am  familiar.     I  shall  be  pleased  to  commend 
Dr.  Kyle's  work  as  the  best  text-book." 


SAUNDERS'  BOOKS  ON 


Greene  and  Brooks* 
Genito-Urinary  Diseases 


A  Text=Book  of  Qenito=Urinary  Diseases.  By  Robert  H.  Greene, 
M.  D.,  Professor  of  Genito-Urinary  Surgery  at  Fordham  University; 
and  Harlow  Brooks,  M.  D.,  Assistant  Professor  of  Pathology,  Univer- 
sity and  Bellevue  Hospital  Medical  School.  Octavo  of  550  pages, 
profusely  illustrated. 

JUST  READY 

This  new  work  covers  completely  the  subject  of  genito-urinary  diseases,  pre- 
senting both  the  medical  and  stcrgical  sides.  It  has  been  designed  as  a  work  of 
quick  reference,  and  has  therefore  been  written  in  a  clear,  condensed  style,  so 
that  the  information  can  be  readily  grasped  and  retained.  Kidney  diseases  are 
very  elaborately  detailed,  and  especially  well  presented  is  surgery  of  the  kidney. 
The  text  is  profusely  illustrated  with  original  line-drawings. 


Gleason  on  Nose,  Throat, 
and  Ear 


A  Manual    of    Diseases   of   the    Nose,  Throat,  and    Ear.     By  E. 

Baldwin  Gleason,  M.  D.,  LL.  D.,  Clinical  Professor  of  Otology, 
Medico-Chirurgical  College,  Philadelphia.  i2mo  of  556  pages,  pro- 
fusely illustrated.     Flexible  leather,  ^2.50  net. 

JUST   ISSUED 

Anatomy,  physiology,  and  pathology  of  the  upper  respiratory  tract  and  ear 
have  been  carefully  presented,  the  author  rightly  beheving  such  knowledge  essen- 
tial to  the  efficacious  treatment  of  diseases  of  these  organs.  Methods  of  treat- 
ment have  been  simphfied  as  much  as  possible,  so  that  in  most  instances  only 
those  methods,  drugs,  and  operations  have  been  advised  which  have  proved 
essential.     A  valuable  feature  consists  of  the  collection  of  formulas. 


American  Text=Book  of  Genito=Urinary  Diseases,  Syphilis,  and 
Diseases  of  the  Skin.  Edited  by  L.  Bolton  Bangs,  M.  D.,  late 
Professor  of  Genito-Urinary  Surgery,  University  and  Bellevue  Hospital 
Medical  College,  New  York ;  and  W.  A.  Hardaway,  M.  D.,  Professor 
of  Diseases  of  the  Skin,  Missouri  Medical  College.  Octavo,  1229 
pao-es,  300  engravings,  20  colored  plates.     Cloth,  ^7.00  net. 


DISEASES   OF   THE  SKIN. 


Mracek  and  Stelwagon's 
Diseases  of  the  Skin 

Atlas  and  Epitome  of  Diseases  of  the  Skin.  By  Prof.  Dr.  Franz 
Mracek,  of  Vienna.  Edited,  with  additions,  by  Henry  W.  Stelwagon, 
M.  D.,  Professor  of  Dermatology  in  the  Jefferson  Medical  College, 
Philadelphia.  With  77  colored  plates,  50  half-tone  illustrations,  and 
280  pages  of  text.     I71  Saunders'  Hand- Atlas  Series.  Clo.,  ;^4.oonet. 

RECENTLY   ISSUED— NEW  (2nd)  EDITION 

This  volume,  the  outcome  of  years  of  scientific  and  artistic  work,  contains, 
together  with  colored  plates  of  unusual  beauty,  numerous  illustrations  in  black, 
and  a  text  comprehending  the  entire  field  of  dermatology.  The  illustrations  are 
all  original  and  prepared  from  actual  cases  in  Mracek' s  clinic,  and  the  execution 
of  the  plates  is  superior  to  that  of  any,  even  the  most  expensive,  dermatologic 
atlas  hitherto  pubhshed. 

American  Journal  of  the  Medical  Sciences 

"  The  advantages  which  we  see  in  this  book  and  which  recommend  it  to  our  minds  are: 
First,  its  handiness;  secondly,  the  plates,  which  are  excellent  as  regards  drawing,  color,  and  the 
diagnostic  points  which  they  bring  out." 

Mracek  and  Bangs' 
Syphilis  and  Venereal 

Atlas    and    Epitome   of    Syphilis    and    the    Venereal    Diseases. 

By  Prof.  Dr.  Franz  Mracek,  of  Vienna.  Edited,  with  additions,  by 
L.  Bolton  Bangs,  M.  D.,  late  Prof,  of  Genito-Urinary  Surger>-,  Univer- 
sity and  Bellevue  Hospital  Medical  College,  New  York.  With  71 
colored  plates  and  122  pages  of  text.  Cloth,  $3.50  net.  In  Saunders' 
Hand-Atlas  Series. 

CONTAINING   71    COLORED   PLATES 

According  to  the  unanimous  opinion  of  numerous  authorities,  to  whom  the 
original  illustrations  of  this  book  were  presented,  they  surpass  in  beauty  anything 
of  the  kind  that  has  been  produced  in  this  field,  not  only  in  Germany,  but 
throughout  the  literature  of  the  world. 

Robert  L.  Dickinson,  M.  D., 

Art  Editor  of  "  The  American  Text-Book  of  Obstetrics." 
"  The  book  that  appeals  instantly  to  me  for  the  strikingly  successful,  valuable,  and  graphic 
character  of  its  illustrations  is  the  'Atlas  of  Syphilis  and  the  Venereal  Diseases.'     I  know  of 
nothing  in  this  country  that  can  compare  with  it." 


12  SALWDERS'  BOOKS   ON 

Holland's  Medical 
Chemistry  and  Toxicolog(y 

A  Text=Book  of  Medical  Chemistry  and  Toxicology.     By   James 

W.  Holland,  M.  D.,  Professor  of  ]\Iedical  Chemistry  and  Toxicology^ 
and  Dean,  Jefferson  Medical  College,  Philadelphia.  Octavo  of  592 
pages,  fully  illustrated.     Cloth,  33.00  net. 

RECENTLY   ISSUED 

Dr.  Holland's  work  is  an  entirely  new  one,  and  is  based  on  his  thirty -five 
years'  practical  experience  in  teaching  chemistry  and  medicine.  Recognizing 
that  to  understand  physiologic  chemistr}',  students  must  first  be  informed  upon 
points  not  referred  to  in  most  medical  text-books,  the  author  has  included  in  his 
work  the  latest  views  of  equilibrium  of  equations,  mass  action,  cryoscopy,  os- 
motic pressure,  dissociation  of  salts  into  ions,  effects  of  ionization  upon  electric 
conductivity,  and  the  relationship  between  purin  bodies,  uric  acid,  and  urea. 
More  space  is  given  to  toxicology  than  in  any    other  text-book  on  chemistry, 

Americzin  Medicine 

"  Its  statements  are  clear  and  terse  ;  its  illustrations  well  chosen;  its  development  logical,- 
systematic,  and  comparatively  easy  to  follow.  .  .  .  We  heartily  commend  the  work." 

Griinwald  and  Newcomb*s 
Mouth,  Pharynx,  and  Nose 

Atlas  and  Epitome  of  Diseases  of  the  Mouth,  Pharynx,  and 
Nose.  By  Dr.  L.  Grunwald,  of  Munich,  From  the  Second  Revised 
and  Enlarged  German  Edition.  Edited,  with  additions,  by  James  E, 
Newcomb,  M.  D.,  Instructor  in  Laryngology,  Cornell  University  Medical 
School.  With  102  illustrations  on  42  colored  lithographic  plates,  41 
text-cuts,  and  219  pages  of  text.  Cloth,  ^3.00  net.  In  Saunders*' 
Hand- Atlas  Series. 

INCLUDING  ANATOMY  AND  PHYSIOLOGY 

In  designing  this  atlas  the  needs  of  both  student  and  practitioner  were  kept 
constantly  in  mind,  and  as  far  as  possible  typical  cases  of  the  various  diseases 
were  selected.  The  illustrations  are  described  in  the  text  in  exactly  the  same  way 
as  a  practised  examiner  would  demonstrate  the  objective  findings  to  his  class. 
The  illustrations  themselves  are  numerous  and  exceedingly  well  executed.  The 
editor  has  incorporated  his  own  valuable  experience,  and  has  also  included  exten- 
sive notes  on  the  use  of  the  active  principle  of  the  suprarenal  bodies. 

American  Medicine 

■'  Its  conciseness  without  sacrifice  of  clearness  and  thoroughness,  as  well  as  the  excellence 
of  text  and  illustrations,  are  commendable." 


EYE,    EAR,    NOSE,    AND    THROAT.  13 

Jackson  on  the  Eye 

A  Manual  of  the  Diagnosis  and  Treatment  of  Diseases  of  the  Eye. 

By  Edward  Jackson,  A.M.,  :\I.D,,  Professor  of  Ophthalmolog}-,  Uni- 
versity of  Colorado.  i2mo  volume  of  615  pages,  with  184  beautiful 
illustrations.     Cloth,  S2.50  net. 

JUST  ISSUED— NEW  (2d)  EDITION 

The  Medical  Record,  New  York 

"  It  is  truly  an  admirable  work.  .  .  .  Written  in  a  clear,  concise  manner,  it  bears  evidence 
of  the  author's  comprehensive  grasp  of  the  subject.  The  term  '  multum  in  parvo  '  is  an  appro- 
priate one  to  apply  to  this  work." 

Grant  on  the 
Face,  Mouth,  and  Jaws 

A  Text=Book  of  the  Surgical  Principles  and  Surgical  Diseases  of 
the  Face,  Mouth,  and  Jaws.  For  Dental  Students.  By  H.  Horace 
Grant,  A.  M.,  M.  D.,  Professor  of  Surgery  and  of  Clinical  Surgery, 
Hospital  College  of  Medicine,  Louisville.  Octavo  of  231  pages,  with 
68  illustrations.     Cloth,  ^2.50  net. 

Annals  of  Surgery 

"  The  book  is  well  illustrated,  the  te.xt  is  clear,  and  on  the  whole  it  serves  well  for  the 
purpose  for  which  it  is  intended." 

Friedrich  anb  Curtis* 
Nose,  Larynx,  and  Ear 

Rhinology,  Laryngology,  and  Otology,  and  Their  Significance  in 
General  Medicine.  By  Dr.  E.  P.  Friedrich,  of  Leipzig.  Edited  by 
H.  HoLBRooK  Curtis,  M.  D.,  Consulting  Surgeon  to  the  New  York- 
Nose  and  Throat  Hospital.  Octavo  volume  of  350  pages.  Cloth, 
;$2.50  net. 

Boston  Medical  and  Surgical  Journal 

"  This  task  he  has  performed  admirably,  and  has  given  both  to  the  general  practitioner  and 
to  the  specialist  a  book  for  collateral  reference  which  is  modern,  clear,  and  complete." 


14  SAUNDERS'    BOOKS    ON 

O^den  on  the  Urine 


Clinical  Examination  of  Urine  and  Urinary  Diagnosis.  A  Clinical 
Guide  for  the  Use  of  Practitioners  and  Students  of  Medicine  and  Sur- 
gery. By  J,  Bergen  Ogden,  M.  D.,  Late  Instructor  in  Chemistry, 
Harvard  University  Medical  School ;  Formerly  Assistant  in  Clinical 
Pathology,  Boston  City  Hospital.  Octavo,  418  pages,  54  illustrations, 
and  a  number  of  colored  plates.      Cloth,  ^3.00  net. 

SECOND  REVISED  EDITION— RECENTLY  ISSUED 

In  this  edition  the  work  has  been  brought  absolutely  down  to  the  present  day. 
Important  changes  have  been  made  in  connection  with  the  determination  of  Urea, 
Uric  Acid,  and  Total  Nitrogen  ;  and  the  subjects  of  Cryoscopy  and  Beta-Oxybutyric 
Acid  have  been  given  a  place.  Special  attention  has  been  paid  to  diagnosis  by 
the  character  of  the  urine,  the  diagnosis  of  diseases  of  the  kidneys  and  urinary 
passages  ;  an  enumeration  of  the  prominent  clinical  symptoms  of  each  disease  ; 
and  the  peculiarities  of  the  urine  in  certain  general  diseases. 

The  Lancet,  London 

"  We  consider  this  manual  to  have  been  well  compiled  ;  and  the  author's  own  experience, 
so  clearly  stated,  renders  the  volume  a  useful  one  both  for  study  and  reference." 

Vecki*s  Sexual  Impotence 


The  Pathology  and  Treatment  of  Sexual  Impotence.  By  Victor 
G.  Vecki,  M.  D.  From  the  Second  Revised  and  Enlarged  German. 
Edition.     i2mo  volume  of  329  pages.     Cloth,  ^2.00  net. 

THIRD   EDITION,  REVISED   AND   ENLARGED 

The  subject  of  impotence  has  but  seldom  been  treated  in  this  country  in  the 
truly  scientific  spirit  that  its  pre-eminent  importance  deserves,  and  this  volume  will 
come  to  many  as  a  revelation  of  the  possibilities  of  therapeutics  in  this  important 
field.  The  reading  part  of  the  English-speaking  medical  profession  has  passed 
judgment  on  this  monograph.  The  whole  subject  of  sexual  impotence  and  its 
treatment  is  discussed  by  the  author  in  an  exhaustive  and  thoroughly  scientific 
manner.  In  this  edition  the  book  has  been  thoroughly  revised,  and  new  matter 
has  been  added,  especially  to  the  portion  dealing  with  treatment. 

Johns  Hopkins  Hospital  Bulletin 

"  A  scientific  treatise  upon  an  important  and  much  neglected  subject.  .  .  .  The  treatment 
of  impotence  in  general  and  of  sexual  neurasthenia  is  discriminating  and  judicious." 


CHEMISTRY,  SKIN,  AND   VENEREAL   DISEASES.  15 

American  Pocket  Dictionary  Fifth  Edition.  Revved 

The  American  Pocket  Medical  Dictionary.  Edited  by  W.  A. 
Newman  Borland,  M.  D.,  Assistant  Obstetrician  to  the  Hospital 
of  the  University  of  Pennsylvania.  Containing  the  pronunciation 
and  definition  of  the  principal  words  used  in  medicine  and  kindred 
sciences.  Flexible  leather,  with  gold  edges,  ^i.oo  net;  with  thumb 
index,  ^1.25  net. 
James  W.  Holland,  M.  D., 

Professor  of  Medical  Chemistry  and  Toxicology,  and  Dean,  Jefferson  Medical  College, 
Philadelphia, 

"  I  am  struck  at  once  with  admiration  at  the  compact  size  and  attractive  exterior.  I 
can  recommend  it  to  our  students  without  reserve." 

Stelwagon-s  Essentials  of  Skin  *"£eS„XisSSd°" 

Essentials  of  Diseases  of  the  Skin.  By  Henry  W.  Stel- 
wagon,  M.  D.,  Ph.D.,  Professor  of  Dermatology  in  the  Jeffer- 
son Medical  College,  Philadelphia.  Post-octavo  of  276  pages, 
with  72  text-illustrations  and  8  plates.  Cloth,  ^i.oo  net.  In 
Saunders'  Question- Comp end  Series. 
The  Medical  News 

"  In  Hne  with  our  present  linowledge  of  diseases  of  the  slcin.  .  .  .  Continues  to  main- 
tain the  high  standard  of  excellence  for  which  these  question  compends  have  been  noted." 

Wolffs  Medical  Chemistry  ^'^RefendrissuS"' 

Essentials  of  Medical  Chemistry,  Organic  and  Inorganic 
Containing  also  Questions  on  Medical  Physics,  Chemical  Physiol- 
ogy, Analytical  Processes,  Urinalysis,  and  Toxicology.  By  Law- 
rence Wolff,  M.  D.,  Late  Demonstrator  of  Chemistry,  Jefferson 
Medical  College.  Revised  by  Smith  Ely  Jelliffe,  M.  D.,  Ph.D., 
Professor  of  Pharmacognosy,  College  of  Pharmacy  of  the  City  of 
New  York.  Post-octavo  of  222  pages.  Cloth,  ^i.oo  net.  In 
Saunders'  Question- Compend  Series. 

Martin's  Minor  Surgery,  Bandaging,  and  the  Venereal 

Diseases  second  Edition,  Revised 

Essentials  of  Minor  Surgery,  Bandaging,  and  Venereal 
Diseases.  By  Edward  Martin,  A.  M.,  M.  D.,  Professor  of  Clin- 
ical Surgery,  University  of  Pennsylvania,  etc.  Post-octavo,  166 
pages,  with  jZ  illustrations.  Cloth,  ^i.oo  net.  /;/  Saunders' 
Question- Compend  Series. 

Senn*s  Genito- Urinary  Tuberculosis 

Tuberculosis  of  the  Genito-Urinarv  Organs,  Male  and 
Female.  By  N.  Senn,  M.  D.,  Ph.  D.,  LL.  D.,  Professor  of  Surgery 
in  Rush  Medical  College.  Octavo  of  317  pages,  illustrated. 
Cloth,  $3.00  net. 


1 6  URINE,  EYE,  EAR,  NOSE,  AND    THROAT. 


Wolfs  Examination  of  Urine 

A  Laboratory  Handbook  of  Physiologic  Chemistry  and 
Urine-examination.  By  Charles  G.  L.  Wolf,  M.  D.,  Instructor  in 
Physiologic  Chemistry,  Cornell  University  Medical  College,  New 
York.    i2mo  volume  of  204  pages,  fully  illustrated.   Cloth,  $\.2^  net. 

British  Medicad  JournzJ 

"  The  methods  of  examining  the  urine  are  very  fully  described,  and  there  are  at  the 
end  of  the  book   some   extensive   tables   drawn  up  to  assist  in  urinar}-  diagnosis." 

Jackson's  Essentials  of  Eye  Third  Revised  Edition 

Essentials  of  Refraction  and  of  Diseases  of  the  Eye.  By 
Edward  Jackson,  A.  M.,  M.  D.,  Emeritus  Professor  of  Diseases  of 
the  Eye,  Philadelphia  Polyclinic.  Post-octavo  of  261  pages,  82  illus- 
trations. Cloth,  ^ 1. 00  net.  In  Saunders  Question- Compend  Series. 
Johns  Hopkins  Hospital  Bulletin 

"  The  entire  ground  is  covered,  and  the  points  that  most  need  careful  elucidation 
are  made  clear  and  easy." 

Gleason*s  Nose  and  Throat  Third  Edition,  Revised 

Essentials  of  Diseases  of  the  Nose  and  Throat.  By  E.  B. 
Gleason,  S.  B.,  M.  D.,  Chnical  Professor  of  Otology,  Medico- 
Chirurgical  College,  Philadelphia,  etc.  Post-octavo,  241  pages,  1 12 
illustrations.     Cloth,  Si.oo  net.     In  Saunders"  Question  Compends^ 

The  Lsoicet,  London 

"  The  careful  description  which  is  given  of  the  various  procedures  would  be  suflBcient 
to  enable  most  people  of  average  intelligence  and  of  slight  anatomical  knowledge  to 
make  a  very  good  attempt  at  laryngoscopy." 

Gleason*s  Diseases  of  the  Ear  Third  Edition.  Revised 

Essentials  of  Diseases  of  the  Ear.     By  E.  B.  Gleason,  S.  B., 
M.  D.,  Clinical  Professor  of  Otology,  Medico-Chirurgical  College, 
Phila.,  etc.     Post-octavo   volume  of  214  pages,  with    114  illustra- 
tions.    Cloth,  $1.00  net.      In  Saunders'  Question- Compend  Series. 
Bristol  Medico-Chirurgiced  Journal 

"We  know  of  no  other  small  work  on  ear  diseases  to  compare  with  this,  either  in 
freshness  of  style  or  completeness  of  information." 

Wilcox  on  Genito- Urinary  and  Venereal  Diseases ^^jf^^eJ 

Essentials  of  Genito-Urinary  and  Venereal  Diseases.  By 
Starling  S.  Wilcox,  M.  D.,  Professor  of  Genito-Urinar}^  Diseases 
and  Syphilology,  Starling  Medical  College,  Columbus,  Ohio.  i2mo 
of  313  pages,  illustrated.     Cloth,  ^i.oo  net.     Saunders'  Conipends. 

Stevenson's  Photoscopy  J"st  Ready 

Photoscopy.  (Skiascopy  or  Retinoscopy)     By  Mark  D.  Stev- 
enson, M.  D.,  Ophthalmic  Surgeon  to  the   Akron   City   Hospital, 
I2mo  of  126  pages,  illustrated.  Cloth,  $1.25  net. 

Dr.  Stevenson's  work  fully  and  clearly  explains  the  use  of  this  objective  test  and  eluci- 
dates the  reasons  of  the  various  phenomena  observed.  The  illustrations  have  been  drawn 
with  special  attention  to  their  practical  usefulness. 


COLUMBIA  UNIVERSITY  LIBRA^^^^^ 

0047954043 


RC845  R64 

Copy  1 
Rolleston 

Diseases  of  the  liver,  gall-bladdei 


